METHOD AND COMPOSITIONS FOR THE PREVENTION AND TREATMENT OF A HIV INFECTION

Abstract

Described herein are methods of preventing or treating a HIV infection comprising administering to a mammal in need thereof, a pharmaceutically effective amount of a CD8+ T cell vaccine composition. Such methods comprising using CD8+ T cells which have been pre-stimulated with at least one HIV epitope, to thereby enhance a CD8+ T cell immune response against HIV in said mammal.

Description

BACKGROUND

Despite antiretroviral therapy (ART), HIV-1 persists in a stable latent reservoir^1,2, primarily in resting memory CD4⁺ T cells^{3, 4}. This reservoir presents a major barrier to the cure of HIV-1 infection. To purge the reservoir, pharmacological reactivation of latent HIV-1 has been proposed⁵ and tested both in vitro and in vivo^6-8. A key remaining question is whether virus-specific immune mechanisms including cytolytic T lymphocytes (CTL) can clear infected cells in ART-treated patients after latency is reversed. Here we show that there is a striking all or none pattern for CTL escape mutations in HIV-1 Gag epitopes. Unless ART is started early, the vast majority (>98%) of latent viruses carry CTL escape mutations that render infected cells insensitive to CTLs directed at common epitopes. To solve this problem, we identified CTLs that could recognize epitopes from latent HIV-1 that were unmutated in every chronically infected patient tested. Upon stimulation, these CTLs eliminated target cells infected with autologous virus derived from the latent reservoir, both in vitro and in patient-derived humanized mice. The predominance of CTL-resistant viruses in the latent reservoir poses a major challenge to viral eradication. Our results demonstrate that chronically infected patients retain a broad spectrum viral-specific CTL response and that appropriate boosting of this response may be required for the elimination of the latent reservoir.

HIV-1 establishes latent infection in resting CD4⁺ T cells^{3, 4}. Recent efforts to eradicate HIV-1 infection have focused on reversing latency without global T cell activation⁵. However, inducing HIV-1 gene expression in latently infected cells is not sufficient to cause the death of these cells if they remain in a resting state⁹. Boosting HIV-1-specific immune responses including CTL responses may be required for clearance of the latent reservoir⁹. CTLs play a significant role in suppressing HIV-1 replication in acute infection^10-14. Because of this strong selective pressure, HIV-1 quickly acquires mutations to evade CTL recognition^{12, 13, 15-18}. CTL escape has been studied primarily through the analysis of plasma virus^{12, 13, 16, 18-20}, and CTL-based vaccines have been designed based on conserved epitopes^{21, 22}. A systematic investigation of CTL escape in the latent reservoir will be of great importance to the ongoing CTL-based eradication efforts, because latent HIV-1 likely represents the major source of viral rebound after treatment interruption. Earlier studies have suggested the presence of CTL escape mutations in proviral DNA^{15, 17}, but it still remains unclear to what extent the latent reservoir in resting CD4⁺ T cells is affected by CTL escape, whether mutations detected in proviral DNA are representative of the very small fraction of proviruses that are replication-competent, and most importantly, whether the CTL response can recognize and clear infected cells after latency is reversed. Provided herein, in part, is a CD8⁺ T cell vaccine or therapy for use against latent HIV-1 infection.

SUMMARY OF THE INVENTION

Provided herein are methods of preventing or treating a HIV infection in a mammal, such as a human. The methods involve administrating to a mammal in need thereof, a therapeutically effective amount of a CD8+ T cell vaccine composition. Such methods comprise using a CD8⁺ T cell vaccine composition which has been pre-stimulated with at least one HIV epitope, such as a HIV-1 Gag epitope, or a pool or mixture of HIV epitopes. The vaccine induces and enhances a CD8⁺ T cell immune response against HIV/AIDS in said mammal.

One aspect of the invention relates to a method of preventing or treating a HIV infection comprising administering to a mammal in need thereof, a therapeutically effective amount of a CD8⁺ T cell vaccine composition, wherein the CD8⁺ T cell has been pre-stimulated with at least one HIV epitope, to thereby enhance a CD8⁺ T cell immune response against HIV.

In certain embodiments, the pre-stimulation occurs ex-vivo.

In certain embodiments, the CD8⁺ T cell has been pre-stimulated with at least two, three, four, five, six, seven, eight, nine, or ten HIV epitopes.

In certain embodiments, the at least one HIV epitope is a subdominant epitope.

In certain embodiments, the at least one HIV epitope is a dominant epitope.

In certain embodiments, the HIV epitopes comprise subdominant and dominant epitopes.

In certain embodiments, the at least one HIV epitope is from HIV-1.

In certain embodiments, the at least one HIV epitope is selected from an epitope in the HIV-1 Gag, HIV-1 Nef, HIV-1 Rev, HIV-1 Tat, or HIV-1 Env, or combination thereof.

In certain embodiments, the at least one HIV epitope is provided in a pool or mixture of HIV epitopes.

In certain embodiments, the pool or mixture of HIV epitope is a pool or mixture of HIV-1 Gag, HIV-1 Nef, HIV-1 Rev, HIV-1 Tat, HIV-1 Env, or combination thereof.

In certain embodiments, the pool or mixture of HIV epitope is a pool or mixture of HIV-1 Gag represented by the peptide sequences set forth in Table 2, Table 4, or both.

In certain embodiments, the pool or mixture of HIV epitope is a pool or mixture of HIV-1 Nef represented by the peptide sequences set forth in Table 3.

In certain embodiments, the pool or mixture of HIV epitope is a pool or mixture of HIV-1 Rev represented by the peptide sequences set forth in Table 5.

In certain embodiments, the pool or mixture of HIV epitope is a pool or mixture of HIV-1 Tat represented by the peptide sequences set forth in Table 7.

In certain embodiments, the pool or mixture of HIV epitope is a pool or mixture of HIV-1 Env represented by the peptide sequences set forth in Table 6.

In certain embodiments, the at least one HIV epitope is an epitope in the HIV-1 Gag.

In certain embodiments, the epitope in the HIV-1 Gag is selected from any one of SEQ ID NOs: 1-17, or combination thereof.

In certain embodiments, the HIV-1 Gag is from proviral HIV-1 DNA in resting CD4+ T cells from mammals during the acute phase or chronic phase of infection.

In certain embodiments, the at least one HIV epitope is synthetic.

In certain embodiments, the at least one HIV epitope is unmutated.

In certain embodiments, the at least one HIV epitope is mutated.

In certain embodiments, the CD8⁺ T cell immune response is to subdominant epitope in HIV-1.

In certain embodiments, the CD8⁺ T cell is from CP36 or CP39.

In certain embodiments, the CD8⁺ T cell is autologous.

In certain embodiments, the CD8⁺ T cell has been pre-stimulated with at least one HIV epitope and at lease one cytokine.

In certain embodiments, the at least one cytokine is interleukin-2 (IL-2).

In certain embodiments, the CD8⁺ T cell to CD4⁺ T cell ratio is enhanced.

In certain embodiments, the CD8⁺ T cell response targets latent or reactivated HIV-1 infected cells.

In certain embodiments, the CD8⁺ T cell immune response is greater in magnitude than a CD8⁺ T cell immune response induced by administration of an unstimulated CD8⁺ T cell composition.

In certain embodiments, the CD8⁺ T cell immune response is greater in magnitude than a CD8⁺ T cell immune response induced by administration of the HIV epitope alone.

In certain embodiments, the efficacy of the immune response against HIV results in a reduction of the levels of HIV viral replication.

In certain embodiments, the reduction of levels of HIV viral replication is decreased in log₁₀ reductions of about 2-logs, 3-logs, 4-logs, 5-logs, 6-logs, 7-logs, 8-logs, or 9-logs.

In certain embodiments, the efficacy of the immune response against HIV results in a reduction of levels of plasma HIV-1 RNA.

In certain embodiments, the reduction of the levels of plasma HIV-1 RNA is in log₁₀ reductions of about 2-logs, 3-logs, 4-logs, 5-logs, 6-logs, 7-logs, 8-logs, or 9-logs.

In certain embodiments, the efficacy of the immune response against HIV results in a reduction of levels of proviral HIV-1 DNA.

In certain embodiments, the levels of provrial HIV-1 DNA is decreased 100-, 200-, 300-, 400-, 500-, 600-, 700-, 800-, 900-, 1000-, 1500-, or 2000-fold.

In certain embodiments, the efficacy of the immune response against HIV results in a reduction of the HIV-1 latent reservoir.

In certain embodiments, the HIV-1 latent reservoir is decreased 100-, 200-, 300-, 400-, 500-, 600-, 700-, 800-, 900-, 1000-, 1500-, or 2000-fold when compared to the resting CD4⁺ T cell population in any healthy or infected individual or total latently infected resting CD4⁺ T cell population.

In certain embodiments, the resting CD4⁺ T cell population in any healthy or infected individual about 10¹² cells.

In certain embodiments, the total latently infected resting CD4+T cell population is from about 10⁶ to about 10⁷ cells.

In certain embodiments, the efficacy of the immune response against HIV results in a delay in rebound of HIV viremia after cessation of antiretroviral therapy.

In certain embodiments, the delay is measured in months of about 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, or 11 months.

In certain embodiments, the mammal is a human.

In certain embodiments, the human is afflicted with HIV-1.

In certain embodiments, the human is chronically infected with HIV-1.

In certain embodiments, the human is acutely infected with HIV-1.

In certain embodiments, the CD8⁺ T cell vaccine composition is administered to a human on suppressive antiretroviral therapy.

In certain embodiments, the CD8⁺ T cell vaccine composition is administered to the antiretroviral-treated human followed by antiretroviral treatment interruption.

In certain embodiments, the CD8⁺ T cell vaccine composition is administered to the antiretroviral-treated human in combination with latency reversing therapy.

In certain embodiments, the composition is administered to the mammal more than one time over the course of treating or preventing.

In certain embodiments, the composition is administered to the mammal in need thereof at about weeks two, three, four, five, six, seven, eight, nine, ten, eleven, twelve, thirteen, fourteen, fifteen, and sixteen post-HIV infection.

In certain embodiments, the therapeutically effective amount is about 10², 10³, 10⁴, 10⁵, 10⁶, 10⁷, 10⁸, 10⁹, 10¹⁰, 10¹¹, or 10¹² prestimulated CD8⁺ T cells per infusion into a patient.

In certain embodiments, the effective amount is between about 10⁷ to 10⁹ prestimulated CD8⁺ T cells per infusion into a patient.

Other objects, features and advantages of the present invention will become apparent from the following detailed description. It should be understood, however, that the detailed description and the specific examples, while indicating preferred embodiments of the invention, are given by way of illustration only, since various changes and modifications within the spirit and scope of the invention will become apparent to those skilled in the art from this detailed description.

BRIEF DESCRIPTION OF THE DRAWINGS

FIGS. 1a-1e. CTL escape variants dominate the latent reservoir of CP-treated but not AP-treated patients. a, Frequency of variants in Gag CTL epitopes in proviruses from resting CD4⁺ T cells. Representative results of 6 patients are shown. Only optimal CTL epitopes relevant to each patient's HLA type are listed. Results from both Pacbio (left bar) and MiSeq (right bar) sequencing are shown. The effect on CTL recognition (denoted by color) is determined from information in the Los Alamos National Laboratory (LANL) HIV Molecular Immunology Database. b, CTL escape variants identified by sequencing are specific to HLA type. Frequencies of documented escape-associated variants in four well-characterized epitopes are shown for all 15 CP-treated patients. Median and P value from Mann-Whitney test are shown. c, Comparison of CTL escape variant frequency in proviruses between CP- and AP-treated patients. Only well-characterized epitopes are shown. Median and P value from Mann-Whitney test are shown. d, Characterization of CTL responses against HIV-1 Gag epitopes by interferon-γ ELISpot. The peptides tested are listed below the x-axis (black type, epitopes in which sequence variation was detected; blue type, no variation). The observed mutation is underlined in red, and CTL escape (defined by the lost of positive response) is denoted by * above the bar. The peptide concentration was 10 μg/ml. Error bars represent s.e.m., n=3. e, Sequences in Gag CTL epitopes for proviral DNA and outgrowth virus from resting CD4⁺ T cells in CP39. CTL epitopes with no observed variation are highlighted in blue. Epitopes with documented escape mutations are shaded in red.

FIGS. 2a-2c. CD8⁺ T cells pre-stimulated with a mixture of Gag peptides eliminate autologous CD4⁺ T cells infected with autologous HIV-1 from resting CD4⁺ T cells. a, Pre-stimulated CD8⁺ T cells (sCD8) eliminate autologous infected CD4⁺ T cells more efficiently than unstimulated CD8⁺ T cells (uCD8). Each symbol represents the mean of 3 replicates. Median and P value from Mann-Whitney test are shown. b, sCD8 inhibit viral growth in autologous infected CD4⁺ T cells with higher efficacy than uCD8. c, sCD8 pre-stimulated by different viral peptides eliminate autologous CD4⁺ T cells infected with viruses derived from resting CD4⁺ T cells. For b and c, results are compared with CD4 only using paired t tests. Error bars represent s.e.m., n=3. *: p<0.05; **: p<0.01; ***: p<0.001; ns: p>0.05.

FIGS. 3a-3d. CD8⁺ T cells targeting unmutated epitopes, not epitopes with identified escaped mutations, eliminate CTL escape variants. a, Frequency of variants in Gag CTL epitopes in proviruses from resting CD4⁺ T cells of CP36 and CP39. Epitopes tested with single peptide stimulation herein are denoted in colors (red or pink, epitopes with escape observed; blue, no escape observed). b, Epitope-specific CD8⁺ T cells proliferate significantly after single peptide stimulation. Only CD8⁺ cells are shown. Percentages of CFSE_low, pentamer-positive cells are indicated for unstimulated cultures (uCD8) with or without IL2, for cultures stimulated with Gag peptide mixture (sCD8) and IL2, and for cultures stimulated with the indicated single peptides and IL2. Wild type versions of peptides were used for all single peptide stimulations. c, CD8⁺ T cell proliferative responses after single peptide stimulation. Only CD8⁺ cells are shown. Percentages of CFSE_low cells are indicated. d, CD8⁺ T cells targeting unmutated epitopes, not epitopes with identified escaped mutations, eliminate autologous CD4⁺ T cells infected with CTL escape variants. uCD8: unstimulated CD8⁺ T cells; sCD8: Gag peptide mixture stimulated CD8⁺ T cells. Error bars represent s.e.m., n=3. *: p<0.05; **: p<0.01; ***: p<0.001; ns: p>0.05, paired t test.

FIGS. 4a-4h. Broad-spectrum cytotoxic T lymphocytes suppress in vivo replication of HIV-1 from the latent reservoir of the same patients in patient-derived humanized mice. a, Experimental design. b and c, Efficient engraftment of patient CP18-derived hematopoietic cells in MIS(^KI)TRG mice at week 6. Representative flow cytometry analysis (b) and summary (c) of human CD45⁺ cells, human T-lymphocyte and monocyte subsets. 11 out of 15 mice (enclosed in the rectangle) were used for HIV-1 infection. d, Correlation between frequency of peripheral human CD45⁺ cells (6 weeks after engraftment) and plasma HIV-1 RNA levels (14 days after infection). e, Depletion of peripheral CD4⁺ T cells after HIV-1 infection. *: p<0.05, paired t-test, n=11. f and g, Reduction of levels of plasma HIV-1 RNA and copies of peripheral blood HIV-1 DNA after injection of viral-specific CTLs. Filled: above detection limit; open: below detection limit. *: p<0.05, unpaired t test. h, Effect of CTL on the level of viral replication in vivo. The area under the curve of the viremia vs. time plot for each mouse in f and g before (AUC1) or after (AUC2) injection of CD8⁺ T cells was calculated to quantitatively represent viral replication over time. *: p<0.05, unpaired t test.

FIG. 5. CTL escape variants dominate the latent reservoir of CP-treated HIV-1-positive individuals, but not AP-treated individuals. Frequency of variants in Gag CTL epitopes in proviruses from resting CD4⁺ T cells. Results of all 25 patients tested are shown. Only optimal CTL epitopes relevant to each patient's HLA type are listed in linear positional order on the X axis. Results from both Pacbio (left bar) and MiSeq (right bar) sequencing platforms are shown for each epitope. The absence of bars above a listed epitope indicates that only wild type sequences were detected. For each mutation in a CTL epitope, information regarding the effect of the mutation on CTL recognition from the Los Alamos National Laboratory (LANL) HIV Molecular Immunology Database or from ELISpot assays described herein was used to assign the mutation to one of the categories indicated at the bottom. See Methods for definitions of these categories.

FIG. 6. Characterization of CTL responses against HIV-1 Gag epitopes by interferon-γ ELISpot. Results of 7 patients tested are shown. The peptides tested are listed for each patient in each graph. Error bars represent s.e.m., n=3.

FIG. 7. Partial Gag sequences from proviral DNA and outgrowth virus from resting CD4⁺ T cells of 8 CP-treated patients (following FIG. 1e). CTL epitopes with no observed variation are highlighted in blue. Documented escape mutations (red shading), inferred escape mutations (yellow shading), diminished response (pink shading), susceptible form (green shading) or undetermined variations (gray shading) in relevant optimal epitopes are indicated. See Methods for definitions of these types of mutations.

FIGS. 8a-8d. CD8⁺ T cells pre-stimulated with a mixture of consensus B Gag peptides eliminate autologous CD4⁺ T cells infected with autologous HIV-1 from resting CD4⁺ T cells. a, HIV-1 isolated from ART-treated individuals replicates as well as lab strain virus BaL. p24 values represent mean of 3 replicates. Error bars represent s.e.m., n=3. b, CD8⁺ T cells are not stimulated after co-cultured with PHA-activated CD4⁺ T cells. c, A representative flow cytometric analysis of CTL-mediated killing after co-culture of infected CD4⁺ T cells with autologous CD8⁺ T cells. CTL activity is measured by the percentage of Gag-positive, CD8-negative cells after 3 days of co-culture relative to cultures without CD8⁺ T cells. d, Pre-stimulated CD8⁺ T cells eliminate autologous infected CD4⁺ T cells more efficiently than non-stimulated CD8⁺ T cells. All results were normalized to the CD4 only control group. Error bars represent s.e.m., n=3. *: p<0.05; **: p<0.01; ***: p<0.001; ns: p>0.05, paired t test.

FIGS. 9a-9b. The elimination of infected CD4⁺ T cells is mediated by direct killing by autologous CD8⁺ T cells. a, Killing of infected CD4⁺ T cells is enhanced by increased E:T ratios for both pre-stimulated and non-stimulated CD8⁺ T cells. b, Killing of the infected CD4⁺ T cells depends on direct cell-cell contact between CD4⁺ T cells and CTLs. All results were normalized to the CD4 only control group. Error bars represent s.e.m., n=3. *: p<0.05; **: p<0.01; ***: p<0.001; ns: p>0.05, paired t test.

FIGS. 10a-10d. Viral dynamics and depletion of CD4⁺ T cells in humanized mice. a, Viral dynamics in CP18-infected MIS^(KI)TRG mice. CP18-derived MIS^(KI)TRG mice were infected with autologous HIV-1. Plasma HIV-1 RNA levels were measured from day 0 to day 56. b, Depletion of CD4 T cells in peripheral blood of HIV-1 BaL-infected mice. MIS^(KI)TRG mice engrafted with fetal liver CD34 cells were infected with HIV-1 BaL. CD4 to CD8 ratio in peripheral blood was measured by FACS from day 0 to day 29 after infection. c, Depletion of CD4 T cells in spleen of HIV-1 BaL-infected mice. MIS^(KI)TRG mice engrafted with fetal liver CD34 cells were infected with HIV-1 BaL. CD4 to CD8 ratio in spleen was measured by FACS 20 days after infection. Median and P value from Mann-Whitney test are shown. d, Detection of cell-associated HIV-1 RNA in T cells and macrophages/monocytes. CD3⁺ and CD14⁺ human cells from HIV-1-infected MIS^(KI)TRG mice from spleen and lung were purified by FACS. CD3⁻CD14⁻ cells were also collected as controls. Cell associated HIV-1 RNA was quantified by gag-specific qPCR. *: p<0.05, unpaired t test.

FIGS. 11a-11c. HIV-1 infection occurs in peripheral blood and tissues in humanized mice. a, Engraftment levels of MIS^(KI)TRG mice with fetal liver or patient CD34 cells. b, Memory CD4⁺ T cells are detected in MIS^(KI)TRG mice after infection. MIS^(KI)TRG mice were infected with HIV-1 BaL. Peripheral blood and indicated tissues from infected mice were collected at 20 dpi. Memory CD4 T cells were determined by CD45RO staining. c, Total number of cell associated HIV-1 DNA in blood and tissues. DNA Leukocytes from peripheral blood or indicated tissues were isolated for the measurement of total amount of cell-associated HIV-1 DNA by real-time PCR. For b and c, median and P value from Mann-Whitney test are shown.

FIG. 12. Broad-spectrum cytotoxic T lymphocytes suppress in vivo infection of patient-derived humanized mice with autologous latent HIV-1. Generation of patient CP36-derived humanized mice was described in FIG. 4. Mice were infected with autologous viruses at 6 weeks old. CD8 T cells from CP36 were pre-stimulated with the mixture of Gag peptides or left untreated for 6 days in vitro and were injected into mice by i.v. 9 days after infection. Plasma HIV-1 RNA and HIV-1 DNA in peripheral blood were measured by real-time PCR.

DETAILED DESCRIPTION

A. Definitions

For convenience, certain terms employed in the specification, examples, and appended claims are collected here. Unless defined otherwise, all technical and scientific terms used herein have the same meaning as commonly understood by one of ordinary skill in the art to which this invention belongs.

The articles “a” and “an” are used herein to refer to one or to more than one (i.e., to at least one) of the grammatical object of the article. By way of example, “an element” means one element or more than one element.

The term “administering” includes any method of delivery of a compound of the present invention, including but not limited to, a pharmaceutical composition, therapeutic agent, or CD8⁺ T cell vaccine composition into a subject's system or to a particular region in or on a subject. The phrases “systemic administration,” “administered systemically,” “peripheral administration,” “administered peripherally,” “infusion,” and “reinfusion” as used herein mean the administration of a compound, drug, CD8⁺ T cell vaccine composition, or other material other than directly into the central nervous system, such that it enters the patient's system and, thus, is subject to metabolism and other like processes, for example, subcutaneous administration. “Parenteral administration” and “administered parenterally” means modes of administration other than enteral and topical administration, usually by injection, and includes, without limitation, intravenous, intramuscular, intraarterial, intrathecal, intracapsular, intraorbital, intracardiac, intradermal, intraperitoneal, transtracheal, subcutaneous, subcuticular, intra-articular, subcapsular, subarachnoid, intraspinal and intrasternal injection and infusion.

The term “amino acid” is known in the art. In general the abbreviations used herein for designating the amino acids and the protective groups are based on recommendations of the IUPAC-IUB Commission on Biochemical Nomenclature (see Biochemistry (1972) 11:1726-1732). In certain embodiments, the amino acids used in the application of this invention are those naturally occurring amino acids found in proteins, or the naturally occurring anabolic or catabolic products of such amino acids which contain amino and carboxyl groups. Particularly suitable amino acid side chains include side chains selected from those of the following amino acids: glycine, alanine, valine, cysteine, leucine, isoleucine, serine, threonine, methionine, glutamic acid, aspartic acid, glutamine, asparagine, lysine, arginine, proline, histidine, phenylalanine, tyrosine, and tryptophan.

Also included are the (d) and (l) stereoisomers of such amino acids when the structure of the amino acid admits of stereoisomeric forms. The configuration of the amino acids and amino acid residues herein are designated by the appropriate symbols (d), (l) or (dl). Furthermore, when the configuration is not designated the amino acid or residue can have the configuration (d), (l) or (dl). It is to be understood accordingly that the isomers arising from such asymmetry are included within the scope of this invention. Such isomers can be obtained in substantially pure form by classical separation techniques and by sterically controlled synthesis. For the purposes of this application, unless expressly noted to the contrary, a named amino acid shall be construed to include both the (d) or (l) stereoisomers.

The terms “comprise” and “comprising” are used in the inclusive, open sense, meaning that additional elements may be included.

The term “HIV” is known to one skilled in the art to refer to Human Immunodeficiency Virus. There are two types of HIV: HIV-1 and HIV-2. There are many different strains of HIV-1. The strains of HIV-1 can be classified into three groups: the “major” group M, the “outlier” group O and the “new” group N. These three groups may represent three separate introductions of simian immunodeficiency virus into humans. Within the M-group there are at least ten subtypes or clades: e.g., clade A, B, C, D, E, F, G, H, I, J, and K. A “clade” is a group of organisms, such as a species, whose members share homologous features derived from a common ancestor. Any reference to HIV-1 in this application includes all of these strains.

The term “including” is used to mean “including but not limited to”. “Including” and “including but not limited to” are used interchangeably.

A “patient” or “subject” or “mammal” refers to either a human or non-human animal.

The term “pharmaceutical delivery device” refers to any device that may be used to administer a therapeutic agent or agents to a subject. Non-limiting examples of pharmaceutical delivery devices include hypodermic syringes, multichamber syringes, stents, catheters, transcutaneous patches, microneedles, microabraders, and implantable controlled release devices.

The phrase “pharmaceutically acceptable” is employed herein to refer to those compounds, materials, compositions, and/or dosage forms which are, within the scope of sound medical judgment, suitable for use in contact with the tissues of human beings and animals without excessive toxicity, irritation, allergic response, or other problem or complication, commensurate with a reasonable benefit/risk ratio.

The phrase “pharmaceutically-acceptable carrier” as used herein means a pharmaceutically-acceptable material, composition or vehicle, such as a liquid or solid filler, diluent, excipient, or solvent encapsulating material, involved in carrying or transporting the subject compound from one organ, or portion of the body, to another organ, or portion of the body. Each carrier must be “acceptable” in the sense of being compatible with the other ingredients of the formulation and not injurious to the patient. Some examples of materials which can serve as pharmaceutically-acceptable carriers include: (1) sugars, such as lactose, glucose and sucrose; (2) starches, such as corn starch and potato starch; (3) cellulose, and its derivatives, such as sodium carboxymethyl cellulose, ethyl cellulose and cellulose acetate; (4) powdered tragacanth; (5) malt; (6) gelatin; (7) talc; (8) excipients, such as cocoa butter and suppository waxes; (9) oils, such as peanut oil, cottonseed oil, safflower oil, sesame oil, olive oil, corn oil and soybean oil; (10) glycols, such as propylene glycol; (11) polyols, such as glycerin, sorbitol, mannitol and polyethylene glycol; (12) esters, such as ethyl oleate and ethyl laurate; (13) agar; (14) buffering agents, such as magnesium hydroxide and aluminum hydroxide; (15) alginic acid; (16) pyrogen-free water; (17) isotonic saline; (18) Ringer's solution; (19) ethyl alcohol; (20) pH buffered solutions; (21) polyesters, polycarbonates and/or polyanhydrides; and (22) other non-toxic compatible substances employed in pharmaceutical formulations.

The terms “polypeptide”, “peptide” and “epitope” are used interchangeably herein to refer to polymers of amino acids. The polymer may be linear or branched, it may comprise modified amino acids, and it may be interrupted by non-amino acids. The terms also encompass an amino acid polymer that has been modified; for example, disulfide bond formation, glycosylation, lipidation, acetylation, phosphorylation, or any other manipulation, such as conjugation with a labeling component.

In certain embodiments, peptides of the invention may be synthesized chemically, ribosomally in a cell free system, or ribosomally within a cell. Chemical synthesis of polypeptides of the invention may be carried out using a variety of art recognized methods, including stepwise solid phase synthesis, semi-synthesis through the conformationally-assisted re-ligation of peptide fragments, enzymatic ligation of cloned or synthetic peptide segments, and chemical ligation. Native chemical ligation employs a chemoselective reaction of two unprotected peptide segments to produce a transient thioester-linked intermediate. The transient thioester-linked intermediate then spontaneously undergoes a rearrangement to provide the full length ligation product having a native peptide bond at the ligation site. Full length ligation products are chemically identical to proteins produced by cell free synthesis. Full length ligation products may be refolded and/or oxidized, as allowed, to form native disulfide-containing protein molecules (see e.g., U.S. Pat. Nos. 6,184,344 and 6,174,530; and T. W. Muir et al., Curr. Opin. Biotech. (1993): vol. 4, p 420; M. Miller, et al., Science (1989): vol. 246, p 1149; A. Wlodawer, et al., Science (1989): vol.

245, p 616; L. H. Huang, et al., Biochemistry (1991): vol. 30, p 7402; M. Schnolzer, et al., Int. J. Pept. Prot. Res. (1992): vol. 40, p 180-193; K. Rajarathnam, et al., Science (1994): vol. 264, p 90; R. E. Offord, “Chemical Approaches to Protein Engineering”, in Protein Design and the Development of New therapeutics and Vaccines, J. B. Hook, G. Poste, Eds., (Plenum Press, New York, 1990) pp. 253-282; C. J. A. Wallace, et al., J. Biol. Chem. (1992): vol. 267, p 3852; L. Abrahmsen, et al., Biochemistry (1991): vol. 30, p 4151; T. K. Chang, et al., Proc. Natl. Acad. Sci. USA (1994) 91: 12544-12548; M. Schnlzer, et al., Science (1992): vol., 3256, p 221; and K. Akaji, et al., Chem. Pharm. Bull. (Tokyo) (1985) 33: 184).

As known to one skilled in the art, “retroviruses” are diploid positive-strand RNA viruses that replicate through an integrated DNA intermediate (proviral DNA). In particular, upon infection by the RNA virus, the lentiviral genome is reverse-transcribed into DNA by a virally encoded reverse transcriptase that is carried as a protein in each retrovirus. The viral DNA is then integrated pseudo-randomly into the host cell genome of the infecting cell, forming a “provirus” which is inherited by daughter cells. The retrovirus genome contains at least three genes: Gag codes for core and structural proteins of the virus; Pol codes for reverse transcriptase, protease and integrase; and Env codes for the virus surface proteins. Within the retrovirus family, HIV is classified as a lentivirus, having genetic and morphologic similarities to animal lentiviruses such as those infecting cats (feline immunodeficiency virus), sheep (visna virus), goats (caprine arthritis-encephalitis virus), and non-human primates (simian immunodeficiency virus).

B. Methods of Preventing or Treating a HIV Infection

Provided are methods of preventing or treating a lentiviral infection, such as a HIV infection, comprising administering to a mammal in need thereof, a therapeutically effective amount of a CD8⁺ T cell vaccine composition, wherein the CD8⁺ T cell has been pre-stimulated with at least one HIV epitope, to thereby enhance a CD8⁺ T cell immune response against HIV.

The term “effective amount” as used herein means an amount effective and at dosages and for periods of time necessary to achieve the desired result. The term “mammal” as used herein includes all members of the animal kingdom including non-humans and humans. In certain embodiments, the mammal may be a human. The human may be afflicted with HIV-1. The human may be chronically infected or acutely infected with HIV-1. The human may be on suppressive antiretroviral therapy. In certain embodiments, the pre-stimulated CD8+ T cell vaccine composition can be reinfused only in antiretroviral therapy (ART)-treated individuals, reinfused only in untreated individuals, reinfused only in ART-treated individuals, followed by antiretroviral treatment interruption, or reinfused combined with latency reversing therapy in ART-treated individuals.

In certain embodiments, the CD8⁺ T cell vaccine composition is administered to the patient more than one time over the course of treating or preventing.

In certain embodiments, the efficacy of the CD8⁺ T cell vaccine composition may relate to HIV latency and the ability to remain off of antiretroviral therapy without HIV rebound. In certain embodiments, these measures include reduction in proviral DNA. The estimated number of HIV proviruses per infected person on therapy are 10⁸ to 10⁹. In certain embodiments, the reductions in proviral DNA that result in a delay in rebound may be on the order of about 100- to 1000-fold reductions. In other embodiments, these measures included reduction in the total number of resting CD4⁺ T cells in any healthy or infected individual would be approximately 10¹² using well-known methods in the art of measuring reservoir size. In other embodiments, these measures included reduction in the total latently infected resting CD4 T cell population appears to be between 10⁶ and 10⁷ cells. In certain embodiments, a 1000-fold reduction would result in significant delay in rebound when off antiretroviral therapy. In other embodiments, efficacy is measured in delay in rebound of HIV viremia after cessation of antiretroviral therapy measured in months.

C. Therapeutically Effective CD8⁺ T Cell Vaccine Compositions

A therapeutically effective amount of a CD8⁺ T cell vaccine composition comprises CD8⁺ T cells which have been pre-stimulated with at least one HIV epitope, to thereby enhance a CD8⁺ T cell immune response.

The pre-stimulation occurs ex-vivo and may include incubating the CD8⁺ T cells with at least one cytokine in addition to the at least one HIV epitope. The CD8⁺ T cell may be derived from CP36 or CP39. The CD8⁺ T cell may be autologous to the mammal.

The HIV epitopes may include at least 2, 3, 4, 5, 6, 7, 8, 9, 10, 15, 20, 30, 40, 50, 60, 70, 80, 90, 100, 125, 150, 175, 200, 225, 250, 275, 300, 325, 350, 375, 400, 425, 450, 475, or 500 HIV epitopes. The at least one HIV epitope may be a subdominant or dominant epitope. The at least two HIV epitopes may comprise subdominant and dominant epitopes.

In certain embodiments, the CD8⁺ T cell response may target latent or reactivated HIV-1 infected cells. In certain embodiments, the CD8⁺ T cell immune response may be greater in magnitude than a CD8⁺ T cell immune response induced by administration of an unstimulated CD8⁺ T cell composition. In other embodiments, the CD8⁺ T cell immune response is greater in magnitude than a CD8⁺ T cell immune response induced by administration of the HIV epitope alone. The CD8⁺ T cell immune response may be in response to a subdominant epitope(s) in HIV-1.

In certain embodiments, the at least one HIV epitope may be from HIV-1. In certain embodiments, the at least one HIV epitope may be from HIV-2. In certain embodiments, the at least one HIV epitope may be selected from an epitope in the HIV-1 Gag, HIV-1 Nef, HIV-1 Rev, HIV-1 Tat, or HIV-1 Env. In certain embodiments, the HIV epitope may be provided singly, or in combination as a mixture or pool of HIV peptides. In certain embodiments, the pool or mixture of HIV peptides are defined by the Gag peptides in Table 2 and Table 4 (i.e., NIH AIDS Reagent 8117). In certain embodiments, the pool or mixture of HIV peptides are defined by the Nef peptides in Table 3 (i.e., NIH AIDS Reagent 5189). In certain embodiments, the pool or mixture of HIV peptides are defined by the Rev peptides in Table 5 (i.e., NIH AIDS Reagent 6445). In certain embodiments, the pool or mixture of HIV peptides are defined by the Tat peptides in Table 7 (i.e., NIH AIDS Reagent 5138). In certain embodiments, the pool or mixture of HIV peptides are defined by the Env peptides in Table 6 (i.e., NIH AIDS Reagent 9480). Said mixtures or pools of HIV peptides may comprise different combinations of the HIV peptides set for the in Tables 2-7. In certain embodiments, the at least one HIV epitope is an epitope in HIV-1 Gag. In certain embodiments, the HIV-1 Gag epitopes may be selected from ISPRTLNAW (SEQ ID NO: 1), LSPRTLNAW (SEQ ID NO: 2), TSTLQEQIGW (SEQ ID NO: 3), TSNLQEQIGW (SEQ ID NO: 4), QASQEVKNW (SEQ ID NO: 5), QSTQEVKNW(SEQ ID NO: 6), KAFSPEVIPMF (SEQ ID NO: 7), SLYNTVATL (SEQ ID NO: 8), SLFNTVAVL (SEQ ID NO: 9), WASRELERF (SEQ ID NO: 10), TLNAWVKVV (SEQ ID NO: 11), RLRPGGKKK (SEQ ID NO: 12), RLRPGGKKS (SEQ ID NO: 13), LYNTVATLY (SEQ ID NO: 14), LFNTIAALF (SEQ ID NO: 15), TPQDLNTML (SEQ ID NO: 16), or GPGHKARVL (SEQ ID NO: 17). In certain embodiments, the HIV Env epitope is found in the consensus Subtype B sequence as follows:

(SEQ ID NO: 18)
MRVKGIRKNYQHLWRWGTMLLGMLMICSAAEKLWVTVYYGVPVWKEATTT
LFCASDAKAYDTEVHNVWATHACVPTDPNPQEVVLENVTENFNMWKNNMV
EQMHEDIISLWDQSLKPCVKLTPLCVTLNCTDLMNATNTTNSSSGEKMEK
GEIKNCSFNITTSIRDKVQKEYALFYKLDVVPIDNDNTSSYRLISCNTSV
ITQACPKVSFEPIPIHYCAPAGFAILKCNDKKFNGTGPCTNVSTVQCTHG
IRPVVSTQLLLNGSLAEEEVVIRSENFTNNAKTIIVQLNESVEINCTRPN
NNTRKSIHIGPGRAFYTTGEIIGDIRQAHCNISRAKWNNTLKQIVKKLRE
QFGNKTIVFNQSSGGDPEIVMHSFNCGGEFFYCNTTQLFNSTWNVNGTWN
NNTEGNDTITLPCRIKQIINMWQEVGKAMYAPPIRGQIRCSSNITGLLLT
RDGGNNNTNETEIFRPGGGDMRDNWRSELYKYKVVKIEPLGVAPTKAKRR
VVQREKRAVGIGAMFLGFLGAAGSTMGAASMTLTVQARQLLSGIVQQQNN
LLRAIEAQQHLLQLTVWGIKQLQARVLAVERYLKDQQLLGIWGCSGKLIC
TTTVPWNASWSNKSLDEIWDNMTWMEWEREIDNYTSLIYTLIEESQNQQE
KNEQELLELDKWASLWNWFDITNWLWYIKIFIMIVGGLIGLRIVFAVLSI
VNRVRQGYSPLSFQTRLPAPRGPDRPEGIEEEGGERDRDRSGRLVDGFLA
LIWDDLRSLCLFSYHRLRDLLLIVTRIVELLGRRGWEVLKYWWNLLQYWS
QELKNSAVSLLNATAIAVAEGTDRVIEVVQRACRAILHIPRRIRQGLERA
LL.

In certain embodiments, the HIV epitope may be synthetic and may be chemically synthesized as described in section “A” above. In other embodiments, the HIV epitopes may be mutated or unmutated. Other HIV epitopes may be deep sequences from from proviral HIV-1 DNA in resting CD4⁺ T cells from mammals during the acute phase or chronic phase of infection (see examples section of instant specification).

The present invention further features methods comprising the administration of an effective amount a CD8⁺ T cell vaccine composition, wherein the composition comprises CD8⁺ T cells which have been pre-stimulated with at least one HIV epitope, or a pool or mixure of HlVepitodes set forth in Tables 2-7, to thereby enhance a CD8⁺ T cell immune response, as described above. Dosage levels of between about 10², 10³, 10⁴, 10⁵, 10⁶, 10⁷, 10⁸, 10⁹, 10¹⁰, 10¹¹, or 10¹² cells per infusion into a patient may be useful as a vaccine injection in the methods described herein. The amount of active ingredient that may be combined with the carrier materials to produce a single dosage form will vary depending upon the host treated and the particular mode of administration. The dose of the vaccine may vary according to factors such as the infection state, age, sex, and weight of the individual, and the ability of CD8⁺ T cell vaccine composition to elicit a desired response in the individual. Dosage regime may be adjusted to provide the optimum therapeutic response. For example, several divided doses may be administered daily or the dose may be proportionally reduced as indicated by the exigencies of the therapeutic situation. The dose of the vaccine may also be varied to provide optimum preventative or treatment dose response depending upon the circumstances.

In certain embodiments, the dosage may enhance the CD8⁺ T cell to CD4⁺ T cell ratio. The efficacy of the prevention or treatment of the methods of the present invention may be determined from samples obtained from the mammal after treatment has began using the following. In certain embodiments, the efficacy is determined comparing a sample of a mammal obtained during the course of treatment to a sample which has been previously obtained from the patient, such as at the start of treatment or in an initial sample obtained two, three, or four weeks post HIV infection but prior to treatment. In certain embodiments, the levels of HIV viral replication is decreased in a plasma sample when compared to a plasma sample previously obtained from the mammal prior to initiation of treatment. The levels of HIV viral replication may be decreased in terms of log₁₀ reductions of about 2-logs, 3-logs, 4-logs, 5-logs, 6-logs, 7-logs, 8-logs, or 9-logs. In certain embodiments, the levels of plasma HIV-1 RNA may be decreased in a plasma sample when compared to a plasma sample previously obtained from the mammal prior to initiation of treatment. The levels of plasma HIV-1 RNA may be decreased in terms of log₁₀ reductions of about 2-logs, 3-logs, 4-logs, 5-logs, 6-logs, 7-logs, 8-logs, or 9-logs. In other embodiments, the levels of proviral HIV-1 DNA may be decreased 100-, 200-, 300-, 400-, 500-, 600-, 700-, 800-, 900-, 1000-, 1500-, or 2000-fold. The fold reduction may be calculated as a reduction from an estimated 10⁸ or 10⁹ HIV provirus per infected person on antiretroviral therapy. In other embodiments, the efficacy of the CD8⁺ T cell vaccine composition can be determined when the HIV-1 latent reservoir is decreased 100-, 200-, 300-, 400-, 500-, 600-, 700-, 800-, 900-, 1000-, 1500-, or 2000-fold when compared to the resting CD4+ T cell population in any healthy or infected individual or total latently infected resting CD4+ T cell population using well known methods in the art to measure the reservoir size. In certain embodiments, the resting CD4⁺ T cell population in any healthy or infected individual is about 10¹² cells. In certain embodiments, the total latently infected resting CD4⁺ T cell population is from about 10⁶ to about 10⁷ cells. Such fold reductions may result in significant delay in rebound when off of antiretroviral therapy. In other embodiments, the efficacy of the CD8⁺ T cell vaccine composition relate to HIV latency and the ability of the patient to remain off of antiretroviral therapy without HIV rebound. In certain embodiments, efficacy of the CD8⁺ T cell vaccine composition can be determined by the delay in rebound of HIV viremia after cessation of antiretroviral therapy. Typically, a rebound of HIV viremia may occur in a couple of weeks in patients who have stopped antiretroviral therapy. In certain embodiments a significant delay may be measured in months of about 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, or 11 months.

The compositions of the invention are suitable for administration to subjects in a biologically compatible form in vivo. The expression “biologically compatible form suitable for administration in vivo” as used herein means a form of the substance to be administered in which any toxic effects are outweighed by the therapeutic effects. The substances may be administered to any animal, preferably humans.

The CD8⁺ T cell vaccine composition of the present invention may additionally contain suitable diluents, adjuvants and/or carriers. Preferably, the vaccines contain an adjuvant which can enhance the immunogenicity of the vaccine in vivo. The adjuvant may be selected from many known adjuvants in the art including the lipid-A portion of gram negative bacteria endotoxin, trehalose dimycolate of mycobacteria, the phospholipid lysolecithin, dimethyldictadecyl ammonium bromide (DDA), certain linear polyoxypropylene-polyoxyethylene (POP-POE) block polymers, aluminum hydroxide, liposomes and CpG (cytosine-phosphate-guanidine) polymers. The vaccines may also include cytokines that are known to enhance the immune response including GM-CSF, IL-2, IL-12, TNF and IFNγ.

The vaccines of the instant invention may be formulated and introduced as a vaccine through oral, intradermal, intramuscular, intraperitoneal, intravenous, subcutaneous, intranasal, and intravaginal, or any other standard route of immunization.

In formulations of the subject vaccines, wetting agents, emulsifiers and lubricants, such as sodium lauryl sulfate and magnesium stearate, as well as coloring agents, releasing agents, coating agents, sweetening, flavoring and perfuming agents, preservatives and antioxidants may be present in the formulated agents.

Subject compositions may be suitable for oral, nasal, topical (including buccal and sublingual), rectal, vaginal, aerosol and/or parenteral administration. The formulations may conveniently be presented in unit dosage form and may be prepared by any method well known in the art of pharmacy. The amount of composition that may be combined with a carrier material to produce a single dose may vary depending upon the subject being treated, and the particular mode of administration.

Methods of preparing these formulations include the step of bringing into association compositions of the present invention with the carrier and, optionally, one or more accessory ingredients. In general, the formulations are prepared by uniformly and intimately bringing into association agents with liquid carriers, or finely divided solid carriers, or both, and then, if necessary, shaping the product.

Formulations suitable for oral administration may be in the form of capsules, cachets, pills, tablets, lozenges (using a flavored basis, usually sucrose and acacia or tragacanth), powders, granules, or as a solution or a suspension in an aqueous or non-aqueous liquid, or as an oil-in-water or water-in-oil liquid emulsion, or as an elixir or syrup, or as pastilles (using an inert base, such as gelatin and glycerin, or sucrose and acacia), each containing a predetermined amount of a subject composition thereof as an active ingredient. Compositions of the present invention may also be administered as a bolus, electuary, or paste.

In solid dosage forms for oral administration (capsules, tablets, pills, dragees, powders, granules and the like), the subject composition is mixed with one or more pharmaceutically acceptable carriers, such as sodium citrate or dicalcium phosphate, and/or any of the following: (1) fillers or extenders, such as starches, lactose, sucrose, glucose, mannitol, and/or silicic acid; (2) binders, such as, for example, carboxymethylcellulose, alginates, gelatin, polyvinyl pyrrolidone, sucrose and/or acacia; (3) humectants, such as glycerol; (4) disintegrating agents, such as agar-agar, calcium carbonate, potato or tapioca starch, alginic acid, certain silicates, and sodium carbonate; (5) solution retarding agents, such as paraffin; (6) absorption accelerators, such as quaternary ammonium compounds; (7) wetting agents, such as, for example, acetyl alcohol and glycerol monostearate; (8) absorbents, such as kaolin and bentonite clay; (9) lubricants, such a talc, calcium stearate, magnesium stearate, solid polyethylene glycols, sodium lauryl sulfate, and mixtures thereof; and (10) coloring agents. In the case of capsules, tablets and pills, the compositions may also comprise buffering agents. Solid compositions of a similar type may also be employed as fillers in soft and hard-filled gelatin capsules using such excipients as lactose or milk sugars, as well as high molecular weight polyethylene glycols and the like.

A tablet may be made by compression or molding, optionally with one or more accessory ingredients. Compressed tablets may be prepared using binder (for example, gelatin or hydroxypropylmethyl cellulose), lubricant, inert diluent, preservative, disintegrant (for example, sodium starch glycolate or cross-linked sodium carboxymethyl cellulose), surface-active or dispersing agent. Molded tablets may be made by molding in a suitable machine a mixture of the subject composition moistened with an inert liquid diluent. Tablets, and other solid dosage forms, such as dragees, capsules, pills and granules, may optionally be scored or prepared with coatings and shells, such as enteric coatings and other coatings well known in the pharmaceutical-formulating art.

Liquid dosage forms for oral administration include pharmaceutically acceptable emulsions, microemulsions, solutions, suspensions, syrups and elixirs. In addition to the subject composition, the liquid dosage forms may contain inert diluents commonly used in the art, such as, for example, water or other solvents, solubilizing agents and emulsifiers, such as ethyl alcohol, isopropyl alcohol, ethyl carbonate, ethyl acetate, benzyl alcohol, benzyl benzoate, propylene glycol, 1,3-butylene glycol, oils (in particular, cottonseed, groundnut, corn, germ, olive, castor and sesame oils), glycerol, tetrahydrofuryl alcohol, polyethylene glycols and fatty acid esters of sorbitan, and mixtures thereof.

Suspensions, in addition to the subject composition, may contain suspending agents as, for example, ethoxylated isostearyl alcohols, polyoxyethylene sorbitol and sorbitan esters, microcrystalline cellulose, aluminum metahydroxide, bentonite, agar-agar and tragacanth, and mixtures thereof.

Formulations for rectal or vaginal administration may be presented as a suppository, which may be prepared by mixing a subject composition with one or more suitable non-irritating excipients or carriers comprising, for example, cocoa butter, polyethylene glycol, a suppository wax or a salicylate, and which is solid at room temperature, but liquid at body temperature and, therefore, will melt in the body cavity and release the active agent. Formulations, which are suitable for vaginal administration also include pessaries, tampons, creams, gels, pastes, foams or spray formulations containing such carriers as are known in the art to be appropriate.

Dosage forms for transdermal administration of a subject composition includes powders, sprays, ointments, pastes, creams, lotions, gels, solutions, patches and inhalants. The active component may be mixed under sterile conditions with a pharmaceutically acceptable carrier, and with any preservatives, buffers, or propellants, which may be required.

The ointments, pastes, creams and gels may contain, in addition to a subject composition, excipients, such as animal and vegetable fats, oils, waxes, paraffins, starch, tragacanth, cellulose derivatives, polyethylene glycols, silicones, bentonites, silicic acid, talc and zinc oxide, or mixtures thereof.

Powders and sprays may contain, in addition to a subject composition, excipients such as lactose, talc, silicic acid, aluminum hydroxide, calcium silicates and polyamide powder, or mixtures of these substances. Sprays may additionally contain customary propellants, such as chlorofluorohydrocarbons and volatile unsubstituted hydrocarbons, such as butane and propane.

Compositions of the present invention may alternatively be administered by aerosol. This is accomplished by preparing an aqueous aerosol, liposomal preparation or solid particles containing the compound. A non-aqueous (e.g., fluorocarbon propellant) suspension could be used. Sonic nebulizers may be used because they minimize exposing the agent to shear, which may result in degradation of the compounds contained in the subject compositions.

Ordinarily, an aqueous aerosol is made by formulating an aqueous solution or suspension of a subject composition with conventional pharmaceutically acceptable carriers and stabilizers. The carriers and stabilizers vary with the requirements of the particular subject composition, but typically include non-ionic surfactants (Tweens, Pluronics, or polyethylene glycol), innocuous proteins like serum albumin, sorbitan esters, oleic acid, lecithin, amino acids such as glycine, buffers, salts, sugars or sugar alcohols. Aerosols generally are prepared from isotonic solutions.

In addition, vaccines may be administered parenterally as injections (intravenous, intramuscular or subcutaneous). The vaccine compositions of the present invention may optionally contain one or more adjuvants. Any suitable adjuvant can be used, such as CpG polymers, aluminum hydroxide, aluminum phosphate, plant and animal oils, and the like, with the amount of adjuvant depending on the nature of the particular adjuvant employed. In addition, the anti-infective vaccine compositions may also contain at least one stabilizer, such as carbohydrates such as sorbitol, mannitol, starch, sucrose, dextrin, and glucose, as well as proteins such as albumin or casein, and buffers such as alkali metal phosphates and the like.

Pharmaceutical compositions of this invention suitable for parenteral administration comprise a subject composition in combination with one or more pharmaceutically-acceptable sterile isotonic aqueous or non-aqueous solutions, dispersions, suspensions or emulsions, or sterile powders which may be reconstituted into sterile injectable solutions or dispersions just prior to use, which may contain antioxidants, buffers, bacteriostats, solutes which render the formulation isotonic with the blood of the intended recipient or suspending or thickening agents.

Examples of suitable aqueous and non-aqueous carriers, which may be employed in the pharmaceutical compositions of the invention, include water, ethanol, polyols (such as glycerol, propylene glycol, polyethylene glycol, and the like), and suitable mixtures thereof, vegetable oils, such as olive oil, and injectable organic esters, such as ethyl oleate. Proper fluidity may be maintained, for example, by the use of coating materials, such as lecithin, by the maintenance of the required particle size in the case of dispersions, and by the use of surfactants. Further, the CD8⁺ T cell vaccine compositions may be encapsulated in liposomes and administered via injection.

All references cited herein are all incorporated by reference herein, in their entirety, whether specifically incorporated or not. All publications, patents, or patent applications cited herein are hereby expressly incorporated by reference for all purposes. In case of conflict, the definitions within the instant application govern.

Having now fully described this invention, it will be appreciated by those skilled in the art that the same can be performed within a wide range of equivalent parameters, concentrations, and conditions without departing from the spirit and scope of the invention and without undue experimentation.

The present description is further illustrated by the following examples, which should not be construed as limiting in any way.

EXAMPLES

Methods

• Human subjects. Peripheral blood or bone marrow for the isolation of primary CD4⁺, CD8⁺ or CD34⁺ T cells was obtained from 30 HIV-1-infected patients (Table 1) and 7 healthy adult volunteers. All patients had been on antiretroviral therapy (ART) for at least 2 years and had maintained undetectable plasma HIV-1 RNA levels (<50 copies/ml) for at least 1 year prior to study. 10 AP-treated patients were recruited from the OPTIONS cohort at the University of California San Francisco (UCSF). This study was approved by the Johns Hopkins Internal Review Board and by the UCSF Committee on Human Research. Written informed consent was provided by all study participants. HLA typing for each patient was performed by the Johns Hopkins University Immunogenetics Laboratory.
• Sample preparation for deep sequencing. Peripheral blood mononuculear cells (PBMCs) were isolated from whole blood by Ficoll gradient separation. CD4⁺ T cells were purified from PBMCs by negative selection using CD4⁺ Isolation Kit II (Miltenyi). Resting CD4⁺ T cells were then purified from CD4⁺ T cells by negative selection using CD25, CD69 and HLA-DR microbeads (Miltenyi). Genomic DNA was extracted from 5 million resting CD4⁺ T cells from each patient using QlAamp DNA Mini Kit (Qiagen). The gag gene was amplified from genomic DNA by a two-round nested PCR using these primers: 5′ outer primer (5′-TTGACTAGCGGAGGCTAGAAGG-3′); 3′ outer primer (5′-GATAAAACCTCCAATTCCCCCTATC-3); 5′inner primer (5′-GAGAGATGGGTGCGAGAGCGTC-3′); 3′ inner primer (5′-CTGCTCCTGTATCTAATAGAGC-3′). For each patient, the entire genomic DNA from 5 million of resting CD4⁺ T cells was evenly distributed as template into 80 PCR reactions. The reactions were performed by using High Fidelity Plantinum Taq Polymerase (Life Technologies) following manufacturer's instruction. PCR amplicons were purified by gel extraction after gel electrophoresis.
• Deep sequencing. For PacBio RS single molecule sequencing, amplicons were barcoded with a group of 10 bp indexes and then multiple samples were pooled together to generate smrtbell sequencing library following Pacific Biosciences template preparation and sequencing-C2 user guide for 2 kb insert size and using Pacific Bioscience DNA template preparation kit. For MiSeq Sequencing, the pooled amplicon DNA was end repaired, adenylated, and ligated to Illumina TruSeq adaptors and PCR enriched for 10 cycles. The resulting library was then run on bioanalyzer high sensitivity DNA chip for size and concentration determination. The library was then sequenced on MiSeq for paired end 250 bp reads. The sequence reads from PacBio and MiSeq were demultiplexed using Fastx-Toolkit.
• Data analysis for deep sequencing results. For the paired MiSeq reads, the two reads were first merged using FLASH³¹. MiSeq and PacBio reads from each individual were then aligned to the reference HIV-1 consensus B Gag sequence using Bowtie2³². Custom program was written using perl scripts to identify and compute the frequency of all sequence variants that caused non-synonymous amino acid changes in each individual's relevant optimal Gag epitopes (based on reported information in the HIV Molecular

Immunology Database, Los Alamos National Laboratory, http://www.hiv.lanl.gov/content/immunology/index.html) according to their HLA type. For each individual, variants that occurred at a frequency >3% were retained. Additional for PacBio reads, sequences with identified premature stop codons were eliminated from the analyzed results. For each identified variation, the mutation type regarding CTL recognition was determined by matching with the information in the above-mentioned database. The five mutation types adopted in this paper are: Documented Escape (no CTL response when patient cells are challenged with the variant peptide), Inferred Escape (variant is predicted to be an escape mutant by longitudinal study or transmission study, but the reactivity of the variant is not tested experimentally), Diminished Response (experimental data suggest partial escape as evidenced by decreased CTL response), Susceptible Form (CTL response is elicited when patient cells are challenged with the variant peptide) and Mutation Type Not Determined (no experimental data on CTL recognition of this variant).

• Elispot essays. The Elispot assays were performed using Human IFN-γ ELISpot PLUS kit (Mabtech) according to previously described³³ and manufacturer's instructions. PBMCs were added at 200,000 cells per well and synthetic peptides were added in a final concentration of 0.1, 1 or 10 μg/ml. A response is considered positive if it was 3 fold higher than the mean background (cell only control) and greater than 55 SFC/million cells. The number of specific T cells was calculated by subtracting the mean background values.
• Recovery and sequencing of patient viruses from resting CD4⁺ T cells. Co-culture assays were performed to recover and amplify replication-competent viruses as previously described³⁴. The viruses were recovered from five to ten million resting CD4⁺ T cells. The concentration of outgrowth viruses was determined by p24 ELISA (PerkinElmer). Total RNA of outgrowth viruses was extracted using Trizol LS reagent (Life Technologies). Residual DNA was then removed by TURBO DNase (Life Technologies) treatment. First strand cDNA was synthesized using SuperScript III Reverse Transcriptase (Life Technologies) and the gag gene was amplified from cDNA using the gag outer primer pair mentioned above. The PCR amplicons were then purified by gel extraction and sequenced by regular Sanger sequencing.
• In vitro HIV-1 infection. PBMCs from HIV-1-infected patients and healthy donors were stimulated by adding 0.5 μg/ml Phytohaemagglutinin (PHA) and IL-2 (100 U/ml) to basal media (RPMI with 10% heat-inactivated fetal bovine serum and antibiotics) for three days prior to isolation of CD4⁺ T cells. Each patient's activated CD4⁺ T cells were infected with viruses recovered from the same patient's resting CD4⁺ T cells. Healthy donor's CD4⁺ cells were infected with a lab strain virus, BaL. Virus concentration used in infection was equivalent to the p24 concentration of 200 ng/ml. All infections were performed by centrifugation of target cells with virus at 1,200 g for 2 hours.
• Stimulation of CD8⁺ T cells. PBMCs from CP-treated patients were cultured in the presence of IL-2 (100 U/ml) with a mixture of consensus B Gag (or Nef, Rev, Tat, Env) peptides (800 ng/ml for each) (NIH AIDS Reagent Program), or with individual synthetic peptide (0.5 μ/ml) (Genemed Synthesis). CD8⁺ T cells were purified after six days of incubation by positive selection using human CD8 microbeads (Miltenyi). To monitor CTL proliferation, PBMCs were stained with CFSE (Life Technologies) prior to incubation and with relevant pentamer (Proimmune) after incubation. PBMCs were then stained with CD8-APC (Becton Dickson, BD) and analyzed by flow cytometry using FACS Canto II (BD).
• Co-culture of autologous CD4⁺ and CD8⁺ T cells. Three hours after infection, CD4⁺ T cells were mixed with autologous unstimulated or stimulated CD8⁺ T cells at 1:1 ratio in basal media at 5 million cells per ml. Two days after co-culture, enfuvirtide (T-20, Roche) was added into the culture at 10 μM to prevent further infection events except if the measurement was p24 ELISA. Three days after co-culture, cells were stained with CD8-APC (BD) first, fixed and permeabilized with Cytoperm/Cytofix (BD pharmingen), then stained for intracellular p24 Gag (PE, Coulter). Cells were analyzed by flow cytometry using FACS Canto II (BD). For measurement of viral growth, 5 μl of supernatant was taken from the co-culture at Days 0, 3 and 6, and subjected to p24 ELISA. For analysis of cell contact dependence, CD4⁺ and CD8⁺ T cells were placed in separate chambers of trans-well plates (0.4 μm, Costar).
• Generation and infection of patient-derived humanized mice. The previously reported MISTRG mouse in the Rag2^−/− Il2rg^−/− 129×Balb/c (N2) genetic background harbors knock-in replacement of the endogenous mouse Csf1, Csf2, Il3 and Tpo genes with humanized version and a BAC transgene encoding human SIRPα²⁵. We generate Sirpa^(KI) mouse which harbors a knock-in replacement of the endogenous mouse Sirpa gene with a humanized version. Sirpa^(KI) mouse will be thoroughly described elsewhere. The improved MIS^(KI)TRG mouse was generated by breeding Sirpa^(KI) mice to MITRG mice. All animal experimentations were performed in compliance with Yale Institutional Animal Care and Use Committee protocols. MIS^(KI)TRG mice were maintained with continuous treatment with enrofloxacin in the drinking water (Baytril, 0.27 mg/ml). Patient bone marrow or fetal liver CD34⁺ cells were isolated by CD34 microbeads selection (miltenyi). Newborn mice (within first 3 days of life) were sublethally irradiated (X-ray irradiation with X-RAD 320 irradiator, PXi; 1×150 cGy) and 100,000 fetal liver or 250,000 patient CD34⁺ cells in 20 μl of PBS were injected into the liver with a 22-gauge needle (Hamilton Company). 6-8 weeks after engraftment, mice engrafted with patient CD34⁺ cells were infected by i.v. with HIV-1 (100 ng p24) which was recovered and expanded from the resting CD4⁺ T cells of the same patient (CD34⁺ cell donor), as mentioned above. Mice engrafted with fetal liver CD34⁺ cells were infected by i.v. with HIV-1 BaL (100 ng p24). Mice with less than 5% human CD45⁺ cells in the peripheral blood were excluded from the infection study. Mice with more than 70% human CD45 ⁺ cells in the peripheral blood were also excluded because they were unhealthy due to human macrophage/monocytes caused anemia³³. 20 million autologous CD8⁺ T cells with or without pre-stimulation were injected by i.v. 9 or 14 days after infection. Group allocation was blinded. Peripheral blood samples were collected by retro-orbital bleeding at different time points before and after injection of CD8⁺ T cells. Engraftment of human CD45⁺ cells as well as lymphoid and myeloid subsets was determined by flow cytometry. Plasma HIV-1 RNA in peripheral blood was measured by one-step reverse transcriptase (Invitrogen) real-time PCR using the following primers and probe, described previously⁸: forward (5′→3′) ACATCAAGCAGCCATGCAAAT, reverse (5′→3′) TCTGGCCTGGTGCAATAGG and probe (5′→3′) VIC-CTATCCCATTCTGCAGCTTCCTCATTGATG-TAMRA. Assay sensitivity is 200 RNA copies per ml of plasma. HIV-1 DNA in peripheral blood was also measured by real time PCR using the same primers and probe mentioned above, with assay sensitivity at 5 copies per 100 μl of blood. Total viral DNA in PBMCs was determined by measuring copies of viral DNA/100 μl blood and blood volume per mouse (80 μl blood/1 g body weight). To quantitate total viral DNA in tissues, spleens, livers and lungs of infected mice were collected. For the spleen, single-cell suspensions were treated with ACK lysis buffer. Liver and lung leukocytes were isolated by digesting tissues with 100 U/ml collagenase IV and 0.02 mg/ml DNase I (Sigma), followed by density gradient centrifugation.
• Statistical analysis. For comparison of HIV-1 variant frequency (FIGS. 1b and c) and viral infection in HIV-1 BaL-infected mice (FIGS. 10 and 11), we applied Mann-Whitney tests. For comparison of inhibitory effect of autologous CTLs (FIG. 2a), we applied a Wilcoxon matched pairs test. For comparison of viral replication in humanized mice (FIGS. 4f, g and h), we applied an unpaired t test. For all other comparisons, paired t tests were applied. All tests were calculated by the GraphPad Prism 6 software, and conducted as two-tailed tests with a type I error rate of 5%.

To investigate CTL escape variants in the latent reservoir, the proviral HIV-1 DNA in resting CD4⁺ T cells from 25 patients was deep sequenced (Table 2). Among them, 10 initiated ART during the acute phase (AP, within 3 months of infection) while the other 15 initiated ART during the chronic phase (CP) of infection. The sequencing was focused on Gag because it is an important target of the CTL response²³ and is highly conserved, which facilitates detection of escape variants. Prior data from our lab showed that previously documented CTL escape variants completely dominated the viral reservoirs of nearly all CP-treated patients (FIG. 5 and Table 2). This trend is especially obvious for several well characterized CTL epitopes: the HLA-A2-restricted epitope SLYNTVATL (SL9), the HLA-A3-restricted epitope RLRPGGKKK (RK9) and the HLA-B57/58-restricted epitope TSTLQEQIGW (TW10) (FIG. 1a and FIG. 5). In these epitopes, close to 100% of the sequences harbored escape mutations. Comparison of mutation frequencies between HLA allele-relevant and -irrelevant epitopes in CP-treated patients suggests these CTL escape mutations identified are specific to patient's HLA type (FIG. 1b). By contrast, except for SL9 from AP01 and RK9 from AP08, few if any CTL escape mutations were archived in AP-treated patients (FIG. 1c and FIG. 5). The striking difference between AP- and CP-treated patients (FIG. 1c) indicates that unless treatment is initiated within the first several months of infection, the latent reservoir becomes almost completely dominated by variants resistant to dominant CTL responses.

To confirm variants detected at high frequency in the latent reservoir represent functional CTL escape mutants, cells from 7 CP-treated subjects were tested for reactivity to synthetic peptides representing wild-type and mutant versions of the relevant epitopes. As expected, there were only minimal responses to previously documented CTL escape mutants by patient CD8⁺ T cells, and no de novo response was detected (FIG. 1d and FIG. 6). In contrast, all tested subjects retained a strong response to peptides representing the wild-type epitopes, suggesting wild-type virus was initially transmitted, with subsequent evolution of CTL escape variants. Most HIV-1 proviruses detected in patients are defective²⁴. Therefore, to determine whether these CTL escape variants can be reactivated and lead to viral rebound if therapy is stopped, replication-competent viruses were isolated from the latent reservoirs of 9 CP-treated patients. It was found that all dominant CTL escape mutations identified in proviruses in resting CD4⁺ T cells were also present in the replication-competent viruses that grew out after T cell activation (FIG. 1e and FIG. 7), indicating that these CTL escape variants not only dominate the population of proviruses, but can also be released and replicate once latency is reversed.

Whether the host CTL response could recognize and eliminate the cells infected with these escape variants were investigated next. A ctivated CD4⁺ T cells from these patients were infected with autologous, replication-competent virus derived from the latent reservoir (FIG. 8a). The infected cells were then co-cultured with autologous CD8⁺ T cells, either unstimulated or pre-stimulated, to assess HIV-1-specific cytolytic activity. Non-specific activation of CD8⁺ T cells was not observed after co-cultured with PHA-activated CD4⁺ T cells (FIG. 8b). From all 13 CP-treated subjects tested, CD8⁺ T cells pre-stimulated by a Gag peptide mixture efficiently killed autologous infected CD4⁺ T cells (median 61% elimination), while unstimulated CD8⁺ T cells from most subjects had significantly less effect (median 23% elimination) (FIG. 2a and FIGS. 8c and 8d). CD8⁺ T cells from 7/7 healthy donors completely failed to eliminate autologous infected cells (FIG. 2a), confirming the observed killing was HIV-1-specific. The killing effect was enhanced by increasing the effector to target (E:T) ratio (FIG. 9a), and was cell-cell contact dependent (FIG. 9b). When the co-culture was maintained over time in the absence of ART, viral replication was significantly reduced, but not completely inhibited by pre-stimulated CD8⁺ T cells (FIG. 2b). Itwas found that peptide mixtures from other HIV-1 proteins (Nef, Tat, Rev, and Env) could also boost CTL responses and facilitate the elimination of infected cells (FIG. 2c) and that CTLs pre-stimulated by Gag peptides generally had the highest activity. Together, these results demonstrate that chronically infected patients retain CTL clones that can recognize and eliminate autologous infected CD4⁺ T cells, despite the presence of CTL escape mutations in dominant epitopes. However, these clones require stimulation with antigen for optimal activity.

To further characterize which CTL population contributed to the elimination of cells infected by CTL escape variants, the killing activity of two specific CTL populations were compared: the one that targets epitopes in which escape has been identified and the one that targets unmutated epitopes (FIG. 3a). CD8⁺ T cells from CP36 and CP39 were pre-stimulated with IL-2 and different synthetic peptides representing the wild-type forms of the relevant epitopes. After incubation for 6 days, each CTL population exhibited significant proliferation compared to no treatment or IL-2 alone (FIGS. 3b and c). Pentamer staining for three available epitopes revealed that the number of epitope-specific CD8⁺ T cells increased dramatically after stimulation with wild-type peptides (FIG. 3b). After co-culture with autologous target cells infected with latent reservoir-derived viruses, CTLs targeting unmutated epitopes clearly showed stronger cytolytic activity than the IL-2 only controls, while CTLs targeting epitopes with identified escaped mutations showed no significant killing (FIG. 3d). CTLs pre-stimulated by the Gag peptide mixture exhibited stronger killing than all single peptide-stimulated populations (FIG. 3d).

To test whether CTL that recognize unmutated viral epitopes can inhibit HIV-1 replication and clear infected cells in vivo, patient-derived humanized mice using an improved version of a recently reported mouse system named MISTRG²⁵ were generated. Whereas the previously reported MISTRG mice bear a BAC transgene encoding human SIRPα, the newly generated MIS^(KI)TRG mice harbor a knock-in replacement of the endogenous mouse Sirpa gene with a humanized version. With humanization by knock-in replacement of the Csf1, Csf2, Il3, Tpo and Sirpa genes in the Rag2^−/− Il2rg^−/− genetic background, MIS^(KI)TRG mice are highly permissive for human hematopoiesis and support the reconstitution of robust human lymphoid and myelomonocytic systems. With the demonstrated development of functional T-lymphocytes and monocytes/macrophages, MIS^(KI)TRG mice provide a useful humanized mouse host for HIV-1 infection studies. Bone marrow biopsies were obtained from study participants and purified CD34⁺ cells were used to reconstitute the MIS^(KI)TRG mice. These patient-derived humanized mice were infected with primary HIV-1 isolates grown from resting CD4⁺ T cells of the same patient and then evaluated antiviral effect of autologous CD8⁺ T cells (FIG. 4a). MIS^(KI)TRG mice engrafted with CP18 bone marrow CD34⁺ cells successfully developed human T-lymphocyte and monocyte/macrophage subsets (FIGS. 4b and c), which were sufficient to support HIV-1 infection (FIG. 4d). Plasma HIV-1 RNA levels peaked 20-30 days after infection (FIG. 10a). Depletion of CD4⁺ T cells was clearly evident 12 days after infection in peripheral blood and spleen (FIG. 4e and FIGS. 10b and 10c). Cell-associated HIV-1 RNA was detected in both T cells and macrophages/monocytes (FIG. 10d). Viral infection was also observed in various tissues where a large number of memory CD4⁺ T cells were detected (FIG. 11). In control mice or mice that received autologous patient CD8⁺ T cells pre-stimulated with a peptide representing the unmutated dominant SL9 epitope, levels of plasma HIV-1 RNA and proviral DNA in peripheral blood continued to increase from day 14 to day 29 after infection (FIG. 40. In sharp contrast, mice that received CD8⁺ T cells pre-stimulated with unmutated epitopes (Gag mix or WF9) had a significantly lower level of viral replication (FIG. 4g and h). Dramatic decreases in plasma HIV-1 RNA of 100- to 1,000-fold were observed in all three mice that received CD8⁺ T cells pre-stimulated with the mixture of Gag peptides including dominant and subdominant epitopes. Two of three mice had undetectable levels of plasma HIV-1 RNA and proviral DNA in peripheral blood measured at three time points (FIG. 4g). The same experiments were performed using patient CP36-derived humanized mice and reduction of peripheral HIV-1 RNA and DNA levels was also observed in mice that received CP36 CD8⁺ T cells pre-stimulated with the mixture of Gag peptides (FIG. 12). Since the post-engraftment lifespan of MIS^(KI)TRG mice is only 10-12 weeks³³, the acute phase of HIV-linfection and demonstrate the in vivo functionality of patient CD8⁺ T cells was only investigated. Future developments of the MIS^(KI)TRG model will prolong the post-engraftment lifespan of the mice and will allow the studies of establishment and clearance of HIV-1 latent reservoir in vivo. Together, these in vitro and in vivo experiments demonstrate that only the CTL clones targeting unmutated epitopes are effective against cells infected with the viral variants that are likely to represent the major source of rebound HIV-1 after reversal of latency.

The seeding of the HIV-1 latent reservoir starts just a few days after infection²⁶, prior to the development of robust CTL response¹⁴. This is consistent with the finding that patients who initiated treatment early in acute infection have few if any CTL escape variants archived in the latent reservoir. However, if treatment was initiated in chronic infection, CTL escape variants became dominant in the latent reservoir, indicating a complete replacement of the initially established ‘wild-type’ reservoir. The mechanism behind this replacement warrants further investigation, but likely reflects the dynamic nature of the reservoir in untreated infection. In any event, the overwhelming presence of escape variants in the latent reservoir of chronic patients certainly presents an additional barrier to eradication efforts. The striking difference between AP- and CP-treated patients presents another argument for early treatment of HIV-1 infection; early treatment not only reduces the size of the latent reservoir²⁷, but also alters the composition of the reservoir, as shown here, in a way that may enhance the efficacy of potential CTL-based eradication therapies.

The hierarchy of HIV-1-specific CTL response in acute infection appears to play a significant role in initial viral suppression as demonstrated by the fact that certain immunodominant CTL populations are frequently linked to lower set point viremia later in infection^17,28. These immunodominant responses in acute infection have been identified as the major selection force driving the development of CTL escape mutations^{13, 20}. Here it was shown that these immunodominant response-driven mutations are not only archived in the latent reservoir, but also in fact dominate the latent provirus population in CP-treated patients. Therefore, directing CTL responses to unmutated viral epitopes is essential to clear latent HIV-1. Due to bias in antigen presentation or recognition²⁹, common vaccination strategies will likely re-stimulate immunodominant CTL clones which do not kill infected cells after reversal of latency. Stimulation of CTL responses with viral peptides circumvents antigen processing and is able to elicit broad-spectrum CTL responses against unmutated regions of viral proteins. These study suggests that latent HIV-1 can be eliminated in chronically infected patients despite the overwhelming presence of CTL escape variants. Future directions in therapeutic vaccine design need to focus on boosting broad CTL responses as also reported elsewhere³⁰ and/or manipulating immuno dominance.

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EQUIVALENTS

Those skilled in the art will recognize, or be able to ascertain using no more than routine experimentation, many equivalents to the specific embodiments of the invention described herein. While specific embodiments of the subject invention have been discussed, the above specification is illustrative and not restrictive. Many variations of the invention may become apparent to those skilled in the art upon review of this specification. The full scope of the invention should be determined by reference to the claims, along with their full scope of equivalents, and the specification, along with such variations. Such equivalents are intended to be encompassed by the following claims.

TABLE 1
Peripheral blood or bone marrow for the isolation of primary
CD4+, CD8+ or CD34+ T cells was obtained from
30 HIV-1-infected patients and 7 healthy adult volunteers.
			Plasma		Treatment
		CD4	HIV-1	Time on	start time
	Year of	count*	RNA†	ART	after infection
Patient	Diagnosis	(cells/μl)	(copies/ml)	(years)	(days)
AP01	2006	1251	<50	7	64
AP03	2004	595	<50	9	34
AP04	1998	953	<50	15	77
AP05	2002	618	<50	11	39
AP07	2012	592	<50	1.5	67
AP08	2008	780	<50	6	28
AP09	2012	1069	<50	2	39
AP10	2006	513	<50	7	50
AP11	2007	874	<50	6	10
AP12	2007	629	<50	6	15
CP05	2001	500	<50	10	>180
CP12	1997	1074	<50	15	>180
CP18	1998	773	<50	>4	>180
CP19	2006	620	<50	6	>180
CP26	1994	640	<50	16	>180
CP27	1987	784	<50	4	>180
CP28	1998	614	<50	6	>180
CP31	2000	619	<50	10	>180
CP32	1999	780	<50	2	>180
CP35	2002	738	<50	10	>180
CP36	2003	1119	<50	4	>180
CP37	1999	730	<50	12	>180
CP38	1986	870	<50	3	>180
CP39	1996	1552	<50	10	>180
CP40	2002	544	<50	7	>180
CP42	1987	684	<50	16	>180
CP47	1986	792	<50	14	>180
CP48	1998	641	<50	8	>180
CP49	1992	864	<50	5	>180
CP50	2001	964	<50	4	>180

TABLE 2
Deep sequencing results for viral variants archived in the latent reservoir.
					Variation	Variation
		Epitope			Frequency	Frequency	Mutation
Patient	HLA Type	Name	Epitope1	Variant2	(%) (PacBio)	(%) (MiSeq)	Type3
CP05	A*29:02	RY11	RSLYNTVATLY (A30)	—	0	0	—
	A*30:01	LY9	LYNTVATLY (A29:02)	—	0	0	—
	B*42:01	IW9	ISPRTLNAW (B57:01)	I147L	89.4	92.3	E
	B*57:01	KF11	KAFSPEVIPMF (B57:01)	—	0	0	—
	Cw*06:02	TL9	TPQDLNTML (B42:01)	Q182A	86.6	88.1	MTND
	Cw*17:01	TW10	TSTLQEQIGW (B57:01)	T242N	98.4	98.7	E
		QW9	QASQEVKNW (B57:01)	—	0	0	—
CP12	A*01:01	LY9	LYNTVATLY (A29:02, B44:03)	T81A, V82I	67.1	68.6	MTND
	A*29:02	IW9	ISPRTLNAW (B57:01)	I147L	93	97.3	E
	B*44:03	KF11	KAFSPEVIPMF (B57:01)	—	0	0	—
	B*57:01	TW10	TSTLQEQIGW (B57:01)	T242N	91.3	99.1	B
	Cw*06:02	QW9	QASQEVKNW (B57:01)	S310T	69.8	72.8	MTND
	Cw*16:01
CP18	A*02:01	WF9	WASRELERF (B35:01)	—	0	0	—
	A*33:03	SL9	SLYNTVATL (A02:01)	Y79F, V82I,	97.4	98.8	E
	B*35:01			T84V
	B*81:01	TV9	TLNAWVKVV (A02:01)	—	0	0	—
	Cw*04:01	TL9	TPQDLNTML (B81:01)	Q182G/A/V	87.6	93.4	MTND
	Cw*18:01	HA9	HPVHAGPIA (B35:01)	I223V	53.7	66.6	MTND
		PY9	PPIPVGEIY (B35:01)	—	0	0	—
		FK10	FLGKIWPSHK (A0201)	—	0	0	—
CP19	A*23:01	RY11	RSLYNTVATLY (B58)	V82I, T84V	35.9	24.6	MTND
	A*68:02	VF9	VKVVEEKAF (B15:03)	—	0	0	—
	B*15:03	GHL9	GHQAAMQML (B15)	—	0	0	—
	B*58:01	TW10	TSTLQEQIGW (B58:01)	T242N, G248T	82.9	98.3	E
	Cw*02:10	QW9	QASQEVKNW (B58:01)	E312D	78.1	97.9	MTND
	Cw*07:18
CP31	A*23:01	RY11	RSLYNTVATLY (B58)	R76K, T81A	99.5	92.3	E
	A*66:02	KF11	KAFSPEVIPMF (B58:01)	—	0	0	—
	B*41:01	TL9	TPQDLNTML (C08:02)	Q182G, T186L	0	22.9	MTND
	B*58:01	EW10	ETINEEAAEW (B58)	E203D	95.1	69.2	SF
	Cw*07:18	TW10	TSTLQEQIGW (B58:01)	T242N, G248A	99.1	71.7	E
	Cw*08:02	QW9	QASQEVKNW (B58:01)	E312D	99	70.4	MTND
CP32	A*34:02	LY9	LYNTVATLY (B44:03)	—	0	0	—
	A*68:01	TL9	TPQDLNTML (B53:01)	—	0	0	—
	B*44:03	QW9	QASQEVKNW (B53:01)	S310T	97.2	98.8	E
	B*53:01
	Cw*04:01
CP36	A*02:02	KK9	KIRLRPGGK (A03:01)	—	0	0	—
	A*03:01	RK9	RLRPGGKKK (A03:01)	K28S	94.5	97.5	MTND
	B*35:01	WF9	WASRELERF (B35:01)	—	0	0	—
	B*53:01	SL9	SLYNTVATL (A02:02)	T84V	98.2	99	E
	Cw*04:01	TV9	TLNAWVKVV (A02:02)	V159I	81.6	83.4	DR
		EW10	ETINEEAAEW (B53)	—	0	0	—
		HA9	HPVHAGPIA (B35:01)	—	0	0	—
		QW9	QASQEVKNW (B53:01)	S310T	70.9	78	MTND
CP38	A*03:01	KK9	KIRLRPGGK (A03:01)	K26R	10.4	13.1	E
	A*24:02	RK9	RLRPGGKKK (A03:01)	K26R, K28Q	75.4	78.7	E
	B*44:02	KW9	KYKLKHIVW (A24:02)	K28Q, K30R, I34L	98.3	99.4	E
	B*81:01	TL9	TPQDLNTML (B81:01)	Q182G/S, T186L	95.7	99.4	MTND
	Cw*05:01	RL11	RDYVDRFYKTL (B44:02)	—	0	0	—
	Cw*18:01	AW11	AEQASQEVKNW (B44:02, Cw5)	S310T	12.5	12.3	MTND
CP39	A*03:01	KK9	KIRLRPGGK (A03:01)	—	0	0	—
	A*29:02	RK9	RLRPGGKKK (A03:01)	K28Q	94.7	98.6	E
	B*07:02	LY9	LYNTVATLY (A29:02)	Y79F, V82I,	99	98.6	E
	B*15:16			T84V, Y86F
	Cw*07:02	SV9	SPRTLNAWV (B07:02)	—	0	0	—
	Cw*14:02	TL9	TPQDLNTML (B07:02)	—	0	0	—
		HA9	HPVHAGPIA (B7)	—	0	0	—
		GL9	GPGHKARVL (B07:02)	—	0	0	—
CP40	A*02:02	KK9	KIRLRPGGK (A03:01)	K18R	39.8	40.4	MTND
	A*03:01	RK9	RLRPGGKKK (A03:01)	K28T/R	89.5	91.1	DR
	B*15:16	RL10	RPGGKKKYKL (B51:01)	K28T/R, K30R	91.8	92.4	MTND
	B*51:01	SL9	SLYNTVATL (A02:02, Cw14)	Y79F, T81A,	99.4	99.3	E
	Cw*14:02			V82I, T84V
		TV9	TLNAWVKVV (A02:02)	V159I	3.4	4.2	DR
CP42	A*02:01	KK9	KIRLRPGGK (A03:01)	—	0	0	—
	A*03:01	RK9	RLRPGGKKK (A03:01)	K28Q	97.5	98.9	E
	B*07:02	SL9	SLYNTVATL (A02:01)	Y79F, V82I	98.3	98.7	E
	B*38:01	SV9	SPRTLNAWV (B07:02)	—	0	0	—
	Cw*07:02	TV9	TLNAWVKVV (A02:01)	—	0	0	—
	Cw*12:03	TL9	TPQDLNTML (B07:02)	—	0	0	—
		HA9	HPVHAGPIA (B7)	—	0	0	—
		GL9	GPGHKARVL (B07:02)	—	0	0	—
		FK10	FLGKIWPSHK (A02:01)	—	0	0	—
CP47	A*02:01	SL9	SLYNTVATL (A02:01)	Y79F, T81A,	92.3	96.4	E
				V82I, T84V
	A*25:01	QW11	QAISPRTLNAW (A25:01)	I147L	96.5	96.5	DR
	B*18;01	TV9	TLNAWVKVV (A02:01)	—	0	0	—
	Cw*07:01	EW10	ETINEEAAEW (A25:01)	—	0	0	—
	Cw*12:03	FRK10	FRDYVDRFYK (B18:01)	—	0	0	—
		FK10	FLGKIWPSHK (A02:01)	—	0	0	—
CP48	A*33:03	LY9	LYNTYATLY (B44:03)	T81A, V82I, T84V	94.2	98.7	MTND
	A*37:01	RL11	RDYVDRFYKTL (B44)	—	0	0	—
	B*44:03	AW11	AEQASQEVKNW (B44)	S310T	24.5	27.8	MTND
	Cw*06:02
	Cw*07:06
CP49	A*01:01	GK9	GGKKKYKLK (B08:01)	—	0	0	—
	A*02:01	EV9	ELRSLYNTV (B08:01)	R76K, Y79F	99.2	98.5	MTND
	B*08:01	SL9	SLYNTVATL (A02:01)	Y79F	99.2	98.5	E
	B*13:02	VQV9	VQNLQGQMV (B13)	L138M	97	97.3	MTND
	Cw*06:02	TV9	TLNAWVKVV (A02:01)	—	0	0	—
	Cw*07:01	GI11	GQMKFPRGSD1 (B13)	—	0	0	—
		EI8	EIYKRWII (B08:01)	—	0	0	—
		DL9	DCKTILKAL (B08:01)	—	0	0	—
		R19	RQANFLGKI (B13)	—	0	0	—
		FK10	FLGKIWPSHK (A02:01)	—	0	0	—
CP50	A*03:01	KK9	KIRLRPGGK (A03:01)	—	0	0	—
	A*30:04	RK9	RLRPGGKKK (A03:01)	K28Q	91.8	94	E
	B*35:01	WF9	WASRELERF (B35:01)	—	0	0	—
	B*49:01	RY11	RSLYNTVATLY (A30)	R76K	97.4	98.5	IE
	Cw*04:01	HA9	HPVHAGPIA (B35:01)	—	0	0	—
	Cw*07:01	PY9	PPIPVGEIY (B35:01)	—	0	0	—
AP01	A*02:01	KK9	KIRLRPGGK (A03:01)	—	0	0	—
	A*03:01	RK9	RLRPGGKKK (A03:01)	K28Q	3.4	4.3	E
	B*35:01	WF9	WASRELFRF (B35:01)	—	0	0	—
	B*44:02	SL9	SLYNTVATL (A02:01)	T84V	94.4	98.7	E
	Cw*04:01	TV9	TLNAWVKVV (A02:01)	—	0	0	—
	Cw*05:01	HA9	HPVHAGPIA (B35:01)	I223P	95.2	94.7	MTND
		PY9	PP1PVGEIY (B35:01)	—	0	0	—
		RL11	RDYVDRFYKTL (B44:02)	—	0	0	—
		AW11	AEQASQEVKNW (B44:02, Cw5)	N315G	96.5	94.9	MTND
		FK10	FLGKIWPSHK (A02:01)	1	0	0	—
AP03	A*24:02	IK9	IRLRPGGKK (B27:05)	K26N	66.1	61.5	MTND
	A*24:07	KW9	KYKLKHIVW (A24:02)	K28Q	29.5	36.4	E
	B*15:02	VL8	VIPMFSAL (C01:02)	—	0	0	—
	B*27:05	KK10	KRWIILGLNK (B27:05)	R264K, L268M	25	25.8	E
	Cw*01:02	YL9	YVDRFYKTL (C03:03)	—	0	0	—
	Cw*03:03
AP04	A*02:01	KW9	KYKLKHIVW (A24::02)	K30Q/R	50.4	52.9	MTND
	A*24:02	WF9	WASRELFRF (B35:01)	F44Y	7.7	7	MTND
	B*14:01	SL9	SLYNTVATL (A02:01)	V82I	11.7	12.3	E
	B*35:01	TV9	TLNAWVKVV (A02:01)	V1591	7.6	6.9	DR
	Cw*04:01	HA9	HPVHAGPIA (B35:01)	—	0	0	—
	Cw*15:05	PY9	PPIPVGEIY (B35:01)	—	0	0	—
		CC9	CRAPRKKGC (B14)	K411R	70.5	79.2	MTND
		FK10	FLGKIWPSHK (A02:01)	1437L	7.7	6.9	MTND
AP05	A*02:01	RL10	RPGGKKKYKL, (B51:01)	K28Q	95.8	98.7	MTND
	B*07:02	SL9	SLYNTVATL (A02:03)	—	0	0	—
	B*51:01	SV9	SPRTLNAWV (B07:02)	—	0	0	—
	Cw*01:02	TV9	TLNAWVKVV (A02:01)	V159I	99.2	98.5	DR
	Cw*07:02	VL8	VIPMFSAL (Cw01:02)	—	0	0	—
		TL9	TPQDLNTML (B07:02)	—	0	0	—
		HA9	HPVHAGPIA (B7)	H219P, I223V	99.4	98.7	MTND
		GL9	GPGHKARVL (B07:02)	R361K	6.1	18.3	MTND
		FK10	FLGKIWPSHK (A02:01)	H441N	97.2	98.1	MTND
AP07	A*02:07	RY11	RSLYNTVATLY(B58)	—	0	0	—
	A*33:03	VL8	VIPMFSAL(Cw01:02)	S173T	96.6	97.2	DR
	B*46:01	TW10	TSTLQEQIGW(B58:01)	—	0	0	—
	B*58:01	YL9	YVDRFYKTL(A02:07)	—	0	0	—
	Cw*01:02	QW9	QASQEVKNW(B58)	—	0	0	—
	Cw*03:02
AP08	A*02:01	KK9	KIRLRPGGK (A03:01)	—	0	0	—
	A*03:01	RK9	RLRPGGKKK (A03:01)	R28Q	96.1	98.7	E
	B*07:02	SL9	SLYNTVATL (A02:01)	—	0	0	—
	Cw*07:02	SV9	SPRTLMAWV (B07:02)	—	0	0	—
		TV9	TLNAWVKVV (A02:01)	—	0	0	—
		TL9	TPQDLNTML (B07:02)	Q182S	93.1	96.5	MTND
		HA9	HPVIIAGPIA (B7)	—	0	0	—
		GL9	GPGHKARVL (B07:02)	—	0	0	—
		FK10	FLGKIWPSHK (A02:01)	—	0	0	—
AP09	A*03:01	KK9	KIRLRPGGK (A03:01)	—	0	0	—
	A*11:01	RK9	RLRPGGKKK (A03:01)	—	0	0	—
	B*08:01	GK9	GGKKKYKLK (B08:01)	—	0	0	—
	B*14:02	EV9	ELRSLYNTV (B08:01)	R76K, V82I	98.9	98.9	IE
	Cw*07	EI8	EIYKRWII (B08:01)	—	0	0	—
	Cw*08	DA9	DRFYKTLRA(B14:02)	—	0	0	—
		DL9	DCKTILKAL (B08:01)	—	0	0	—
		AK11	ACQGVGGPGHK(A11:01)	G357S	98	99.1	SF
		CC9	CRAPRKKGC (B14)	—	0	0	—
AP10	A*01:01	GK9	GGKKKYKLK (B08:01)	—	0	0	—
	A*02:01	EV9	ELRSLYNTV (B08:01)	—	0	0	—
	B*08:01	SL9	SLYNTVATL (A02:01)	—	0	0	—
	B*15:01	TV9	TLNAWVKVV (A02:01)	—	0	0	—
	Cw*03	EI8	EIYKRWII (B08:01)	—	0	0	—
	Cw*07	GLY9	GLNKIVRMY(B15:01)	—	0	0	—
		DL9	DCKTILKAL (B08:01)	—	0	0	—
		FK10	FLGKIWPSHK (A02:01)	G435R	31.7	51.6	MTND
AP11	A*02:01	RL10	RPGGKKKYKL (B51:01)	—	0	0	—
	B*35:01	WF9	WASRELERF (B35:01)	—	0	0	—
	B*51:01	SL9	SLYNTVATL (A02:01)	—	0	0	—
	Cw*02:02	TV9	TLNAWVKVV (A02:01)	—	0	0	—
	Cw*04:01	HA9	HPVHAGPIA (B7)	—	0	0	—
		PY9	PPIPVGEIY (B35:01)	—	0	0	—
		FK10	FLGKIWPSHK (A02:01)	G435R	2.1	6.7	MTND
AP12	A*01:01	KK9	KIRLRPGGK (A03:01)	—	0	0	—
	A*03:01	RK9	RLRPGGKKK (A03:01)	—	0	0	—
	B*07:02	SV9	SPRTLNAWV (B07:02)	R150K	2.7	5.6	MTND
	Cw*07	TL9	TPQDLNTML (B07:02)	—	0	0	—
		HA9	HPVHAGPIA (B7)	—	0	0	—
		GL9	GPGHKARVL (B07:02)	—	0	0	—
1Each patient's relevant optimal Gag epitopes are based: on reported information in the HIV Molecular Immunology Database, Los Alamos National Laboratory (http://www.luv.lanl.gov/content/immunology/index.html) according to the HLA type.
2Sequences from each subject were aligned to the reference HIV-1 clade B consensus Gag sequence. Variants were determined by the differences from the reference sequence.
3Mutation Type abbreviations: MTND: mutation type not determined; E: documented escape; IE: inferred escape; DR: diminished response; SF: susceptible form.

TABLE 3
Consensus Subtype 8 Nef (NIH AIDS Reagent 5189)
DATA SHEET
HIV-1 Consensus Subtype B Nef (15-mer) Peptides - Complete Set
(Cat# 5189, Lot# 10 - NOTE solubility data is from lot#9)
	Solubility Data
			Molecular		Peptide			10%
			Wt.	Purity	Content			Acetic
CAT #	Peptide Name	SEQUENCE	Amu	[%]	[%]	Water	PBS	Acid	DMSO
5139	HIV-1 Consensus Subtype B Nef	MGGKWSKRSVVGWPT	1676.0	96.0	71.0	+	+	+	+
5140	HIV-1 Consensus Subtype B Nef	WSKRSVVGWPTVRER	1843.1	91.5	69.0	+	+	+	+
5141	HIV-1 Consensus Subtype B Nef	SVVGWPTVRERMRRA	1800.1	95.9	69.0	+	+	+	+
5142	HIV-1 Consensus Subtype B Nef	WPTVRERMRRAEPAA	1826.1	95.2	71.0	+	+	+	+
5143	HIV-1 Consensus Subtype B Nef	RERMRRAEPAADGVG	1670.9	97.4	70.0	+	+	+	+
5144	HIV-1 Consensus Subtype B Nef	RRAEPAADGVGAVSR	1511.7	94.8	74.0	+	+	+	+
5145	HIV-1 Consensus Subtype B Nef	PAADGVGAVSRDLEK	1484.6	98.4	80.0	+	+	+	+
5146	HIV-1 Consensus Subtype B Nef	GVGAVSRDLEKHGAI	1508.7	96.6	74.0	+	+	+	+
5147	HIV-1 Consensus Subtype B Nef	VSRDLEKHGAITSSN	1613.8	90.8	71.0	+	+	+	+
5148	HIV-1 Consensus Subtype B Nef	LEKHGAITSSNTAAN	1513.6	96.0	76.0	+	+	+	+
5149	HIV-1 Consensus Subtype B Nef	GAITSSNTAANNADC	1409.4	96.2	80.0	−	−	−	−
5150	HIV-1 Consensus Subtype B Nef	SSNTAANNADCAWLE	1566.6	95.0	84.0	−	−	−	−
5151	HIV-1 Consensus Subtype B Nef	AANNADCAWLEAQEE	1634.7	98.1	90.0	+	+	−	+
5152	HIV-1 Consensus Subtype B Nef	ADCAWLEAQEEEEVG	1678.8	94.4	87.0	−	−	−	+
5153	HIV-1 Consensus Subtype B Nef	WLEAQEEEEVGFPVR	1813.0	97.7	82.0	+	−	+	+
5154	HIV-1 Consensus Subtype B Nef	QEEEEVGFPVRPQVP	1739.9	91.7	88.0	+	+	+	+
5155	HIV-1 Consensus Subtype B Nef	EVGFPVRPQVPLRPM	1722.1	96.6	76.0	+	+	+	+
5156	HIV-1 Consensus Subtype B Nef	PVRPQVPLRPMTYKA	1753.1	96.9	72.0	+	+	+	+
5157	HIV-1 Consensus Subtype B Nef	QVPLRPMTYKAAVDL	1702.1	92.4	77.0	+	+	+	+
NOTE: Peptides that are difficult to solubilize can almost always be dissolved in DMSO. Once
a peptide is in solution, the DMSO can be slowly diluted with aqueous medium. Care must be
taken to ensure that the peptide does not begin to precipitate out of solution.
	Solubility Data
					Peptide			10%
			M W	Purity	Content			Acetic
CAT #	Peptide Name	SEQUENCE	g/mol	[%]	[%]	Water	PBS	Acid	DMSO
5158	HIV-1 Consensus Subtype B Nef	RPMTYKAAVDLSHFL	1749.1	91.0	73.0	+	+	+	+
5159	HIV-1 Consensus Subtype B Nef	YKAAVDLSHFLKEKG	1706.0	95.9	69.0	+	+	+	+
5160	HIV-1 Consensus Subtype B Nef	VDLSHFLKEKGGLEG	1628.8	95.1	76.0	+	+	+	+
5161	HIV-1 Consensus Subtype B Nef	HFLKEKGGLEGLIYS	1691.0	95.5	75.0	+	+	+	+
5162	HIV-1 Consensus Subtype B Nef	SKGGLEGLIYSQKRQ	1705.9	97.0	74.0	+	+	+	+
5163	HIV-1 Consensus Subtype B Nef	LEGLIYSQKRQDILD	1791.0	94.8	79.0	+	+	+	+
5164	HIV-1 Consensus Subtype B Nef	IYSQKRQDILDLWVY	1940.2	96.8	74.0	+	−	+	+
5165	HIV-1 Consensus Subtype B Nef	KRQDILDLWVYHTQG	1872.1	95.9	75.0	+	−	+	+
5166	HIV-1 Consensus Subtype B Nef	ILDLWVYHTGGYFPD	1867.1	96.0	81.0	−	−	+	+
5167	HIV-1 Consensus Subtype B Nef	WVYHTQGYFPDWQNY	2004.0	95.1	75.0	−	−	+	+
5168	HIV-1 Consensus Subtype B Nef	TQGYFPDWQNYTPGP	1770.9	95.5	78.0	+	+	+	+
5169	HIV-1 Consensus Subtype B Nef	FPDWQNYTPGPGIRY	1811.0	95.3	74.0	+	+	+	+
5170	HIV-1 Consensus Subtype B Nef	QNYTPGPGIRYPLTF	1723.9	97.2	76.0	+	+	+	+
5171	HIV-1 Consensus Subtype B Nef	PGPGIRYPLTFGWCF	1711.0	96.9	79.0	−	−	+	+
5172	HIV-1 Consensus Subtype B Nef	IRYPLTFGWCFKLVP	1840.3	96.6	80.0	+	+	+	+
5173	HIV-1 Consensus Subtype B Nef	LTFGWCFKLVPVEPE	1765.1	95.9	82.0	−	−	+	+
5174	HIV-1 Consensus Subtype B Nef	WCFKLVPVEPEKVEE	1832.2	97.6	81.0	−	−	+	+
5175	HIV-1 Consensus Subtype B Nef	LVPVEPEKVEEANEG	1638.8	96.4	84.0	+	+	+	+
5176	HIV-1 Consensus Subtype B Nef	EPEKVEEANEGENNS	1674.7	96.1	83.0	+	+	+	+
5177	HIV-1 Consensus Subtype B Nef	VEEANEGENNSLLHP	1651.7	97.2	82.0	+	+	+	+
5178	HIV-1 Consensus Subtype B Nef	NEGENNSLLHPMSLH	1691.9	95.5	77.0	+	+	+	+
5179	HIV-1 Consensus Subtype B Nef	NNSLLHPMSLHGMDD	1680.9	96.4	70.0	+	+	+	+
5180	HIV-1 Consensus Subtype B Nef	LHPMSLHGMDDPERE	1764.0	94.9	66.0	+	+	+	+
5181	HIV-1 Consensus Subtype B Nef	SLHGMDDPEREVLEW	1813.0	96.1	74.0	+	+	+	+
5182	HIV-1 Consensus Subtype B Nef	MDDPEREVLEWKFDS	1896.1	95.5	74.0	−	−	+	+
5183	HIV-1 Consensus Subtype B Nef	EREVLEWKFDSRLAF	1925.2	98.5	74.0	−	−	+	+
5184	HIV-1 Consensus Subtype B Nef	LEWKFDSRLAFHHMA	1888.2	96.3	74.0	+	−	+	+
5185	HIV-1 Consensus Subtype B Nef	FDSRLAFHHMARELH	1867.1	93.0	71.0	+	+	+	+
5186	HIV-1 Consensus Subtype B Nef	LAFHHMARELHPEYY	1914.2	96.6	72.0	+	+	+	+
5187	HIV-1 Consensus Subtype B Nef	HMARELHPEYYKDC	1792.0	97.0	67.0	+	+	+	+
Determination of solubility: appr, 0.25 mg of the respective peptide was incubated with 1 ml of
solvent.
Solubility was assessed by visual inspection of the resulting solution/suspension.
“+”: complete dissolution
“−”: incomplete dissolution

Brown 20232 delivery list
					MW (1)		MW (2)
					detected	MW (1)	detected	MW (2)	MW (3) detected	MW (3)
Index	JPT-4	Sequence	Peptide Name	Batch#	[g/mol]	label	[g/mol]	label	[g/mol]	label
1	20232_001	H-MGARASVLSGGELDR-OH	7872_HIV-1 Consensus B Gag_001	070213R-06	—	—	759.9	[M + 2H]2+	507	[M + 3H]3+
2	20232_002	H-ASVLSGGELDRNEKI-OH	7872_HIV-1 Consensus B Gag_002	070213R-07	—	—	830.4	[M + 2H]2+	554.1	[M + 3H]3+
3	20232_003	H-SGGKLDRWEKIRLRP-OH	7872_HIV-1 Consensus B Gag_003	190213F-02	—	—	906.8	[M + 2H]2+	604.5	[M + 3H]3+
4	20232_004	H-LURWEKIRLRPGGKK-OH	7872_HIV-1 Consensus B Gag_004	070213R-08	—	—	927	[M + 2H]2+	616.2	[M + 3H]3+
5	20232_005	H-EKIRLRPGGKKKYKL-OH	7872_HIV-1 Consensus B Gag_005	070213R-09	—	—	906	[M + 2H]2+	605.5	[M + 3H]3+
6	20232_006	H-LRPGGKKKYKLKHTV-OH	7872_HIV-1 Consensus B Gag_006	190213F-04	1765.6	[M + H]+	883.4	[M + 2H]2+	589.4	[M + 3H]3+
7	20232_007	H-GKKKYKLKHIVWASR-OH	7872_HIV-1 Consensus B Gag_007	190213F-06	—	—	921.9	[M + 2H]2+	814.8	[M + 3H]3+
8	20232_008	H-YKLKHIVWASREKER-OH	7872_HIV-1 Consensus B Gag_008	190213F-08	—	—	964.9	[M + 2H]2+	643.8	[M + 3H]3+
9	20232_009	H-HIVWASRELKRFAVH-OH	7872_HIV-1 Consensus B Gag_009	190213F-10	—	—	913.9	[M + 2H]2+	609.0	[M + 3H]3+
10	20232_010	H-ASRELERFAVNPGLL-OH	7872_HIV-1 Consensus B Gag_010	190213K-01	—	—	836.4	[M + 2H]2+	658.1	[M + 3H]3+
11	20232_011	H-LERFAVNPGLLETSE-OH	7872_HIV-1 Consensus B Gag_011	190213K-03	1874.9	[M + H]+	838.1	[M + 2H]2+	659	[M + 3H]3+
12	20232_012	H-AVNPGLLETSEGCRQ-OH	7872_HIV-1 Consensus B Gag_012	190213K-05	1575.2	[M + H]+	787.8	[M + 2H]2+	—	—
13	20232_013	H-GLLETSEGCRQILGQ-OH	7872_HIV-1 Consensus B Gag_013	190213K-07	1604.4	[M + H]+	802.4	[M + 2H]2+	535.5	[M + 3H]3+
14	20232_014	H-TSEGCRQILGQLQPS-OH	7872_HIV-1 Consensus B Gag_014	190213K-09	1816.4	[M + H]+	806.9	[M + 2H]2+	539.7	[M + 3H]3+
15	20232_015	H-CRQILGQLQPSLQTG-OH	7872_HIV-1 Consensus B Gag_015	190213K-11	1642.8	[M + H]+	821.5	[M + 2H]2+	548.2	[M + 3H]3+
16	20232_016	H-LGQLQPSLQTGSRHL-OH	7872_HIV-1 Consensus B Gag_016	190213K-13	1000.4	[M + H]+	800.4	[M + 2H]2+	—	—
17	20232_017	H-QPSLQTGSEHLRSLY-OH	7872_HIV-1 Consensus B Gag_017	190213K-15	—	—	854.4	[M + 2H]2+	570.1	[M + 3H]3+
18	20232_018	H-QTGSEELRSLYNTVA-OH	7872_HIV-1 Consensus B Gag_018	190213K-17	—	—	834.5	[M + 2H]2+	556.8	[M + 3H]3+
19	20232_019	H-EKLRSLYMTVATLYC-OH	7872_HIV-1 Consensus B Gag_019	190213K-19	1775.4	[M + H]+	886.4	[M + 2H]2+	—	—
20	20232_020	H-SLYNTVATLYCVHQR-OH	7872_HIV-1 Consensus B Gag_020	190213K-21	—	—	885	[M + 2H]2+	590.1	[M + 3H]3+
21	20232_021	H-TVATLYCVHQRIEVK-OH	7872_HIV-1 Consensus B Gag_021	190213K-23	1762.3	[M + H]+	680.8	[M + 2H]2+	587.7	[M + 3H]3+
22	20232_022	H-LYCVHQRIEVKDTKE-OH	7872_HIV-1 Consensus B Gag_022	190213K-25	1552.4	[M + H]+	931.4	[M + 2H]2+	621.4	[M + 3H]3+
23	20232_023	H-HQRIEVKDTKEALEK-OH	7872_HIV-1 Consensus B Gag_023	190213K-27	—	—	912.4	[M + 2H]2+	606.8	[M + 3H]3+
24	20232_024	H-EVKDTKEALEKIERH-OH	7872_HIV-1 Consensus B Gag_024	190213K-29	—	—	895.3	[M + 2H]2+	597.4	[M + 3H]3+
25	20232_025	H-TKEALEKIEEEQNKS-OH	7872_HIV-1 Consensus B Gag_025	190213K-31	—	—	888.8	[M + 2H]2+	592.7	[M + 3H]3+
26	20232_026	H-LEKIEEEQNKSKKKA-OH	7872_HIV-1 Consensus B Gag_026	190213K-33	1603.3	[M + H]+	901.8	[M + 2H]2+	601.7	[M + 3H]3+
27	20232_027	H-KEEQNKSKKKAQQAA-OH	7872_HIV-1 Consensus B Gag_027	190213K-35	1717.8	[M + H]+	859.1	[M + 2H]2+	573.2	[M + 3H]3+
28	20232_028	H-NKSKKKAQQAAADTG-OH	7872_HIV-1 Consensus B Gag_028	190213K-37	1547.1	[M + H]+	773.7	[M + 2H]2+	516.2	[M + 3H]3+
29	20232_029	H-KKAQQAAADTGGSSQ-OH	7872_HIV-1 Consensus B Gag_029	190213K-39	1505.2	[M + H]+	753.1	[M + 2H]2+	—	—
30	20232_030	H-QAAADTGGSSQVSQN-OH	7872_HIV-1 Consensus B Gag_030	190213K-41	1477.7	[M + H]+	739.5	[M + 2H]2+	—	—
31	20232_031	H-DTGNSSQVSQNYPIV-OH	7872_HIV-1 Consensus B Gag_031	190213K-43	1610.1	[M + H]+	805.2	[M + 2H]2+	—	—
32	20232_032	H-SSQVSQNTPIVQNLQ-OH	7872_HIV-1 Consensus B Gag_032	190213K-45	1707.8	[M + H]+	853.1	[M + 2H]2+	560	[M + 3H]3+
33	20232_033	H-SQNYPTVQNLQGQMV-OH	7872_HIV-1 Consensus B Gag_033	190213K-47	—	—	859.8	[M + 2H]2+	—	—
34	20232_034	H-PIVQNLQGQMVRQAI-OH	7872_HIV-1 Consensus B Gag_034	220213Z-10	1675.5	[M + H]+	838.4	[M + 2H]2+	559.5	[M + 3H]3+
35	20232_035	H-NLQGQMVEQAISPRT-OH	7872_HIV-1 Consensus B Gag_035	220213Z-12	1682.2	[M + H]+	840.8	[M + 2H]2+	561.5	[M + 3H]3+
36	20232_036	H-QMVHQAISPRTLNAW-OH	7872_HIV-1 Consensus B Gag_036	220213Z-14	—	—	876.8	[M + 2H]2+	564.8	[M + 3H]3+
37	20232_037	H-QAISPRTLNAMVKVV-OH	7872_HIV-1 Consensus B Gag_037	220213Z-16	—	—	841.5	[M + 2H]2+	561.5	[M + 3H]3+
38	20232_038	H-PRTLNAWVKVVEEKA-OH	7872_HIV-1 Consensus B Gag_038	220213Z-18	—	—	870.8	[M + 2H]2+	580.7	[M + 3H]3+
39	20232_039	H-NAWVKVVEEKAFSPE-OH	7872_HIV-1 Consensus B Gag_039	220213Z-20	1732.5	[M + H]+	866.9	[M + 2H]2+	578.4	[M + 3H]3+
40	20232_040	H-KVVEEKAFSFEVIPM-OH	7872_HIV-1 Consensus B Gag_040	220213Z-22	1703.5	[M + H]+	851.9	[M + 2H]2+	568.4	[M + 3H]3+
41	20232_041	H-EKAPSPEVIPNFSAL-OH	7872_HIV-1 Consensus B Gag_041	220213Z-24	1666.5	[M + H]+	833.3	[M + 2H]2+	556.1	[M + 3H]3+
42	20232_042	H-SPEVIPMFSALSEGA-OH	7872_HIV-1 Consensus B Gag_042	220213Z-26	1535.7	[M + H]+	768	[M + 2H]2+	—	—
43	20232_043	H-IPMFSALSEGATPQD-OH	7872_HIV-1 Consensus B Gag_043	220213Z-28	1565.2	[M + H]+	762.8	[M + 2H]2+	—	—
44	20232_044	H-SALSEGATPQDLNTM-OH	7872_HIV-1 Consensus B Gag_044	220213Z-30	1535.2	[M + H]+	768.2	[M + 2H]2+	—	—
45	20232_045	H-EGATPQDLNTMLNTV-OH	7872_HIV-1 Consensus B Gag_045	220213Z-32	1604.3	[M + H]+	802.7	[M + 2H]2+	—	—
46	20232_046	H-PQDLNTNLNTVGGHQ-OH	7872_HIV-1 Consensus B Gag_046	220213Z-34	1625.4	[M + H]+	812.8	[M + 2H]2+	542.4	[M + 3H]3+
47	20232_047	H-NTNLNTVGGHQAAHQ-OH	7872_HIV-1 Consensus B Gag_047	220213Z-36	1574.2	[M + H]+	787.2	[M + 2H]2+	—	—
48	20232_048	H-NTVGGHQAAMQMLKE-OH	7872_HIV-1 Consensus B Gag_048	220213Z-38	1615.4	[M + H]+	807.8	[M + 2H]2+	539	[M + 3H]3+
49	20232_049	H-GHQAAMQMLKETINE-OH	7872_HIV-1 Consensus B Gag_049	220213Z-40	1701.8	[M + H]+	851	[M + 2H]2+	567.8	[M + 3H]3+
50	20232_050	H-AMQMLKETINEEAAE-OH	7872_HIV-1 Consensus B Gag_050	220213Z-42	1709.3	[M + H]+	854.8	[M + 2H]2+	—	—
51	20232_051	H-LKETINEEAAENDRL-OH	7872_HIV-1 Consensus B Gag_051	220213Z-44	—	—	909.3	[M + 2H]2+	606.5	[M + 3H]3+
52	20232_052	H-INBEAAEWDRLHPVH-OH	7872_HIV1 Consensus B Gag_052	220213R-01	—	—	908.4	[M + 2H]2+	506	[M + 3H]3+
53	20232_053	H-AAEWDRLHFVHAGPI-OH	7872_HIV1 Consensus B Gag_053	040313Y-01	—	—	834.9	[M + 2H]2+	557.1	[M + 3H]3+
54	20232_054	H-DRLHPVHAGPIAPGO-OH	7872_HIV1 Consensus B Gag_054	040313Y-03	1565.4	[M + H]+	782.9	[M + 2H]2+	522.5	[M + 3H]3+
55	20232_055	H-PVHAGPIAPGQMREP-OH	7872_HIV1 Consensus B Gag_055	040313Y-05	1658.8	[M + H]+	779	[M + 2H]2+	519.8	[M + 3H]3+
56	20232_056	H-GPIAPGQMREPRGSD-OH	7872_HIV1 Consensus B Gag_056	040313Y-07	1568.3	[M + H]+	784.7	[M + 2H]2+	523.5	[M + 3H]3+
57	20232_057	H-PGOMREPRGSDIAGT-OH	7872_HIV1 Consensus B Gag_057	040313Y-09	1572.2	[M + H]+	766.7	[M + 2H]2+	—	[M + 3H]3+
58	20232_058	H-REPRGSDIAGTTSTL-OH	7872_HIV1 Consensus B Gag_058	040313Y-11	—	—	780.9	[M + 2H]2+	521	[M + 3H]3+
59	20232_059	H-GSDIAGTTSTLQEQI-OH	7872_HIV1 Consensus B Gag_059	040313Y-13	1521.3	[M + H]+	760.8	[M + 2H]2+	—	[M + 3H]3+
60	20232_060	H-AGITSTLOEOIGWWT-OH	7872_HIV1 Consensus B Gag_060	040313Y-15	1625.2	[M + H]+	612.7	[M + 2H]2+	—	[M + 3H]3+
61	20232_061	H-STLQEQIGWMTNNPP-OH	7872_HIV1 Consensus B Gag_061	06021306	1716.3	[M + H]+	858.8	[M + 2H]2+	—	[M + 3H]3+
62	20232_062	H-EQIGWMTNNPPIPVG-OH	7872_HIV1 Consensus B Gag_062	040313Y-17	1653.4	[M + H]+	826.8	[M + 2H]2+	—	[M + 3H]3+
63	20232_063	H-MMTNNPPIPVGEIYK-OH	7872_HIV1 Consensus B Gag_063	040313Y-19	1761.2	[M + H]+	880.5	[M + 2H]2+	—	[M + 3H]3+
64	20232_064	H-NPPIPVGEIYKRWIT-OH	7872_HIV1 Consensus B Gag_064	040313Y-21	—	—	898.3	[M + 2H]2+	599.1	[M + 3H]3+
65	20232_065	H-PVGEIYKRWIILGLN-OH	7872_HIV1 Consensus B Gag_065	040313Y-23	1770.3	[M + H]+	886.4	[M + 2H]2+	591.2	[M + 3H]3+
66	20232_066	H-IYKRWIILGLNKIVR-OH	7872_HIV1 Consensus B Gag_066	040313Y-25	—	—	943.5	[M + 2H]2+	629.2	[M + 3H]3+
67	20232_067	H-WIILGLWKIVRMYSP-OH	7872_HIV1 Consensus B Gag_067	040313Y-27	1805.2	[M + H]+	902.5	[M + 2H]2+	601.9	[M + 3H]3+
68	20232_068	H-GLNKIVRNYSPTSIL-OH	7872_HIV1 Consensus B Gag_068	040313Y-29	1692.7	[M + H]+	846.8	[M + 2H]2+	—	[M + 3H]3+
69	20232_069	H-IVRMYSPTSILDIRQ-OH	7872_HIV1 Consensus B Gag_069	040313Y-31	1792.5	[M + H]+	896.8	[M + 2H]2+	598.4	[M + 3H]3+
70	20232_070	H-ISPTSILOIRQGPKE-OH	7872_HIV1 Consensus B Gag_070	040313Y-33	—	—	852.4	[M + 2H]2+	588.8	[M + 3H]3+
71	20232_071	H-SILDIRDGPKEPPRD-OH	7872_HIV1 Consensus B Gag_071	040313Y-35	—	—	885.9	[M + 2H]2+	591.1	[M + 3H]3+
72	20232_072	H-IRQGPKEPPRDYVDR-OH	7872_HIV1 Consensus B Gag_072	040313Y-37	—	—	938.9	[M + 2H]2+	626.1	[M + 3H]3+
73	20232_073	H-PKEPPRDIVDRFYET-OH	7872_HIV1 Consensus B Gag_073	040313Y-39	—	—	980.9	[M + 2H]2+	654.5	[M + 3H]3+
74	20232_074	H-PRDYVDRFYKTLRAE-OH	7872_HIV1 Consensus B Gag_074	270213M-17	—	—	990.8	[M + 2H]2+	660.7	[M + 3H]3+
75	20232_075	H-VDRFYKTLRAEQASQ-OH	7872_HIV1 Consensus B Gag_075	270213M-19	—	—	906.9	[M + 2H]2+	604.7	[M + 3H]3+
76	20232_076	H-YKTLRASQASQEVEN-OH	7872_HIV1 Consensus B Gag_076	270213M-21	—	—	862.9	[M + 2H]2+	589.1	[M + 3H]3+
77	20232_077	H-RAEQASQIVQNWMTE-OH	7872_HIV1 Consensus B Gag_077	270213M-23	1807.3	[M + H]+	904.2	[M + 2H]2+	—	[M + 3H]3+
78	20232_078	H-ASQEVKNWMTETLLV-OH	7872_HIV1 Consensus B Gag_078	270213M-25	1750.3	[M + H]+	875.3	[M + 2H]2+	—	[M + 3H]3+
79	20232_079	H-VONWMTETLLVQNAN-OH	7872_HIV1 Consensus B Gag_079	270213M-27	1763.2	[M + H]+	861.4	[M + 2H]2+	—	[M + 3H]3+
80	20232_080	H-MTETLLVQNANPDCK-OH	7872_HIV1 Consensus B Gag_080	270213M-29	1678.4	[M + H]+	838.8	[M + 2H]2+	558.7	[M + 3H]3+
81	20232_081	H-LLVQNANPDCKTILK-OH	7872_HIV1 Consensus B Gag_081	270213M-31	1672.4	[M + H]+	835.9	[M + 2H]2+	557.7	[M + 3H]3+
82	20232_082	H-NANPDCKIILKALGP-OH	7872_HIV1 Consensus B Gag_082	270213M-33	1555.8	[M + H]+	778	[M + 2H]2+	—	[M + 3H]3+
83	20232_083	H-DCKTLLKALGPAATL-OH	7872_HIV1 Consensus B Gag_083	270213M-35	1515.5	[M + H]+	757.9	[M + 2H]2+	505.7	[M + 3H]3+
84	20232_084	H-ILKALGPAATLEEMN-OH	7872_HIV1 Consensus B Gag_084	270213M-37	1588.5	[M + H]+	794.4	[M + 2H]2+	530	[M + 3H]3+
85	20232_085	H-LGPAATLEEMNTACQ-OH	7872_HIV1 Consensus B Gag_085	270213M-39	1566.3	[M + H]+	783.8	[M + 2H]2+	—	[M + 3H]3+
86	20232_086	H-ATLEEMMTACQGVGG-OH	7872_HIV1 Consensus B Gag_086	270213M-41	1498.2	[M + H]+	749.7	[M + 2H]2+	—	[M + 3H]3+
87	20232_087	H-EMNTACQGVGGPGHK-OH	7872_HIV1 Consensus B Gag_087	270213M-43	1504.3	[M + H]+	751.8	[M + 2H]2+	501.7	[M + 3H]3+
88	20232_088	H-ACQGVGGPGHKARVL-OH	7872_HIV1 Consensus B Gag_088	270213M-45	1450.4	[M + H]+	725.4	[M + 2H]2+	464	[M + 3H]3+
89	20232_089	H-VGGPGHKARVLAEAM-OH	7872_HIV1 Consensus B Gag_089	270213M-47	1493.4	[M + H]+	746.9	[M + 2H]2+	498.4	[M + 3H]3+
90	20232_090	H-GHKARVLAEAMSQVT-OH	7872_HIV1 Consensus B Gag_090	08031307	1599.3	[M + H]+	799.7	[M + 2H]2+	—	[M + 3H]3+
91	20232_091	H-RVLAEAHSQVTNSAT-OH	7872_HIV1 Consensus B Gag_091	150313812	—	—	789.6	[M + 2H]2+	526.8	[M + 3H]3+
92	20232_092	H-EAMSQVTMSATIMMO-OH	7872_HIV1 Consensus B Gag_092	18031387	1642	[M + H]+	821.5	[M + 2H]2+	—	[M + 3H]3+
93	20232_093	H-QVTNSATIMMQRGNF-OH	7872_HIV1 Consensus B Gag_093	18031388	1697.2	[M + H]+	846.5	[M + 2H]2+	—	[M + 3H]3+
94	20232_094	H-SATIKMQKGNFRNQR-OH	7872_HIV1 Consensus B Gag_094	14031387	—	—	906.2	[M + 2H]2+	804.3	[M + 3H]3+
95	20232_095	H-MMQRGNFRNQRKTVK-OH	7872_HIV1 Consensus B Gag_095	080313C11	—	—	947.6	[M + 2H]2+	632.4	[M + 3H]3+
96	20232_096	H-GNFRNQRKTVKCFMC-OH	7872_HIV1 Consensus B Gag_096	070313C4	1815.4	[M + H]+	907.5	[M + 2H]2+	605.3	[M + 3H]3+
97	20232_097	H-HORKTVKCFNCGKRG-OH	7872_HIV1 Consensus B Gag_097	070313C5	—	—	856.5	[M + 2H]2+	571.5	[M + 3H]3+
98	20232_098	H-TVKCFNOGKEGHIAK-OH	7872_HIV1 Consensus B Gag_098	070313C6	—	—	817.8	[M + 2H]2+	545.8	[M + 3H]3+
99	20232_099	H-FNCGKEGHIAKNCRA-OH	7872_HIV1 Consensus B Gag_099	070313C8	1648.2	[M + H]+	824.7	[M + 2H]2+	550.3	[M + 3H]3+
100	20232_100	H-KEGHIAKNCRAPRKK-OH	7872_HIV1 Consensus B Gag_100	070313C9	—	—	860.1	[M + 2H]2+	579.5	[M + 3H]3+
101	20232_101	H-IAKNCRAPKKKGCWK-OH	7872_HIV1 Consensus B Gag_101	070313C10	1759.8	[M + H]+	880.4	[M + 2H]2+	587.3	[M + 3H]3+
102	20232_102	H-CRAPRKKGCWKCGKE-OH	7872_HIV1 Consensus B Gag_102	25021384	1750.5	[M + H]+	876.8	[M + 2H]2+	584.4	[M + 3H]3+
103	20232_103	H- -OH	7872_HIV1 Consensus B Gag_103	250213B5	—	—	8 .4	[M + 2H]2+	582.7	[M + 3H]3+
104	20232_104	H- -OH	7872_HIV1 Consensus B Gag_104	250213B6	—	—	877.3	[M + 2H]2+	585.4	[M + 3H]3+
105	20232_105	H- -OH	7872_HIV1 Consensus B Gag_105	250213B7	—	—	859.3	[M + 2H]2+	573.4	[M + 3H]3+
106	20232_106	H- -OH	7872_HIV1 Consensus B Gag_106	250213B8	—	—	859.3	[M + 2H]2+	593.4	[M + 3H]3+
107	20232_107	H- -OH	7872_HIV1 Consensus B Gag_107	250213B9	.2	[M + H]+	893	[M + 2H]2+	593.7	[M + 3H]3+
108	20232_108	H- -OH	7872_HIV1 Consensus B Gag_108	250213B10	—	—	869.6	[M + 2H]2+		[M + 3H]3+
109	20232_109	H- -OH	7872_HIV1 Consensus B Gag_109	260213C2	16 .2	[M + H]+	847.8	[M + 2H]2+	585.7	[M + 3H]3+
110	20232_110	H- -OH	7872_HIV1 Consensus B Gag_110	260213C3	1728.2	[M + H]+	852.8	[M + 2H]2+	575.7	[M + 3H]3+
111	20232_111	H- -OH	7872_HIV1 Consensus B Gag_111	260213C4	—	—	860.4	[M + 2H]2+	574.1	[M + 3H]3+
112	20232_112	H- -OH	7872_HIV1 Consensus B Gag_112	260213C5	1619.2	[M + H]+	8 .0	[M + 2H]2+	—	[M + 3H]3+
113	20232_113	H- -OH	7872_HIV1 Consensus B Gag_113	260213C6	1658.2	[M + H]+	843.2	[M + 2H]2+	—	[M + 3H]3+
114	20232_114	H- -OH	7872_HIV1 Consensus B Gag_114	260213C7	.3	[M + H]+	848.	[M + 2H]2+	—	[M + 3H]3+
115	20232_115	H- -OH	7872_HIV1 Consensus B Gag_115	040313C3	.1	[M + H]+	8.7	[M + 2H]2+	—	[M + 3H]3+
116	20232_116	H- -OH	7872_HIV1 Consensus B Gag_116	040313C4	—	—	872.4	[M + 2H]2+	562.1	[M + 3H]3+
117	20232_117	H- -OH	7872_HIV1 Consensus B Gag_117	040313C5	—	—	848.3	[M + 2H]2+	564.7	[M + 3H]3+
118	20232_118	H- -OH	7872_HIV1 Consensus B Gag_118		—	—	857.9	[M + 2H]2+	577.4	[M + 3H]3+
119	20232_119	H- -OH	7872_HIV1 Consensus B Gag_119	280213C8	1761.3	[M + H]+	860.4	[M + 2H]2+	587.5	[M + 3H]3+
120	20232_120	H- -OH	7872_HIV1 Consensus B Gag_120	280213C9	—	—	865.9	[M + 2H]2+	577.7	[M + 3H]3+
121	20232_121	H- -OH	7872_HIV1 Consensus B Gag_121	280213C10	—	—	854.4	[M + 2H]2+	576.2	[M + 3H]3+
122	20232_122	H- -OH	7872_HIV1 Consensus B Gag_122	11031384	1861.3	[M + H]+	781.2	[M + 2H]2+	—	[M + 3H]3+
123	20232_123	H- -OH	7872_HIV1 Consensus B Gag_123	280213C11	1821.1	[M + H]+	81.1	[M + 2H]2+	—	[M + 3H]3+
		Theor. MW
		(average)	Theor. MW + TFA	Exp. MW vs.
	Index	[g/mol]	[g/mol]	Theor. MW	Purity [%]	Amount [mg]	Purified	Comment
	1	1518.72	1860.72	pass	96.4	50	Y
	2	1659.87	2001.87	pass	90.1	50	Y
	3	1812.08	2382.08	pass	93.1	50	Y
	4	1852.21	2850.21	pass	90.9	50	Y
	5	1814.25	2726.25	pass	87.7	50	Y
	6	1785.21	2677.21	pass	81.7	50	Y
	7	1842.25	2754.25	pass	91.7	50	Y
	8	1928.28	2612.26	pass	88.1	50	Y
	9	1827.09	2283.09	pass	85.7	50	Y
	10	1671.94	2013.94	pass	96.2	50	Y
	11	1674.9	1902.8	pass	81.5	50	Y
	12	1573.78	1801.76	pass	81	50	Y
	13	1603.83	1831.83	pass	90.7	50	Y
	14	1616.83	1844.83	pass	90.4	50	Y
	15	1641.92	1669.92	pass	88.7	50	Y
	16	1599.78	1713.78	pass	93.2	50	Y
	17	1707.89	1935.69	pass	80.4	50	Y
	18	1667.82	1895.82	pass	86.1	50	Y
	19	1775.04	2003.84	pass	82	50	Y
	20	1768.04	2110.04	pass	82.2	50	Y	5)
	21	1760.1	2216.1	pass	85.2	50	Y
	22	1861.16	2431.16	pass	80.4	50	Y
	23	1824.08	2508.08	pass	91.1	50	Y
	24	1789.98	2245.98	pass	94	50	Y
	25	1775.95	2231.95	pass	94.5	50	Y
	26	1802.06	2486.06	pass	81.9	50	Y	5)
	27	1716.87	2286.67	pass	50.4	50	Y
	28	1545.71	2115.71	pass	87.5	50	Y	5)
	29	1504.58	1846.58	pass	81.9	50	Y	5)
	30	1477.47	1591.47	pass	86.5	50	Y
	31	1508.69	1722.69	pass	89.1	50	Y
	32	1704.86	1818.86	pass	84.3	50	Y	1)
	33	1716.94	1632.94	pass	89	50	Y
	34	1675.96	1903.96	pass	82.1	50	Y
	35	1679.92	2021.92	pass	93.5	50	Y
	36	1752.03	2094.03	pass	85.4	50	Y
	37	1682	2024	pass	84.6	50	Y
	38	1740.04	2196.04	pass	95.2	50	Y
	39	1732.96	2074.96	pass	93.9	50	Y
	40	1703.04	2045.04	pass	86.8	50	Y
	41	1665.99	1893.99	pass	58.6	50	Y
	42	1534.77	1546.77	pass	83.8	50	Y	5)
	43	1563.77	1677.77	pass	81.2	50	Y
	44	1534.68	1646.68	pass	81.7	50	Y
	45	1603.78	1717.78	pass	81.6	50	Y
	46	1624.79	1652.79	pass	81.6	50	Y
	47	1572.77	1800.77	pass	84.4	50	Y
	48	1614.85	1956.85	pass	83.4	50	Y
	49	1700.95	2042.95	pass	95.1	50	Y
	50	1707.95	1935.95	pass	88.8	50	Y
	51	1817.01	2158.01	pass	88.5	50	Y
	52	1815.98	2271.98	pass	96	50	Y
	53	1668.80	2124.89	pass	93.85	50	Y
	54	1564.78	2020.78	pass	94.9	50	Y
	55	1656.62	1896.82	pass	84.1	50	Y
	56	1567.76	1909.76	pass	84.5	50	Y
	57	1571.75	1913.75	pass	84.7	50	Y
	58	1560.72	1902.72	pass	82.3	50	Y	5)
	59	1520.64	1634.64	pass	81.7	50	Y
	60	1623.82	1737.82	pass	81.5	50	Y
	61	1715.91	1829.91	pass	85.2	50	Y
	62	1852.89	1766.89	pass	89.5	50	Y
	63	1759.06	1987.06	pass	91	50	Y
	64	1795.17	2137.17	pass	83.4	50	Y
	65	1771.14	2113.14	pass	92.5	50	Y
	66	1885.37	2455.37	pass	90.7	50	Y
	67	1803.24	2145.24	pass	93.4	50	Y
	68	1692.06	2034.06	pass	83.9	50	Y
	69	1792.15	2134.15	pass	83.1	50	Y
	70	1703.94	2045.94	pass	92.3	50	Y
	71	1771.03	2227.03	pass	92.7	50	Y
	72	1876.13	2446.13	pass	87.7	50	Y
	73	1961.24	2531.24	pass	85.5	50	Y
	74	1979.26	2549.26	pass	88	50	Y
	75	1812.04	2268.04	pass	89.5	50	Y
	76	1764.97	2220.07	pass	85.4	50	Y
	77	1800.68	2148.96	pass	85.3	50	Y
	78	1749.02	1977.02	pass	88.6	50	Y
	79	1781.02	1989.02	pass	82.9	50	Y
	80	1676.93	1904.93	pass	89.8	50	Y
	81	1670	2012	pass	88.1	50	Y	5)
	82	1654.83	1896.83	pass	89.7	50	Y
	83	1514.86	1856.86	pass	81	50	Y
	84	157.97	1815.97	pass	92.8	50	Y
	85	1565.86	1679.86	pass	81.8	50	Y
	86	1497.73	1611.73	pass	89.2	50	Y
	87	1502.74	1844.74	pass	84.3	50	Y
	88	1449.69	1905.69	pass	86.7	50	Y
	89	1492.76	1946.76	pass	97.1	50	Y
	90	1597.88	2053.86	pass	81.6	50	Y
	91	1577.79	1805.79	pass	92.9	50	Y
	92	1641.9	1755.9	pass	87.7	50	Y
	93	1697.95	1925.95	pass	86	50	Y
	94	1810.09	2266.09	pass	86.8	50	Y
	95	1894.24	2578.24	pass	84.3	50	Y	5)
	96	1815.1	2385.1	pass	95.3	50	Y
	97	1711.97	2281.97	pass	85.5	50	Y
	98	1834.93	2204.93	pass	86.45	50	Y
	99	1847.80	2217.89	pass	86.6	50	Y
	100	1738.07	2648.07	pass	87.3	50	Y
	101	1759.18	2557.16	pass	82	50	Y
	102	1750.13	2548.13	pass	82.9	50	Y
	103	1776.11	2578.11	pass	86.3	50	Y
	104	1754.	2324.04	pass	81.3	50	Y
	105	1717.9	2287.9	pass	82.6	50	Y
	106	1778	2234	pass	87.2	50	Y
	107	1778.03	2120.03	pass	91.5	50	Y
	108	1739.01	2309.01	pass	94	50	Y
	109	1893.	2253.97	pass	89	50	Y
	110	17	2179.28	pass	81.7	50	Y	1)
	111		2289.84	pass	84.7	50	Y
	112	1687.83	1639.52	pass	81.9	50	Y
	113		1812.67	pass	82.4	50	Y
	114		1817.65	pass	82.3	50	Y
	115	1697.83	1825.83	pass	81.1	50	Y
	116	1743.89		pass	86.1	50	Y
	117			pass	89.2	50	Y
	118	1714.82		pass	94.8	50	Y
	119	1759.81	2101.61	pass	94.5	50	Y
	120		2828.61	pass	93.7	50	Y
	121			pass	96.8	50	Y
	122	1580.75	1788.75	pass	92	50	Y
	123	1320.44	1548.44	pass	82.7	50	Y
	Comments:
	1) C  isomerization of protein
	2) no HPLC possible-MALDI performed
	3) dissolved in CMSO
	4) dissolved in TFA/water
	5) dissolved in ACN-
	indicates data missing or illegible when filed

TABLE 5
HIV-1 Consensus B Rev (NIH AIDS Reagent 6445)
DATA SHEET
HIV-1 Consensus B REV (15-mer) Peptides - Complete Set (Cat# 6445, Lot# 7)
					Peptide
Cat #	Peptide Name	Sublot #	Lot #	HPLC Purity	Content	Solubility Data
5991	HIV-1 Consensus B REV (15-mer)	5	5991	91.4%	77.6%	1 mg/ml in water
	Peptide MAGRSGDSDEELLKT
5992	HIV-1 Consensus B REV (15-mer)	5	5992	89.1%	75.5%	1 mg/ml in water
	Peptide SGDSDEELLKTVRLI
5993	HIV-1 Consensus B REV (15-mer)	5	5993	85.2%	85.5%	1 mg/ml in water
	Peptide DEELLKTVRLIKFLY
5994	HIV-1 Consensus B REV (15-mer)	5	5994	92.5%	80.0%	1 mg/ml in water
	Peptide LKTVRLIKFLYQSNP
5995	HIV-1 Consensus B REV (15-mer)	5	5995	89.7%	80.3%	1 mg/ml in water
	Peptide RLIKPLYQSNPPPSP
5996	HIV-1 Consensus B REV (15-mer)	5	5996	95.3%	89.1%	1 mg/ml in water
	Peptide FLYQSNPPPSPEGTR
5997	HIV-1 Consensus B REV (15-mer)	5	5997	93.2%	65.5%	1 mg/ml in water
	Peptide SNPPPSPEGTRQARR
5998	HIV-1 Consensus B REV (15-mer)	5	5998	80.3%	67.3%	1 mg/ml in water
	Peptide PSPEGTRQARRNRRR
5999	HIV-1 Consensus B REV (15-mer)	5	5999	94.5%	73.0%	1 mg/ml in water
	Peptide GTRQARRNRRRRWRE
6000	HIV-1 Consensus B REV (15-mer)	5	6000	89.7%	67.8%	1 mg/ml in water
	Peptide ARRNRRRRWRERGRQ
6001	HIV-1 Consensus B REV (15-mer)	5	6001	91.7%	67.0%	1 mg/ml in water
	Peptide RRRRWRERQRQIRSI
6002	HIV-1 Consensus B REV (15-mer)	5	6002	89.3%	77.0%	1 mg/ml in water
	Peptide WRERQRQIRSISGWI
6003	HIV-1 Consensus B REV (15-mer)	5	6003	82.8%	74.9%	1 mg/ml in water
	Peptide QRQIRSISGWILSTY
6004	HIV-1 Consensus B REV (15-mer)	5	6004	93.0%	88.7%	1 mg/ml in water
	Peptide RSISGWILSTYLGRP
6005	HIV-1 Consensus B REV (15-mer)	5	6005	91.9%	86.1%	1 mg/ml in water
	Peptide GWILSTYLGRPAEPV
6006	HIV-1 Consensus B REV (15-mer)	5	6006	85.0%	87.5%	1 mg/ml in water
	Peptide STYLGRPAEPVPLQL
6007	HIV-1 Consensus B REV (15-mer)	5	6007	83.8%	82.9%	1 mg/ml in water
	Peptide GRPAEPVPLQLPPLE
6008	HIV-1 Consensus B REV (15-mer)	5	6008	84.2%	89.1%	1 mg/ml in water
	Peptide EPVPLQLPPLERLTL
6009	HIV-1 Consensus B REV (15-mer)	5	6009	85.4%	85.2%	1 mg/ml in water
	Peptide LQLPPLERLTLDCNE
6010	HIV-1 Consensus B REV (15-mer)	5	6010	74.8%	82.8%	1 mg/ml in water
	Peptide PLERLTLDCNEDCGT
6011	HIV-1 Consensus B REV (15-mer)	5	6011	83.4%	82.7%	1 mg/ml in water
	Peptide LTLDCNEDCGTSGTQ
6012	HIV-1 Consensus B REV (15-mer)	5	6012	82.1%	87.4%	1 mg/ml in water
	Peptide CNEDCGTSGTQGVGS
6013	HIV-1 Consensus B REV (15-mer)	5	6013	89.9%	88.0%	1 mg/ml in water
	Peptide CGTSGTQGVGSPQIL
6014	HIV-1 Consensus B REV (15-mer)	5	6014	90.5%	91.0%	1 mg/ml in water
	Peptide GTQGVGSPQILVESP
6015	HIV-1 Consensus B REV (15-mer)	5	6015	81.8%	84.5%	1 mg/ml in water
	Peptide VGSPQILVESPAVLE
6016	HIV-1 Consensus B REV (15-mer)	5	6016	82.3%	75.1%	1 mg/ml in water
	Peptide QILVESPAVLESGTK
6017	HIV-1 Consensus B REV (15-mer)	5	6017	89.2%	85.2%	1 mg/ml in water
	Peptide ESPAVLESGTKEE
NOTE:
Peptides that are difficult to solubilize can almost always be dissolved in DMSO. Once a peptide is in solution, the DMSO can be slowly diluted with aqueous medium. Care must be taken to ensure that the pepside does not begin to precipitate out of solution.

TABLE 6
Consensus B Env (NIH AIDS reagent 9480)
Data for Cat# 9480
Lot 140223 and #12540 Lot 140347	Solubility	Solvent
	Cat #	Peptide	Sequence	mg/ml	Water	PBS	10% Acetic Acid	DMSO
1	8763	HIV-1 Con B Env	MRVKGIRKNYQHLWR	0.25	−	−	−	+
2	8764	HIV-1 Con B Env	GIRKNYQHLWRWGTM	0.25	−	−	−	+
3	8765	HIV-1 Con B Env	NYQHLWRWGTMLLGM	0.25	−	−	−	+
4	8766	HIV-1 Con B Env	LWRWGTMLLGMLMIC	0.25	−	−	−	+
5	8767	HIV-1 Con B Env	GTMLLGMLMICSAAE	0.25	−	−	−	+
6	8768	HIV-1 Con B Env	LGMLMICSAAEKLWV	0.25	−	−	−	+
7	8769	HIV-1 Con B Env	MICSAAEKLWVTVYY	0.25	−	−	−	+
8	8770	HIV-1 Con B Env	AAEKLWVTVYYGVPV	0.25	−	−	−	+
9	8771	HIV-1 Con B Env	LWVTVYYGVPVWKEA	0.25	−	−	−	+
10	8772	HIV-1 Con B Env	VYYGVPVWKEATTTL	0.25	−	−	−	+
11	8773	HIV-1 Con B Env	VPVWKEATTTLFCAS	0.25	−	−	−	+
12	8774	HIV-1 Con B Env	KEATTTLFCASDAKA	0.25	−	−	−	+
13	8775	HIV-1 Con B Env	TTLFCASDAKAYDTE	0.25	−	−	−	+
14	8776	HIV-1 Con B Env	CASDAKAYDTEVHNV	0.25	−	−	−	+
15	8777	HIV-1 Con B Env	AKAYDTEVHNVWATH	0.25	−	−	−	+
16	8778	HIV-1 Con B Env	DTEVHNVWATHACVP	0.25	−	−	−	+
17	8779	HIV-1 Con B Env	HNVWATHACVPTDPN	0.25	−	−	−	+
18	8780	HIV-1 Con B Env	ATHACVPTDPNPQEV	0.25	−	−	−	+
19	8781	HIV-1 Con B Env	CVPTDPNPQEVVLEN	0.25	−	−	−	+
20	8782	HIV-1 Con B Env	DPNPQEVVLENVTEN	0.25	−	−	−	+
21	8783	HIV-1 Con B Env	QEVVLENVTENFNMW	0.25	−	−	−	+
22	8784	HIV-1 Con B Env	LENVTENFNMWKNNM	0.25	−	−	−	+
23	8785	HIV-1 Con B Env	TENFNMWKNNMVEQM	0.25	−	−	−	+
24	8786	HIV-1 Con B Env	NMWKNNMVEQMHEDI	0.25	−	−	−	+
25	8787	HIV-1 Con B Env	NNMVEQMHEDIISLW	0.25	−	−	−	+
26	8788	HIV-1 Con B Env	EQMHEDIISLWDQSL	0.25	−	−	−	+
27	8789	HIV-1 Con B Env	EDIISLWDQSLKPCV	0.25	−	−	−	+
28	8790	HIV-1 Con B Env	SLWDQSLKPCVKLTP	0.25	−	−	−	+
29	8791	HIV-1 Con B Env	QSLKPCVKLTPLCVT	0.25	−	−	−	+
30	8792	HIV-1 Con B Env	PCVKLTPLCVTLNCT	0.25	−	−	−	+
31	8793	HIV-1 Con B Env	LTPLCVTLNCTDLMN	0.25	−	−	−	+
32	8794	HIV-1 Con B Env	CVTLNCTDLMNATNT	0.25	−	−	−	+
33	8795	HIV-1 Con B Env	NCTDLMNATNTTNSS	0.25	−	−	−	+
34	8796	HIV-1 Con B Env	LMNATNTTNSSSGEK	0.25	−	−	−	+
35	8797	HIV-1 Con B Env	TNTTNSSSGEKMEKG	0.25	−	−	−	+
36	8798	HIV-1 Con B Env	NSSSGEKMEKGEIKN	0.25	−	−	−
37	8799	HIV-1 Con B Env	GEKMEKGEIKNCSFN	0.25	−	−	−	+
38	8800	HIV-1 Con B Env	EKGEIKNCSFNITTS	0.25	−	−	−	+
39	8801	HIV-1 Con B Env	IKNCSFNITTSIRDK	0.25	−	−	−	+
40	8802	HIV-1 Con B Env	SFNITTSIRDKVQKE	0.25	−	−	−	+
41	8803	HIV-1 Con B Env	TTSIRDKVQKEYALF	0.25	−	−	−	+
42	8804	HIV-1 Con B Env	RDKVQKEYALFYKLD	0.25	−	−	−	+
43	8805	HIV-1 Con B Env	QKEYALFYKLDVVPI	0.25	−	−	−	+
44	8806	HIV-1 Con B Env	ALFYKLDVVPIDNDN	0.25	−	−	−	+
45	8807	HIV-1 Con B Env	KLDVVPIDNDNTSSY	0.25	−	+	−	+
46	8808	HIV-1 Con B Env	VPIDNDNTSSYRLIS	0.25	−	−	−	+
47	8809	HIV-1 Con B Env	NDNTSSYRLISCNTS	0.25	−	−	−	+
48	8810	HIV-1 Con B Env	SSYRLISCNTSVITQ	0.25	−	−	−	+
49	8811	HIV-1 Con B Env	LISCNTSVITQACPK	0.25	−	−	−	+
50	8812	HIV-1 Con B Env	NTSVITQACPKVSFE	0.25	−	−	−	+
51	8813	HIV-1 Con B Env	ITQACPKVSFEPIPI	0.25	−	−	−	+
52	8814	HIV-1 Con B Env	CPKVSFEPIPIHYCA	0.25	−	−	−	+
53	8815	HIV-1 Con B Env	SFEPIPIHYCAPAGF	0.25	−	−	−	+
54	8816	HIV-1 Con B Env	IPIHYCAPAGFAILK	0.25	−	−	−	+
55	8817	HIV-1 Con B Env	YCAPAGFAILKCNDK	0.25	−	−	−	+
56	8818	HIV-1 Con B Env	AGFAILKCNDKKFNG	0.25	−	−	−	+
57	8819	HIV-1 Con B Env	ILKCNDKKFNGTGPC	0.25	−	−	−	+
58	8820	HIV-1 Con B Env	NDKKFNGTGPCTNVS	0.25	−	−	−	+
59	8821	HIV-1 Con B Env	FNGTGPCTNVSTVQC	0.25	−	−	−	+
60	8822	HIV-1 Con B Env	GPCTNVSTVQCTHGI	0.25	−	−	−	+
61	8823	HIV-1 Con B Env	NVSTVQCTHGIRPVV	0.25	−	−	−	+
62	8824	HIV-1 Con B Env	VQCTHGIRPVVSTQL	0.25	−	−	−	+
63	8825	HIV-1 Con B Env	HGIRPVVSTQLLLNG	0.25	−	−	−	+
64	8826	HIV-1 Con B Env	PVVSTQLLLNGSLAE	0.25	−	−	−	+
65	8827	HIV-1 Con B Env	TQLLLNGSLAEEEVV	0.25	−	−	−	+
66	8828	HIV-1 Con B Env	LNGSLAEEEVVIRSE	0.25	−	+	−	+
67	8829	HIV-1 Con B Env	LAEEEVVIRSENFTN	0.25	−	+	−	+
68	8830	HIV-1 Con B Env	EVVIRSENFTNNAKT	0.25	−	−	−	+
69	8831	HIV-1 Con B Env	RSENFTNNAKTIIVQ	0.25	−	−	−	+
70	8832	HIV-1 Con B Env	FTNNAKTIIVQLNES	0.25	−	−	−	+
71	8833	HIV-1 Con B Env	AKTIIVQLNESVEIN	0.25	−	−	−	+
72	8834	HIV-1 Con B Env	IVQLNESVEINCTRP	0.25	−	−	−	+
73	8835	HIV-1 Con B Env	NESVEINCTRPNNNT	0.25	−	−	−	+
74	8836	HIV-1 Con B Env	EINCTRPNNNTRKSI	0.25	−	−	−	+
75	8837	HIV-1 Con B Env	TRPNNNTRKSIHIGP	0.25	−	−	−	+
76	8838	HIV-1 Con B Env	NNTRKSIHIGPGRAF	0.25	−	−	−	+
77	8839	HIV-1 Con B Env	KSIHIGPGRAFYTTG	0.25	−	−	−	+
78	8840	HIV-1 Con B Env	IGPGRAFYTTGEIIG	0.25	−	−	−	+
79	8841	HIV-1 Con B Env	RAFYTTGEIIGDIRQ	0.25	−	−	−	+
80	8842	HIV-1 Con B Env	TTGEIIGDIRQAHCN	0.25	−	−	−	+
81	8843	HIV-1 Con B Env	IIGDIRQAHCNISRA	0.25	−	−	−	+
82	8844	HIV-1 Con B Env	IRQAHCNISRAKWNN	0.25	−	−	−	+
83	8845	HIV-1 Con B Env	HCNISRAKWNNTLKQ	0.25	−	−	−	+
84	8846	HIV-1 Con B Env	SRAKWNNTLKQIVKK	0.25	−	−	−	+
85	8847	HIV-1 Con B Env	WNNTLKQIVKKLREQ	0.25	−	−	−	+
86	8848	HIV-1 Con B Env	LKQIVKKLREQFGNK	0.25	−	−	−	+
87	8849	HIV-1 Con B Env	VKKLREQFGNKTIVF	0.25	−	−	−	+
88	8850	HIV-1 Con B Env	REQFGNKTIVFNQSS	0.25	−	−	−	+
89	8851	HIV-1 Con B Env	GNKTIVFNQSSGGDP	0.25	−	−	−	+
90	8852	HIV-1 Con B Env	IVFNQSSGGDPEIVM	0.25	−	−	−	+
91	8853	HIV-1 Con B Env	QSSGGDPEIVMHSFN	0.25	−	−	−	+
92	8854	HIV-1 Con B Env	GDPEIVMHSFNCGGE	0.25	−	−	−	+
93	8855	HIV-1 Con B Env	IVMHSFNCGGEFFYC	0.25	−	−	−	+
94	8856	HIV-1 Con B Env	SFNCGGEFFYCNTTQ	0.25	−	−	−	+
95	8857	HIV-1 Con B Env	GGEFFYCNTTQLFNS	0.25	−	−	−	+
96	8858	HIV-1 Con B Env	FYCNTTQLFNSTWNV	0.25	−	−	−	+
97	8859	HIV-1 Con B Env	TTQLFNSTWNVNGTW	0.25	−	−	−	+
98	8860	HIV-1 Con B Env	FNSTWNVNGTWNNNT	0.25	−	−	−	+
99	8861	HIV-1 Con B Env	WNVNGTWNNNTEGND	0.25	−	−	−	+
100	8862	HIV-1 Con B Env	GTWNNNTEGNDTITL	0.25	−	−	−	+
101	8863	HIV-1 Con B Env	NNTEGNDTITLPCRI	0.25	−	−	−	+
102	8864	HIV-1 Con B Env	GNDTITLPCRIKQII	0.25	−	−	−	+
103	8865	HIV-1 Con B Env	ITLPCRIKQIINMWQ	0.25	−	−	−	+
104	8866	HIV-1 Con B Env	CRIKQIINMWQEVGK	0.25	−	−	−	+
105	8867	HIV-1 Con B Env	QIINMWQEVGKAMYA	0.25	−	−	−	+
106	8868	HIV-1 Con B Env	MWQEVGKAMYAPPIR	0.25	−	−	−	+
107	8869	HIV-1 Con B Env	VGKAMYAPPIRGQIR	0.25	−	−	−	+
108	8870	HIV-1 Con B Env	MYAPPIRGQIRCSSN	0.25	−	−	−	+
109	8871	HIV-1 Con B Env	PIRGQIRCSSNITGL	0.25	−	−	−	+
110	8872	HIV-1 Con B Env	QIRCSSNITGLLLTR	0.25	−	−	−	+
111	8873	HIV-1 Con B Env	SSNITGLLLTRDGGN	0.25	−	−	−	+
112	8874	HIV-1 Con B Env	TGLLLTRDGGNNNTN	0.25	−	−	−	+
113	8875	HIV-1 Con B Env	LTRDGGNNNTNETEI	0.25	−	−	−	+
114	8876	HIV-1 Con B Env	GGNNNTNETEIFRPG	0.25	−	−	−	+
115	8877	HIV-1 Con B Env	NTNETEIFRPGGGDM	0.25	−	−	−	+
116	8878	HIV-1 Con B Env	TEIFRPGGGDMRDNW	0.25	−	−	−	+
117	8879	HIV-1 Con B Env	RPGGGDMRDNWRSEL	0.25	−	−	−	+
118	8880	HIV-1 Con B Env	GDMRDNWRSELYKYK	0.25	−	−	−	+
119	8881	HIV-1 Con B Env	DNWRSELYKYKVVKI	0.25	−	−	−	+
120	8882	HIV-1 Con B Env	SELYKYKVVKIEPLG	0.25	−	−	+	+
121	8883	HIV-1 Con B Env	KYKVVKIEPLGVAPT	0.25	−	−	+	+
122	8884	HIV-1 Con B Env	VKIEPLGVAPTKAKR	0.25	−	−	−	+
123	8885	HIV-1 Con B Env	PLGVAPTKAKRRVVQ	0.25	−	−	+	+
124	8886	HIV-1 Con B Env	APTKAKRRVVQREKR	0.25	−	−	+	+
125	8887	HIV-1 Con B Env	AKRRVVQREKRAVGI	0.25	−	−	+	+
126	8888	HIV-1 Con B Env	VVQREKRAVGIGAMF	0.25	−	−	−	+
127	8889	HIV-1 Con B Env	EKRAVGIGAMFLGFL	0.25	−	−	−	+
128	8890	HIV-1 Con B Env	VGIGAMFLGFLGAAG	0.25	−	−	−	+
129	8891	HIV-1 Con B Env	AMFLGFLGAAGSTMG	0.25	−	−	−	+
130	8892	HIV-1 Con B Env	GFLGAAGSTMGAASM	0.25	−	−	−	+
131	8893	HIV-1 Con B Env	AAGSTMGAASMTLTV	0.25	−	−	−	+
132	8894	HIV-1 Con B Env	TMGAASMTLTVQARQ	0.25	−	−	−	+
133	8895	HIV-1 Con B Env	ASMTLTVQARQLLSG	0.25	−	−	−	+
134	8896	HIV-1 Con B Env	LTVQARQLLSGIVQQ	0.25	−	−	−	+
135	8897	HIV-1 Con B Env	ARQLLSGIVQQQNNL	0.25	−	−	−	+
136	8898	HIV-1 Con B Env	LSGIVQQQNNLLRAI	0.25	−	−	−	+
137	8899	HIV-1 Con B Env	VQQQNNLLRAIEAQQ	0.25	−	−	−	+
138	8900	HIV-1 Con B Env	NNLLRAIEAQQHLLQ	0.25	−	−	−	+
139	8901	HIV-1 Con B Env	RAIEAQQHLLQLTVW	0.25	−	−	−	+
140	8902	HIV-1 Con B Env	AQQHLLQLTVWGIKQ	0.25	−	−	−	+
141	8903	HIV-1 Con B Env	LLQLTVWGIKQLQAR	0.25	−	−	−	+
142	8904	HIV-1 Con B Env	TVWGIKQLQARVLAV	0.25	−	−	−	+
143	8905	HIV-1 Con B Env	IKQLQARVLAVERYL	0.25	−	−	−	+
144	8906	HIV-1 Con B Env	QARVLAVERYLKDQQ	0.25	−	−	−	+
145	8907	HIV-1 Con B Env	LAVERYLKDQQLLGI	0.25	−	−	−	+
146	8908	HIV-1 Con B Env	RYLKDQQLLGIWGCS	0.25	−	−	−	+
147	8909	HIV-1 Con B Env	DQQLLGIWGCSGKLI	0.25	−	−	−	+
148	8910	HIV-1 Con B Env	LGIWGCSGKLICTTT	0.25	−	−	−	+
149	8911	HIV-1 Con B Env	GCSGKLICTTTVPWN	0.25	−	−	−	+
150	8912	HIV-1 Con B Env	KLICTTTVPWNASWS	0.25	−	−	−	+
151	8913	HIV-1 Con B Env	TTTVPWNASWSNKSL	0.25	−	−	−	+
152	8914	HIV-1 Con B Env	PWNASWSNKSLDEIW	0.25	−	−	−	+
153	8915	HIV-1 Con B Env	SWSNKSLDEIWDNMT	0.25	−	−	−	+
154	8916	HIV-1 Con B Env	KSLDEIWDNMTWMEW	0.25	−	−	−	+
155	8917	HIV-1 Con B Env	EIWDNMTWMEWEREI	0.25	−	−	−	+
156	8918	HIV-1 Con B Env	NMTWMEWEREIDNYT	0.25	−	−	−	+
157	8919	HIV-1 Con B Env	MEWEREIDNYTSLIY	0.25	−	−	−	+
158	8920	HIV-1 Con B Env	REIDNYTSLIYTLIE	0.25	−	−	−	+
159	8921	HIV-1 Con B Env	NYTSLIYTLIEESQN	0.25	−	−	−	+
160	8922	HIV-1 Con B Env	LIYTLIEESQNQQEK	0.25	−	−	−	+
161	8923	HIV-1 Con B Env	LIEESQNQQEKNEQE	0.25	−	−	−	+
162	8924	HIV-1 Con B Env	SQNQQEKNEQELLEL	0.25	−	−	−	+
163	8925	HIV-1 Con B Env	QEKNEQELLELDKWA	0.25	−	−	−	+
164	8926	HIV-1 Con B Env	EQELLELDKWASLWN	0.25	−	−	−	+
165	8927	HIV-1 Con B Env	LELDKWASLWNWFDI	0.25	−	−	−	+
166	8928	HIV-1 Con B Env	KWASLWNWFDITNWL	0.25	−	−	−	+
167	8929	HIV-1 Con B Env	LWNWFDITNWLWYIK	0.25	−	−	−	+
168	8930	HIV-1 Con B Env	FDITNWLWYIKIFIM	0.25	−	−	−	+
169	8931	HIV-1 Con B Env	NWLWYIKIFIMIVGG	0.25	−	−	−	+
170	8932	HIV-1 Con B Env	YIKIFIMIVGGLIGL	0.25	−	−	−	+
171	8933	HIV-1 Con B Env	FIMIVGGLIGLRIVF	0.25	−	−	−	+
172	8934	HIV-1 Con B Env	VGGLIGLRIVFAVLS	0.25	−	−	−	+
173	8935	HIV-1 Con B Env	IGLRIVFAVLSIVNR	0.25	−	−	−	+
174	8936	HIV-1 Con B Env	IVFAVLSIVNRVRQG	0.25	−	−	−	+
175	8937	HIV-1 Con B Env	VLSIVNRVRQGYSPL	0.25	−	−	−	+
176	8938	HIV-1 Con B Env	VNRVRQGYSPLSFQT	0.25	−	−	−	+
177	8939	HIV-1 Con B Env	RQGYSPLSFQTRLPA	0.25	−	−	−	+
178	8940	HIV-1 Con B Env	SPLSFQTRLPAPRGP	0.25	−	−	−	+
179	8941	HIV-1 Con B Env	FQTRLPAPRGPDRPE	0.25	−	−	−	+
180	8942	HIV-1 Con B Env	LPAPRGPDRPEGIEE	0.25	−	−	−	+
181	8943	HIV-1 Con B Env	RGPDRPEGIEEEGGE	0.25	−	+	−	+
182	8944	HIV-1 Con B Env	RPEGIEEEGGERDRD	0.25	−	+	−	+
183	8945	HIV-1 Con B Env	IEEEGGERDRDRSGR	0.25	−	+	−	+
184	8946	HIV-1 Con B Env	GGERDRDRSGRLVDG	0.25	−	+	−	+
185	8947	HIV-1 Con B Env	DRDRSGRLVDGFLAL	0.25	−	+	−	+
186	8948	HIV-1 Con B Env	SGRLVDGFLALIWDD	0.25	−	−	−	+
187	8949	HIV-1 Con B Env	VDGFLALIWDDLRSL	0.25	−	−	−	+
188	8950	HIV-1 Con B Env	LALIWDDLRSLCLFS	0.25	−	−	−	+
189	8951	HIV-1 Con B Env	WDDLRSLCLFSYHRL	0.25	−	−	−	+
190	8952	HIV-1 Con B Env	RSLCLFSYHRLRDLL	0.25	−	−	−	+
191	8953	HIV-1 Con B Env	LFSYHRLRDLLLIVT	0.25	−	−	−	+
192	8954	HIV-1 Con B Env	HRLRDLLLIVTRIVE	0.25	−	−	−	+
193	8955	HIV-1 Con B Env	DLLLIVTRIVELLGR	0.25	−	−	−	+
194	8956	HIV-1 Con B Env	IVTRIVELLGRRGWE	0.25	−	−	−	+
195	8957	HIV-1 Con B Env	IVELLGRRGWEVLKY	0.25	−	−	−	+
196	8958	HIV-1 Con B Env	LGRRGWEVLKYWWNL	0.25	−	−	−	+
197	8959	HIV-1 Con B Env	GWEVLKYWWNLLQYW	0.25	−	−	−	+
198	8960	HIV-1 Con B Env	LKYWWNLLQYWSQEL	0.25	−	−	−	+
199	8961	HIV-1 Con B Env	WNLLQYWSQELKNSA	0.25	−	−	−	+
200	8962	HIV-1 Con B Env	QYWSQELKNSAVSLL	0.25	−	−	−	+
201	8963	HIV-1 Con B Env	QELKNSAVSLLNATA	0.25	−	−	−	+
202	8964	HIV-1 Con B Env	NSAVSLLNATAIAVA	0.25	−	−	−	+
203	8965	HIV-1 Con B Env	SLLNATAIAVAEGTD	0.25	−	−	−	+
204	8966	HIV-1 Con B Env	ATAIAVAEGTDRVIE	0.25	−	−	−	+
205	8967	HIV-1 Con B Env	AVAEGTDRVIEVVQR	0.25	−	−	−	+
206	8968	HIV-1 Con B Env	GTDRVIEVVQRACRA	0.25	−	−	−	+
207	8969	HIV-1 Con B Env	VIEVVQRACRAILH1	0.25	−	−	−	+
208	8970	HIV-1 Con B Env	VQRACRAILHIPRRI	0.25	−	−	+	+
209	8971	HIV-1 Con B Env	CRAILHIPRRIRQGL	0.25	−	−	+	+
210	8972	HIV-1 Con B Env	LHIPRRIRQGLERAL	0.25	+	−	+	+
211	8973	HIV-1 Con B Env	RRIRQGLERALL	0.25	−	−	+	+
Molecular Weight and Purity Data:
Catalog #9480 Lot 140223 and #12540 Lot 140347
					MW (1)		MW (2)
					detected		detected
	JPT-#	Sequence	Peptide Name	Batch#	[g/mol]	MW (1) label	[g/mol]
1	23651_294	H-MRVKGIRKNYQHLWR-OH	8763_HIV-1 Con B Env_001	270114F-04	—	—	993.4
2	23651_295	H-GIRKNYQHLWRWGTM-OH	8764_HIV-1 Con B Env_002	270114F-06	—	—	976.6
3	23651_296	H-NYQHLWRWGTMLLGM-OH	8765_HIV-1 Con B Env_003	270114F-08	1906.2	[M + H]+	953.7
4	23651_297	H-LWRWGTMLLGMLMIC-OH	8766_HIV-1 Con B Env_004	270114F-10	1824.7	[M + H]+	912.7
5	23651_298	H-GTMLLGMLMICSAAE-OH	8767_HIV-1 Con B Env_005	270114F-12	1540.01	[M + H]+	1562.55
6	23651_299	H-LGMLMICSAAEKLWV-OH	8768_HIV-1 Con B Env_006	270114F-14	1665.7	[M + H]+	833.0
7	23651_300	H-MICSAAEKLWVTVYY-OH	8769_HIV-1 Con B Env_007	270114F-16	1777.8	[M + H]+	889.0
8	23651_301	H-AAEKLWVTVYYGVPV-OH	8770_HIV-1 Con B Env_008	270114F-18	1695.7	[M + H]+	848.1
9	23651_302	H-LWVTVYYGVPVWKEA-OH	8771_HIV-1 Con B Env_009	270114F-20	1809.8	[M + H]+	905.6
10	23651_303	H-VYYGVPVWKEATTTL-OH	8772_HIV-1 Con B Env_010	270114F-22	1726.8	[M + H]+	64.1
11	23651_304	H-VPVWKEATTTLFCAS-OH	8773_HIV-1 Con B Env_011	270114F-24	1654.2	[M + H]+	827.2
12	23651_305	H-KEATTTLFCASDAKA-OH	8774_HIV-1 Con B Env_012	270114F-26	1558.6	[M + H]+	779.0
13	23651_306	H-TTLFCASDAKAYDTE-OH	8775_HIV-1 Con B Env_013	270114F-28	1636.6	[M + H]+	818.5
14	23651_307	H-CASDAKAYDTEVHNV-OH	8776_HIV-1 Con B Env_014	270114F-30	1624.6	[M + H]+	812.0
15	23651_308	H-AKAYDTEVHNVWATH-OH	8777_HIV-1 Con B Env_015	270114F-32	1743.1	[M + H]+	871.7
16	23651_309	H-DTEVHNVWATHACVP-OH	8778_HIV-1 Con B Env_016	270114F-34	1679.3	[M + H]+	840.2
17	23651_310	H-HNVWATHACVPTDPN-OH	8779_HIV-1 Con B Env_017	270114F-36	1662.7	[M + H]+	831.5
18	23651_311	H-ATHACVPTDPNPQEV-OH	8780_HIV-1 Con B Env_018	270114F-38	1578.6	[M + H]+	790.0
19	23651_312	H-CVPTDPNPQEVVLEN-OH	8781_HIV-1 Con B Env_019	270114F-40	1655.6	[M + H]+	827.5
20	23651_313	H-DPNPQEVVLENVTEN-OH	8782_HIV-1 Con B Env_020	270114F-42	1696.8	[M + H]+	849.0
21	23651_314	H-QEVVLENVTENFNMW-OH	8783_HIV-1 Con B Env_021	270114F-44	1853.7	[M + H]+	927.0
22	23651_315	H-LENVTENFNMWKNNM-OH	8784_HIV-1 Con B Env_022	270114F-46	1885.7	[M + H]+	942.6
23	23651_316	H-TENFNMWKNNMVEQM-OH	8785_HIV-1 Con B Env_023	270114F-48	1915.7	[M + H]+	959.0
24	23651_317	H-NMWKNNMVEQMHEDI-OH	8786_HIV-1 Con B Env_024	300114C3	—	—	960.0
25	23651_318	H-NNMVEQMHEDIISLW-OH	8787_HIV-1 Con B Env_025	300114C4	1860.7	[M + H]+	930.0
26	23651_319	H-EQMHEDIISLWDQSL-OH	8788_HIV-1 Con B Env_026	300114C5	1845.6	[M + H]+	922.5
27	23651_320	H-EDIISLWDQSLKPCV-OH	8789_HIV-1 Con B Env_027	300114C6	1746.7	[M + H]+	873.5
28	23651_321	H-SLWDQSLKPCVKLTP-OH	8790_HIV-1 Con B Env_028	300114C10	1716.8	[M + H]+	858.0
29	23651_322	H-QSLKPCVKLTPLCVT-OH	8791_HIV-1 Con B Env_029	310114B4	1630.7	[M + H]+	815.6
30	23651_323	H-PCVKLTPLCVTLNCT-OH	8792_HIV-1 Con B Env_030	310114B5	1604.7	[M + H]+	803.0
31	23651_324	H-LTPLCVTLNCTDLMN-OH	8793_HIV-1 Con B Env_031	310114B6	1651.7	[M + H]+	826.5
32	23651_325	H-CVTLNCTDLMNATNT-OH	8794_HIV-1 Con B Env_032	310114B7	1615.6	[M + H]+	807.5
33	23651_326	H-NCTDLMNATNTTNSS-OH	8795_HIV-1 Con B Env_033	310114B11	1588.5	[M + H]+	974.0
34	23651_327	H-LMNATNTTNSSSGEK-OH	8796_HIV-1 Con B Env_034	310114C11	1555.6	[M + H]+	778.0
35	23651_328	H-TNTTNSSSGEKMEKG-OH	8797_HIV-1 Con B Env_035	310114C12	1570.6	[M + H]+	786.0
36	23651_329	H-NSSSGEKMEKGEIKN-OH	8798_HIV-1 Con B Env_036	310114Y-15	1639.9	[M + H]+	816.6
37	23651_330	H-GEKMEKGEIKNCSFN-OH	8799_HIV-1 Con B Env_037	310114Y-17	1713.7	[M + H]+	857.5
38	23651_331	H-EKGEIKNCSFNITTS-OH	8800_HIV-1 Con B Env_038	310114Y-19	1670.7	[M + H]+	836.0
39	23651_332	H-IKNCSFNITTSIRDK-OH	8801_HIV-1 Con B Env_039	310114Y-22	1739.8	[M + H]+	870.6
40	22651_333	H-SFNITTSIRDKVQKE-OH	8802_HIV-1 Con B Env_040	310114Y-23	1765.7	[M + H]+	883.6
41	22651_334	H-TTSIRDKVQKEVALF-OH	8803_HIV-1 Con B Env_041	310114Y-25	—	—	900.1
42	22651_335	H-ROKVQKEYALFYKLD-OH	8804_HIV-1 Con B Env_042	310114Y-27	1917.3	[M + H]+	959.2
43	22651_336	H-QKEYALFYKLDVVPI-OH	8805_HIV-1 Con B Env_043	310114Y-29	1827.8	[M + H]+	913.6
44	22651_337	H-ALFYKLDVVPIDNDN-OH	8806_HIV-1 Con B Env_044	310114Y-31	1736.3	[M + H]+	868.7
45	22651_338	H-KLDVVPIDNDNTSSV-OH	8807_HIV-1 Con B Env_045	310114Y-33	1680.7	[M + H]+	840.5
46	22651_339	H-VPIONDNTSSYRLIS-OH	8808_HIV-1 Con B Env_046	310114Y-35	1693.7	[M + H]+	847.5
47	22651_340	H-NDNTSSYRLISCNTS-OH	8809_HIV-1 Con B Env_047	030214Z-18	1675.6	[M + H]+	838.0
48	22651_341	H-SSYRLISONTSVITQ-OH	8810_HIV-1 Con B Env_048	030214Z-20	1673.7	[M + H]+	836.6
49	22651_342	H-LISCNTSVITQACPK-OH	8811_HIV-1 Con B Env_049	030214Z-22	1578.7	[M + H]+	789.6
50	22651_343	H-NTSVITQACPKVSFE-OH	8812_HIV-1 Con B Env_050	030214Z-24	1625.7	[M + H]+	812.5
51	22651_344	H-ITQACPKVSFEPIPI-OH	8813_HIV-1 Con B Env_051	030214Z-26	1643.7	[M + H]+	822.1
52	22651_345	H-CPKVSFEPIPIHYCA-OH	8814_HIV-1 Con B Env_052	050214V-01	1704.7	[M + H]+	853.0
53	22651_346	H-SFEPIPIHYCAPAGF-OH	8815_HIV-1 Con B Env_053	050214V-02	1650.2	[M + H]+	825.2
54	22651_347	H-IPIHYCAPAGFAILK-OH	8816_HIV-1 Con B Env_054	050214V-03	1615.3	[M + H]+	807.7
55	22651_348	H-YCAPAGFAILKCNDK-OH	8817_HIV-1 Con B Env_055	050214V-04	1614.7	[M + H]+	807.5
56	22651_349	H-AGFAILKCNDKKFNG-OH	8818_HIV-1 Con B Env_056	050214V-05	1627.2	[M + H]+	813.7
57	22651_350	H-ILKCNDKKFNGTGPC-OH	8819_HIV-1 Con B Env_057	050214V-06	1638.7	[M + H]+	819.5
58	22651_351	H-NDKKFNGTGPCTNVS-OH	8820_HIV-1 Con B Env_058	050214V-07	1582.5	[M + H]+	791.5
59	22651_352	H-FNGTGPCTNVSTVQC-OH	8821_HIV-1 Con B Env_059	050214V-08	1529.6	[M + H]+	764.5
60	22651_353	H-GPCTNVSTVQCTHGI-OH	8822_HIV-1 Con B Env_060	050214V-09	1517.6	[M + H]+	759.0
61	22651_354	H-NVSTVQCTHGIRPVV-OH	8823_HIV-1 Con B Env_061	050214V-10	1610.7	[M + H]+	805.5
62	22651_355	H-VQCTHGIRPVVSTQL-OH	8824_HIV-1 Con B Env_062	050214V-11	1638.4	[M + H]+	819.7
63	22651_356	H-HGIRPVVSTQLLLNG-OH	8825_HIV-1 Con B Env_063	050214V-12	1605.8	[M + H]+	802.6
64	22651_357	H-PVVSTQLLLNGSLAE-OH	8826_HIV-1 Con B Env_064	050214V-13	1542.7	[M + H]+	771.0
65	22651_358	H-TQLLLNGSLAEEEVV-OH	8827_HIV-1 Con B Env_065	050214V-14	1615.7	[M + H]+	808.5
66	22651_359	H-LNGSLAEEEVVIRSE-OH	8828_HIV-1 Con B Env_066	050214V-15	1645.7	[M + H]+	823.0
67	22651_360	H-LAEEEVVIRSENFTN-OH	8829_HIV-1 Con B Env_067	050214V-16	1751.7	[M + H]+	875.6
68	22651_361	H-EVVIRSENFTNNAKT-OH	8830_HIV-1 Con B Env_068	050214V-17	1721.7	[M + H]+	861.5
69	22651_362	H-RSENFTNNAKTIIVQ-OH	8631_HIV-1 Con B Env_069	050214V-18	1734.8	[M + H]+	868.1
70	22651_363	H-FTNNAKTIIVCLNES-OH	8832_HIV-1 Con B Env_070	050214V-19	1693.7	[M + H]+	846.5
71	22651_364	H-AKTIIVQLNESVEIN-OH	8833_HIV-1 Con B Env_071	050214V-20	1672.60	[M + H]+	1695.08
72	22651_365	H-IVQLNESVEINCTRP-OH	8834_HIV-1 Con B Env_072	050214V-21	1715.7	[M + H]+	858.0
73	22651_366	H-NESVEINCTRPNNNT-OH	8835_HIV-1 Con B Env_073	050214V-22	1705.6	[M + H]+	853.0
74	22651_367	H-EINCTRPNNNTRKSI-OH	8836_HIV-1 Con B Env_074	050214V-23	1759.8	[M + H]+	880.6
75	22651_368	H-TRPNNNTRKSIHIGP-OH	8837_HIV-1 Con B Env_075	050214V-24	—	—	853.1
76	22651_369	H-NNTRKSIHIGPGRAF-OH	8838_HIV-1 Con B Env_076	050214V-25	—	—	834.6
77	22651_370	H-KSIHIGPGRAFYTTG-OH	8839_HIV-1 Con B Env_077	050214V-26	1605.7	[M + H]+	803.0
78	22651_371	H-IGPGRAFYTTGEIIG-OH	8840_HIV-1 Con B Env_078	050214V-27	1551.7	[M + H]+	776.6
79	22651_372	H-RAFYTTGEIIGDlRQ-OH	8841_HIV-1 Con B Env_079	050214V-28	1740.7	[M + H]+	870.6
80	22651_373	H-TTGEIIGDIRQAHCN-OH	8842_HIV-1 Con B Env_080	050214V-29	1629.2	[M + H]+	814.7
81	22651_374	H-IIGDIRQAHCNISRA-OH	8843_HIV-1 Con B Env_081	050214V-30	1669.2	[M + H]+	834.2
82	22651_375	H-IRQAKCNISRAKWNN-OH	8844_HIV-1 Con B Env_082	050214V-31	—	—	906.1
83	22651_376	H-HCNISRAKWNNTLKQ-OH	8845_HIV-1 Con B Env_083	050214V-32	1813.8	[M + H]+	907.1
84	22651_377	H-SRAKWNNTLKQIVKK-OH	8846_HIV-1 Con B Env_084	050214V-33	1814.9	[M + H]+	907.7
85	22651_378	H-WNNTLKQIVKKLREQ-OH	8847_HIV-1 Con B Env_085	050214V-34	—	—	949.7
86	22651_379	H-LKQIVKKLREQFGNK-OH	8848_HIV-1 Con B Env_086	050214V-35	1829.0	[M + H]+	915.6
87	22651_380	H-VKKLREQFGNKTIVF-OH	8849_HIV-1 Con B Env_087	050214V-36	1806.9	[M + H]+	904.2
88	22651_381	H-REQFGNKTIVFNQSS-OH	8850_HIV-1 Con B Env_088	050214V-37	1754.8	[M + H]+	878.0
89	22651_382	H-GNKTIVFNQSSGGDP-OH	8851_HIV-1 Con B Env_089	050214V-38	1520.6	[M + H]+	761.0
90	22651_383	H-IVFNQSSGGDPEIVM-OH	8852_HIV-1 Con B Env_090	050214V-39	1593.6	[M + H]+	797.0
91	22651_384	H-QSSGGDPEIVMHSFN-OH	8853_HIV-1 Con B Env_091	050214V-40	1606.5	[M + H]+	803.0
92	22651_385	H-GDPEIVMHSFNCGGE-OH	8854_HIV-1 Con B Env_092	050214V-41	1593.5	[M + H]+	796.5
93	22651_386	H-IVMHSFNCGGEFFYC-OH	8855_HIV-1 Con B Env_093	050214V-42	1756.6	[M + H]+	877.9
94	22651_387	H-SFNCGGEFFVCNTTQ-OH	8856_HIV-1 Con B Env_094	050214V-43	1717.6	[M + H]+	859.5
95	22651_388	H-GGEFFYCNTTQLFNS-OH	8857_HIV-1 Con B Env_095	050214V-44	1729.6	[M + H]+	864.5
96	22651_389	H-FYCNTTQLFNSTWNV-OH	8858_HIV-1 Con B Env_096	050214V-45	1838.7	[M + H]+	919.6
97	22651_390	H-TTQLFNSTWNVNGTW-OH	8859_HIV-1 Con B Env_097	050214V-46	1769.9	[M + H]+	885.1
98	22651_391	H-FNSTWNVNGTWNNNT-OH	8860_HIV-1 Con B Env_098	050214V-47	1769.7	[M + H]+	885.5
99	22651_392	H-WNVNGTWNNNTEGND-OH	8861_HIV-1 Con B Env_099	050214V-48	1734.6	[M + H]+	868.0
100	22651_393	H-GTWNNNTEGNDTITL-OH	8862_HIV-1 Con B Env_100	060214Y-18	1651.6	[M + H]+	825.5
101	22651_394	H-NNTEGNDTITLPCRI-OH	8863_HIV-1 Con B Env_101	060214Y-20	1662.7	[M + H]+	831.0
102	22651_395	H-GNDTITLPCRIKQII-OH	8864_HIV-1 Con B Env_102	060214Y-22	1686.2	[M + H]+	843.2
103	22651_396	H-ITLPCRIKQIINMWQ-OH	8865_HIV-1 Con B Env_103	060214C8	1858.3	[M + H]+	929.3
104	22651_397	H-CRIKQIINMWQEVGK-OH	8866_HIV-1 Con B Env_104	060214C10	1848.2	[M + H]+	924.0
105	22651_398	H-QIINMWQEVGKAMYA-OH	8867_HIV-1 Con B Env_105	060214C12	1781.7	[M + H]+	891.5
106	22651_399	H-MWQEVGKAMYAPPIR-OH	8868_HIV-1 Con B Env_106	140214C5	1776.8	[M + H]+	889.1
107	22651_400	H-VGKAMYAPPIRGQIR-OH	8869_HIV-1 Con B Env_107	140214C7	1657.3	[M + H]+	829.3
108	22651_401	H-MYAPPIRGQIRCSSN-OH	8870_HIV-1 Con B Env_108	140214C9	1692.7	[M + H]+	847.0
109	22651_402	H-PIRGQIRCSSNITGL-OH	8871_HIV-1 Con B Env_109	140214C11	—	—	808.1
110	22651_403	H-QIRCSSNITGLLLTR-OH	8872_HIV-1 Con B Env_110	140214B9	1675.8	[M + H]+	838.1
111	22651_404	H-SSNITGLLLTRDGGN-OH	8373_HIV-1 Con B Env_111	110214G-03	1518.4	[M + H]+	759.7
112	22651_405	H-TGLLLTRDGGNNNTN-OH	8874_HIV-1 Con B Env_112	110214G-05	1560.7	[M + H]+	780.5
113	22651_406	H-LTRDGGNNNTNETEI-OH	8875_HIV-1 Con B Env_113	110214G-07	1648.6	[M + H]+	824.5
114	22651_407	H-GGNNNTNETEIFRPG-OH	8676_HIV-1 Con B Env_114	110214G-09	1621.6	[M + H]+	810.5
115	22651_408	H-NTNETEIFRPGGGDM-OH	8877_HIV-1 Con B Env_115	110214G-11	1639.6	[M + H]+	819.5
116	22651_409	H-TEIFRPGGGDMRDNW-OH	8878_HIV-1 Con B Env_116	110214G-13	—	—	876.0
117	22651_410	H-RPGGGDMRDNWRSEL-OH	8679_HIV-1 Con B Env_117	110214G-15	1745.9	[M + H]+	873.5
118	22651_411	H-GDMRDNWRSELYKYK-OH	8880_HIV-1 Con B Env_118	110214G-17	—	—	981.1
119	22651_412	H-DNWRSELYKYKVVKI-OH	8881_HIV-1 Con B Env_119	110214G-19	—	—	971.5
120	22651_413	H-SELYKYKVVKIEPLG-OH	8882_HIV-1 Con B Env_120	110214G-21	1767.9	[M + H]+	883.7
121	22651_414	H-KYKVVKIEPLGVAPT-OH	8883_HIV-1 Con B Env_121	110214G-23	1642.8	[M + H]+	821.6
122	22651_415	H-VKIEPLGVAPTKAKR-OH	8884_HIV-1 Con B Env_122	110214G-25	1606.8	[M + H]+	804.1
123	22651_416	H-PLGVAPTKAKRRVVQ-OH	8885_HIV-1 Con B Env_123	110214V-02	1620.9	[M + H]+	810.6
124	22651_417	H-APTKAKRRVVQREKR-OH	8886_HIV-1 Con B Env_124	110214V-04	—	—	912.2
125	22651_418	H-AKRRVVQREKRAVGI-OH	8887_HIV-1 Con B Env_125	110214V-06	—	—	883.7
126	22651_419	H-VVQREKRAVGIGAMF-OH	8888_HIV-1 Con B Env_126	110214V-08	1662.8	[M + H]+	831.1
127	22651_420	H-EKRAMGLGAMFLGFL-OH	8889_HIV-1 Con B Env_127	110214V-10	1610.7	[M + H]+	805.1
128	22651_421	H-VGIGAMFLGFLGAAG-OH	8890_HIV-1 Con B Env_128	110214V-12	1380.7	[M + H]+	891.0
129	22651_422	H-AMFLGFLGAAGSTMG-OH	8891_HIV-1 Con B Env_129	110214V-14	1480.9	[M + H]+	718.5
130	22651_423	H-GFLGAAGEIMGAASM-OH	8892_HIV-1 Con B Env_130	110214V-16	1326.4	[M + H]+	565.0
131	22651_424	H-AAGSTMGAASMTLTV-OH	8893_HIV-1 Con B Env_131	110214V-15	1368.5	[M + H]+	635.0
132	22651_425	H-TMGAASMTLIVQARQ-OH	8894_HIV-1 Con B Env_132	110214V-20	1565.7	[M + H]+	783.5
133	22651_426	H-ASMTLTVOARQLLSG-OH	8895_HIV-1 Con B Env_133	110214V-22	1576.5	[M + H]+	788.8
134	22651_427	H-LTVQARQLLSGIVQQ-OH	8896_HIV-1 Con B Env_134	110214V-24	1655.7	[M + H]+	817.6
135	22651_428	H-ARQLLSGIVQGQNNL-OH	8897_HIV-1 Con B Env_135	110214V-25	1631.8	[M + H]+	841.6
136	22651_429	H-LSGIVQQQNNLLRAI-OH	8898_HIV-1 Con B Env_136	110214V-25	1666.3	[M + H]+	834.1
137	22651_430	H-VQQQNNLLRAIEAQQ-OH	8899_HIV-1 Con B Env_137	110214V-30	1754.6	[M + H]+	827.5
138	22651_431	H-NNLLRAIEAQQHLIQ-OH	8900_HIV-1 Con B Env_138	110214V-32	1762.8	[M + H]+	851.1
139	22651_432	H-RAIEAQQHLLQLTVW-OH	8901_HIV-1 Con B Env_139	110214V-34	1807.1	[M + H]+	903.7
140	22651_433	H-AQQHLLQLTVWGIKQ-OH	8902_HIV-1 Con B Env_140	110214V-36	1763.8	[M + H]+	882.1
141	22651_434	H-LLQLTVWGIKQLQAR-OH	8903_HIV-1 Con B Env_141	110214V-35	1768.2	[M + H]+	834.2
142	22651_435	H-TVWGIKCLQARVLAV-OH	8904_HIV-1 Con B Env_142	110214V-40	1682.9	[M + H]+	341.2
143	22651_436	H-IKQLOARVLAVERYL-OH	8905_HIV-1 Con B Env_143	110214V-42	1800.0	[M + H]+	900.7
144	22651_437	H-QARVIAVERVLKQQQ-OH	8906_HIV-1 Con B Env_144	110214V-44	—	—	909.2
145	22651_438	H-RYVERYLKDQQLLGI-OH	8907_HIV-1 Con B Env_145	110214V-46	1760.7	[M + H]+	890.2
146	22651_439	H-RYVERYLKDQQLLGI-OH	8908_HIV-1 Con B Env_146	110214V-48	1780.2	[M + H]+	891.1
147	22651_440	H-OQQLLGFWGCSGKLI-OH	8909_HIV-1 Con B Env_147	180214V-02	1631.7	[M + H]+	816.0
148	22651_441	H-LGIWGCSGKLICTIT-OH	8910_HIV-1 Con B Env_148	180214V-04	1553.3	[M + H]+	777.1
149	22651_442	H-GCSGKLKIITTTVPWN-OH	8911_HIV-1 Con B Env_149	180214V-06	1580.7	[M + H]+	790.5
150	22651_443	H-KLICTTTVPWNASWS-OH	8912_HIV-1 Con B Env_150	180214V-08	1707.7	[M + H]+	854.0
151	22651_444	H-TITVPWNASWSNKSL-OH	8913_HIV-1 Con B Env_151	180214V-10	1592.7	[M + H]+	845.5
152	22651_445	H-PWNASWSNKSLDDW-OH	8914_HIV-1 Con B Env_152	180214V-12	1633.1	[M + H]+	917.5
153	22651_446	H-SWSNKSLDEIWDNMT-OH	8915_HIV-1 Con B Env_153	180214V-14	1826.7	[M + H]+	914.0
154	22651_447	H-KSLDEIWDNMTWMEW-OH	8916_HIV-1 Con B Env_154	180214V-16	1986.0	[M + H]+	983.0
155	22651_448	H-EIWDNMTWMIWEREI-OH	8917_HIV-1 Con B Env_155	180214V-18	2069.8	[M + H]+	1035.1
156	22651_449	H-HMTWMEWEREIDNVT-OH	8918_HIV-1 Con B Env_156	180214V-20	—	—	1009.3
157	22651_450	H-MEWEREIDNYISLSY-OH	8919_HIV-1 Con B Env_157	180214V-27	1962.8	[M + H]+	981.3
158	22651_451	H-REIDNYTSLSNTBE-OH	8920_HIV-1 Con B Env_158	180214V-24	1842.9	[M + H]+	922.1
159	22651_452	H-NYISUYTUEESQN-OH	8921_HIV-1 Con B Env_159	180214V-28	1768.3	[M + H]+	894.6
160	22651_453	H-LNTUEESQNQQEK-OH	8922_HIV-1 Con B Env_160	180214V-28	1636.8	[M + H]+	915.6
161	22651_454	H-LIEESQNQQEBNEQE-OH	8923_HIV-1 Con B Env_161	180214V-30	1847.7	[M + H]+	923.3
162	22651_455	H-SQNQQEKNEQQIEL-OH	8924_HIV-1 Con B Env_162	180214V-32	1829.8	[M + H]+	915.6
163	22651_456	H-QEKNEQELLELOKWA-OH	8925_HIV-1 Con B Env_163	180214V-34	1871.9	[M + H]+	937.2
164	22651_457	H-EQELLELDKWASLWN-OH	8926_HIV-1 Con B Env_164	180214V-38	1874.6	[M + H]+	937.8
165	22651_458	H-ELDKWASIWNWFDI-OH	8927_HIV-1 Con B Env_165	180214V-38	3937.3	[M + H]+	969.2
166	22651_459	H-LWASLWNWFWTNWL-OH	8928_HIV-1 Con B Env_166	180214V-40	1981.3	[M + H]+	991.0
167	22651_460	H-LWMWFOMNWDAYIK-OH	8929_HIV-1 Con B Env_167	180214V-42	2100.8	[M + H]+	1050.1
168	22651_461	H-DITNWLWYIKIRM-OH	8930_HIV-1 Con B Env_168	180214V-44	2000.8	[M + H]+	1002.5
169	22651_462	H-NWLWMKAMNGG-OH	8931_HIV-1 Con B Env_169	180214V-48	1855.30	[M + H]+	—
170	22651_463	H-VIKIFIMIMVGGLIG-OH	8932_HIV-1 Con B Env_170	180214V-48	1649.9	[M + H]+	825.7
171	22651_464	H-FIMIVGGLIGIRIVF-OH	8833_HIV-1 Con B Env_171	130214Z-02	1648.9	[M + H]+	824.5
172	22651_465	H-VGGLIGLRIVFAVLS-OH	8834_HIV-1 Con B Env_172	130214Z-04	1514.8	[M + H]+	737.6
173	22651_466	H-IGLRIVFAVLSIVNR-OH	8835_HIV-1 Con B Env_173	130214Z-06	3671.3	[M + H]+	835.8
174	22651_467	H-IVFAVLSIVNRYRGG-OH	8836_HIV-1 Con B Env_174	130214Z-03	1672.8	[M + H]+	836.2
175	22651_468	H-VLSIVNRVRQGYSPI-OH	8837_HIV-1 Con B Env_175	130214Z-10	1700.8	[M + H]+	851.1
176	22651_469	H-VNRYFQGYSPLSFQT-OH	8838_HIV-1 Con B Env_176	130214Z-12	1751.8	[M + H]+	876.6
177	22651_470	H-RQGYSPLSFQTRLPA-OH	8839_HIV-1 Con B Env_177	130214Z-14	1722.2	[M + H]+	861.3
178	22651_471	H-SPLSFQTRIPAPRGP-OH	8840_HIV-1 Con B Env_178	170214Y-04	1625.7	[M + H]+	8126.6
179	22651_472	H-FQTRLPAPRGPDRPE-OH	8841_HIV-1 Con B Env_179	170214Y-05	1739.2	[M + H]+	869.3
180	22651_473	H-LPAPRGPORPEGIEE-OH	8842_HIV-1 Con B Env_180	170214Y-08	1632.8	[M + H]+	817.0
181	22651_474	H-RGPDEPEGIEEGGGE-OH	8843_HIV-1 Con B Env_181	170214Y-10	1627.5	[M + H]+	814.0
182	22651_475	H-RPEGIEEEGGERDRD-OH	8844_HIV-1 Con B Env_182	170214Y-12	—	—	872.5
183	22651_476	H-IEEEGGERDRDSSGR-OH	8845_HIV-1 Con B Env_183	170214Y-14	—	—	881.0
184	22651_477	H-GGERDSDRSGRIVDG-OH	8846_HIV-1 Con B Env_184	170214Y-15	1649.1	[M + H]+	878.0
185	22651_478	H-DRDRSGRLVDGFLAL-OH	8847_HIV-1 Con B Env_185	170214Y-18	1690.3	[M + H]+	845.7
186	22651_479	H-SGRLVDGFIAIIWDD-OH	8848_HIV-1 Con B Env_186	170214Y-20	1678.7	[M + H]+	839.0
187	22651_480	H-VDGFLALIWDDLASL-OH	8849_HIV-1 Con B Env_187	210214R-03	1734.8	[M + H]+	867.1
188	22651_481	H-LALIWDDLRSLCLFS-OH	8850_HIV-1 Con B Env_188	210214R-05	1765.4	[M + H]+	883.3
189	22651_482	H-WDDLASLCLFSYHRL-OH	8851_HIV-1 Con B Env_189	210214R-07	1926.2	[M + H]+	963.1
190	22651_483	H-RSLCLFSYHRLRDIL-OH	8852_HIV-1 Con B Env_190	210214R-08	—	—	947.0
191	22651_484	H-LFSYERLRDLILIVT-OH	8853_HIV-1 Con B Env_191	210214R-11	1859.9	[M + H]+	830.2
192	22651_485	H-HRLRQLLLIVERIVE-OH	8854_HIV-1 Con B Env_192	210214R-13	—	—	922.7
193	22651_486	H-DLLLIVYARVELLGR-OH	8855_HIV-1 Con B Env_193	210214R-15	1725.4	[M + H]+	862.4
194	22651_487	H-IVTRIVELLGREGWE-OH	8856_HIV-1 Con B Env_194	210214R-17	—	—	839.2
195	22651_488	H-IVELLGRRGWEVLKY-OH	8857_HIV-1 Con B Env_195	210214R-19	1632.9	[M + H]+	916.2
196	22651_489	H-LGRRGWEVLKYWWNL-OH	8858_HIV-1 Con B Env_196	210214R-21	1977.0	[M + H]+	938.7
197	22651_490	H-GWEVLKVWWMLLQYW-OH	8859_HIV-1 Con B Env_197	210214R-23	—	—	1043.1
198	22651_491	H-LKYWWNLLQVWSQEL-OH	8860_HIV-1 Con B Env_198	210214R-25	2072.2	[M + H]+	1036.2
199	22651_492	H-WNLLQVWSQELKNSA-OH	8861_HIV-1 Con B Env_199	210214R-27	1881.8	[M + H]+	941.0
200	22651_493	H-QYWSQELKNSAVSLL-OH	8862_HIV-1 Con B Env_200	210214R-29	1767.8	[M + H]+	384.0
201	22651_494	H-QELKNSAVSLINATA-OH	8863_HIV-1 Con B Env_201	210214R-31	1559.3	[M + H]+	780.2
202	22651_495	H-NSAVSLLNATAIAVA-OH	8864_HIV-1 Con B Env_202	210214R-33	1414.2	[M + H]+	708.1
203	22651_496	H-SLINATAIAVAGGTD-OH	8865_HIV-1 Con B Env_203	210214R-35	1446.2	[M + H]+	724.0
204	22651_497	H-ATAIAVAEGTDRVIE-OH	8866_HIV-1 Con B Env_204	210214R-37	1515.7	[M + H]+	758.5
205	22651_498	H-AVAEGTDRVIEVVQR-OH	8867_HIV-1 Con B Env_205	210214R-38	1641.8	[M + H]+	821.6
206	22651_499	H-GTDRVIEVVQFACRA-OH	8868_HIV-1 Con B Env_206	210214R-41	1673.3	[M + H]+	837.2
207	22651_500	H-VIEVVQRACRAELHI-OH	8869_HIV-1 Con B Env_207	210214R-43	1720.4	[M + H]+	850.8
208	22651_501	H-VQRACRAILHIFRFI-OH	8870_HIV-1 Con B Env_208	210214R-45	—	—	901.7
209	22651_502	H-CRAILHIPRRIRQGL-OH	8871_HIV-1 Con B Env_209	210214R-47	—	—	901.7
210	22651_503	H-LHIPRRIRQGLERAL-OH	8872_HIV-1 Con B Env_210	210214Z-02	—	—	914.7
211	22651_504	H-RRIFQGLERALL-OH	8373_HIV-1 Con B Env_211	19021482	—	—	741.1
					Theor.		Exp. MW
			MW (3)		MW	Theor.	vs.
		MW (2)	detected	MW (3)	(average)	MW + TFA	Theor.		Amount
		label	[g/mol]	label	[g/mol]	[g/mol]	MW	Purity [%]	[mg]	Purified	Comment
	1	[M + 2H]2+	662.8	[M + 3H]3+	1985.38	2783.38	pass	85.3	65.0	Y
	2	[M + 2H]2+	649.7	[M + 3H]3+	1946.25	2516.25	pass	87.8	65.0	Y
	3	[M + 2H]2+	—	—	1906.24	2248.24	pass	87.1	65.0	Y
	4	[M + 2H]2+	—	—	1824.34	2052.34	pass	80.2	66.0	Y
	5	[M + 2H]2+	1584.37	[M + 2Na]2+	1540.92	1654.92	pass	approx. 80	65.0	N	2)
	6	[M + 2H]2+	555.8	[M + 3H]3+	1665.09	1893.09	pass	90.0	65.0	Y
	7	[M + 2H]2+	1777.56	[M + H]+	1777.12	2005.12	pass	approx. 80	65.0	N	1)
	8	[M + 2H]2+	565.8	[M + 3H]3+	1694.98	1922.98	pass	94.7	66.0	Y
	9	[M + 2H]2+	604.2	[M + 3H]3+	1810.11	2038.11	pass	87.2	67.0	Y
	10	[M + 2H]2+	576.4	[M + 3H]3+	1726.97	1954.97	pass	88.8	67.0	Y
	11	[M + 2H]2+	—	—	1652.91	1880.91	pass	85.9	67.0	Y
	12	[M + 2H]2+	519.8	[M + 3H]3+	1556.74	1898.74	pass	87.0	66.0	Y
	13	[M + 2H]2+	—	—	1635.76	1863.76	pass	84.7	66.0	Y
	14	[M + 2H]2+	541.9	[M + 3H]3+	1622.72	1964.72	pass	89.4	67.0	Y
	15	[M + 2H]2+	581.7	[M + 3H]3+	1741.86	2197.86	pass	85.3	66.0	Y
	16	[M + 2H]2+	—	—	1678.82	2020.82	pass	82.3	65.0	Y
	17	[M + 2H]2+	555.0	[M + 3H]3+	1661.80	2003.80	pass	88.0	66.0	Y
	18	[M + 2H]2+	527.2	[M + 3H]3+	1578.71	1806.71	pass	93.9	66.0	Y
	19	[M + 2H]2+	—	—	1653.81	1653.81	pass	91.1	66.0	Y
	20	[M + 2H]2+	566.5	[M + 3H]3+	1696.76	1696.76	pass	86.0	66.0	Y
	21	[M + 2H]2+	—	—	1852.01	1852.01	pass	80.5	66.0	Y	5)
	22	[M + 2H]2+	628.9	[M + 3H]3+	1884.07	1884.07	pass	93.6	66.0	Y
	23	[M + 2H]2+	639.5	[M + 3H]3+	1916.13	1916.13	pass	95.5	65.0	Y
	24	[M + 2H]2+	640.5	[M + 3H]3+	1919.14	1919.14	pass	94.8	65.0	Y
	25	[M + 2H]2+	620.5	[M + 3H]3+	1859.08	1859.08	pass	85.9	65.0	Y
	26	[M + 2H]2+	615.5	[M + 3H]3+	1844.02	1844.02	pass	82.9	67.0	Y
	27	[M + 2H]2+	582.9	[M + 3H]3+	1746.01	1746.01	pass	89.3	65.0	Y
	28	[M + 2H]2+	572.6	[M + 3H]3+	1715.04	2057.04	pass	87.1	65.0	Y
	29	[M + 2H]2+	544.2	[M + 3H]3+	1630.03	1972.03	pass	88.1	66.0	Y
	30	[M + 2H]2+	535.7	[M + 3H]3+	1604.99	1832.99	pass	88.2	66.0	Y
	31	[M + 2H]2+	—	—	1650.97	1764.97	pass	82.4	65.0	Y
	32	[M + 2H]2+	—	—	1613.81	1727.81	pass	81.9	66.0	Y
	33	[M + 2H]2+	—	—	1586.64	1700.64	pass	80.4	66.0	Y
	34	[M + 2H]2+	—	—	1554.62	1782.62	pass	84.6	65.0	Y
	35	[M + 2H]2+	524.5	[M + 3H]3+	1570.61	1912.61	pass	84.4	65.0	Y	3)
	36	[M + 2H]2+	546.7	[M + 3H]3+	1637.75	2093.75	pass	85.7	65.0	Y
	37	[M + 2H]2+	572.2	[M + 3H]3+	1713.91	2169.91	pass	87.7	65.0	Y
	38	[M + 2H]2+	557.8	[M + 3H]3+	1670.83	2012.83	pass	95.0	66.0	Y
	39	[M + 2H]2+	580.8	[M + 3H]3+	1740.00	2196.00	pass	89.3	67.0	Y
	40	[M + 2H]2+	589.6	[M + 3H]3+	1765.97	2221.97	pass	81.9	66.0	Y
	41	[M + 2H]2+	600.5	[M + 3H]3+	1799.05	2255.05	pass	90.5	65.0	Y
	42	[M + 2H]2+	639.7	[M + 3H]3+	1916.21	2486.21	pass	91.6	65.0	Y
	43	[M + 2H]2+	609.5	[M + 3H]3+	1826.17	2168.17	pass	95.2	66.0	Y
	44	[M + 2H]2+	—	—	1735.96	1963.96	pass	86.0	65.0	Y
	45	[M + 2H]2+	—	—	1679.80	1907.80	pass	86.9	65.0	Y
	46	[M + 2H]2+	565.5	[M + 3H]3+	1693.84	1921.84	pass	85.4	65.0	Y
	47	[M + 2H]2+	—	—	1674.76	1902.76	pass	85.3	65.0	Y
	48	[M + 2H]2+	558.1	[M + 3H]3+	1671.89	1899.89	pass	88.0	65.0	Y
	49	[M + 2H]2+	526.9	[M + 3H]3+	1577.87	1805.87	pass	91.2	67.0	Y
	50	[M + 2H]2+	542.3	[M + 3H]3+	1623.89	1851.83	pass	85.5	65.0	Y
	51	[M + 2H]2+	548.5	[M + 3H]3+	1642.98	1870.98	pass	93.8	65.0	Y
	52	[M + 2H]2+	568.8	[M + 3H]3+	1704.05	2046.05	pass	90.5	66.0	Y
	53	[M + 2H]2+	—	—	1648.92	1876.92	pass	87.6	66.0	Y
	54	[M + 2H]2+	—	—	1614.00	1956.00	pass	84.0	66.0	Y
	55	[M + 2H]2+	538.8	[M + 3H]3+	1613.92	1955.92	pass	91.7	67.0	Y
	56	[M + 2H]2+	—	—	1625.90	2081.90	pass	92.6	66.0	Y
	57	[M + 2H]2+	546.8	[M + 3H]3+	1637.92	2093.92	pass	89.1	66.0	Y
	58	[M + 2H]2+	528.2	[M + 3H]3+	1581.70	1923.70	pass	89.2	66.0	Y
	59	[M + 2H]2+	—	—	1527.67	1641.67	pass	81.6	66.0	Y	3)
	60	[M + 2H]2+	—	—	1516.69	1744.69	pass	91.2	67.0	Y
	61	[M + 2H]2+	5375	[M + 3H]3+	1609.85	1951.85	pass	86.9	65.0	Y
	62	[M + 2H]2+	—	—	1637.91	1979.91	pass	89.3	65.0	Y
	63	[M + 2H]2+	535.5	[M + 3H]3+	1603.88	1945.88	pass	87.7	66.0	Y
	64	[M + 2H]2+	—	—	1540.77	1654.77	pass	90.4	66.0	Y	3)
	65	[M + 2H]2+	—	—	1614.79	1728.79	pass	92.8	66.0	Y
	66	[M + 2H]2+	549.1	[M + 3H]3+	1644.78	1872.78	pass	94.0	66.0	Y
	67	[M + 2H]2+	—	—	1749.87	1977.87	pass	93.7	65.0	Y
	68	[M + 2H]2+	574.8	[M + 3H]3+	1721.86	2063.86	pass	88.0	65.0	Y
	69	[M + 2H]2+	579.2	[M + 3H]3+	1734.91	2076.91	pass	95.9	65.0	Y
	70	[M + 2H]2+	—	—	1691.88	1919.88	pass	94.6	65.0	Y
	71	[M + Na]+	1717.22	[M + 2Na]2+	1670.90	1898.90	pass	approx. 80	66.0	Y	2)
	72	[M + 2H]2+	572.5	[M + 3H]3+	1714.94	1942.94	pass	92.8	67.0	Y
	73	[M + 2H]2+	—	—	1704.76	1932.76	pass	87.3	67.0	Y
	74	[M + 2H]2+	587.5	[M + 3H]3+	1759.94	2215.94	pass	81.6	68.0	Y
	75	[M + 2H]2+	569.2	[M + 3H]3+	1704.90	2274.90	pass	85.9	72.0	Y
	76	[M + 2H]2+	556.9	[M + 3H]3+	1667.89	2237.89	pass	93.2	74.0	Y
	77	[M + 2H]2+	535.8	[M + 3H]3+	1604.83	2060.83	pass	87.0	74.0	Y
	78	[M + 2H]2+	—	—	1551.76	1779.76	pass	86.9	73.0	Y
	79	[M + 2H]2+	580.9	[M + 3H]3+	1739.95	2081.95	pass	84.7	70.0	Y
	80	[M + 2H]2+	543.5	[M + 3H]3+	1627.78	1969.78	pass	84.5	69.0	Y
	81	[M + 2H]2+	556.7	[M + 3H]3+	1666.93	2122.93	pass	91.1	67.0	Y
	82	[M + 2H]2+	604.6	[M + 3H]3+	1811.05	2381.05	pass	92.7	67.0	Y
	83	[M + 2H]2+	605.3	[M + 3H]3+	1813.05	2383.05	pass	85.4	65.0	Y
	84	[M + 2H]2+	605.7	[M + 3H]3+	1814.14	2498.14	pass	96.0	65.0	Y
	85	[M + 2H]2+	633.6	[M + 3H]3+	1898.21	2468.21	pass	96.9	65.0	Y
	86	[M + 2H]2+	610.7	[M + 3H]3+	1829.20	2513.20	pass	92.9	65.0	Y
	87	[M + 2H]2+	603.3	[M + 3H]3+	1807.15	2377.15	pass	89.6	65.0	Y
	88	[M + 2H]2+	585.8	[M + 3H]3+	1754.91	2096.91	pass	89.3	65.0	Y
	89	[M + 2H]2+	—	—	1520.61	1748.61	pass	91.4	66.0	Y
	90	[M + 2H]2+	—	—	1592.78	1706.78	pass	93.6	66.0	Y
	91	[M + 2H]2+	—	—	1604.71	1832.71	pass	88.3	65.0	Y
	92	[M + 2H]2+	—	—	1591.72	1819.72	pass	82.7	65.0	Y
	93	[M + 2H]2+	—	—	1754.03	1982.03	pass	81.6	66.0	Y
	94	[M + 2H]2+	1718.10	[M + 3H]3+	1717.34	1831.84	pass	approx. 80	69.0	Y	1)
	95	[M + 2H]2+	—	—	1727.86	1841.86	pass	92.3	67.0	Y
	96	[M + 2H]2+	—	—	1838.01	1952.01	pass	89.8	65.0	Y
	97	[M + 2H]2+	—	—	1768.87	1882.87	pass	87.9	66.0	Y
	98	[M + 2H]2+	—	—	1768.78	1882.78	pass	85.7	65.0	Y
	99	[M + 2H]2+	—	—	1734.67	1848.67	pass	92.1	66.0	Y
	100	[M + 2H]2+	—	—	1649.65	1763.65	pass	87.0	66.0	Y
	101	[M + 2H]2+	554.5	[M + 3H]3+	1660.80	1888.80	pass	84.9	65.0	Y
	102	[M + 2H]2+	—	—	1685.01	2027.01	pass	86.3	6.0	Y
	103	[M + 2H]2+	620.0	[M + 3H]3+	1857.30	2199.30	pass	82.5	66.0	Y
	104	[M + 2H]2+	616.3	[M + 3H]3+	1846.22	2302.22	pass	81.0	67.0	Y
	105	[M + 2H]2+	594.8	[M + 3H]3+	1782.09	2010.09	pass	85.7	66.0	Y
	106	[M + 2H]2+	593.2	[M + 3H]3+	1777.13	2119.13	pass	93.3	66.0	Y
	107	[M + 2H]2+	553.3	[M + 3H]3+	1657.02	2113.02	pass	95.9	66.0	Y
	108	[M + 2H]2+	565.2	[M + 3H]3+	1692.99	2034.99	pass	89.1	65.0	Y
	109	[M + 2H]2+	539.2	[M + 3H]3+	1614.89	1956.89	pass	88.7	67.0	Y
	110	[M + 2H]2+	559.3	[M + 3H]3+	1674.98	2016.98	pass	80.8	67.0	Y
	111	[M + 2H]2+	—	—	1517.65	1745.65	pass	91.2	67.0	Y	3)
	112	[M + 2H]2+	—	—	1559.63	1787.63	pass	90.7	65.0	Y
	113	[M + 2H]2+	550.2	[M + 3H]3+	1647.64	1875.64	pass	92.7	66.0	Y
	114	[M + 2H]2+	—	—	1619.64	1847.64	pass	85.3	65.0	Y
	115	[M + 2H]2+	—	—	1637.72	1865.72	pass	91.6	65.0	Y
	116	[M + 2H]2+	584.5	[M + 3H]3+	1750.90	2092.90	pass	83.5	66.0	Y
	117	[M + 2H]2+	582.5	[M + 3H]3+	1745.89	2201.89	pass	84.7	70.0	Y
	118	[M + 2H]2+	654.7	[M + 3H]3+	1961.18	2531.18	pass	89.7	66.0	Y
	119	[M + 2H]2+	647.9	[M + 3H]3+	1941.25	2511.25	pass	94.0	66.0	Y
	120	[M + 2H]2+	589.7	[M + 3H]3+	1766.10	2222.10	pass	97.3	65.0	Y
	121	[M + 2H]2+	548.5	[M + 3H]3+	1642.00	2098.00	pass	95.7	66.0	Y
	122	[M + 2H]2+	536.6	[M + 3H]3+	1606.96	2176.96	pass	93.4	68.0	Y
	123	[M + 2H]2+	541.0	[M + 3H]3+	1619.97	2189.97	pass	92.9	67.0	Y
	124	[M + 2H]2+	608.7	[M + 3H]3+	1823.17	2735.17	pass	94.2	66.0	Y
	125	[M + 2H]2+	589.5	[M + 3H]3+	1766.12	2564.12	pass	96.5	67.0	Y
	126	[M + 2H]2+	554.5	[M + 3H]3+	1660.99	2116.99	pass	97.6	67.0	Y
	127	[M + 2H ]2+	537.2	[M + 3H]3+	1606.96	1950.96	pass	96.0	67.0	Y
	128	[M + 2H ]2+	1403.00	[M + 3H]3+	1380.67	1494.67	pass	Approx. 80	67.0	Y	1)
	129	[M + 2H ]2+	—	—	1430.70	1544.70	pass	86.7	68.0	Y
	130	[M + 2H ]2+	—	—	1328.52	1442.52	pass	91.7	67.0	Y
	131	[M + 2H ]2+	—	—	1366.57	1482.57	pass	83.6	56.0	Y	4)
	132	[M + 2H ]2+	522.8	[M + 3H]3+	1569.81	1793.81	pass	93.3	67.0	Y	3)
	133	[M + 2H ]2+	—	—	1575.84	1803.84	pass	83.3	68.0	Y	3)
	134	[M + 2H ]2+	532.2	[M + 3H]3+	1693.94	1881.94	pass	87.5	67.0	Y
	135	[M + 2H ]2+	561.6	[M + 3H]3+	1681.91	1908.91	pass	96.8	67.0	Y
	136	[M + 2H ]2+	556.5	[M + 3H]3+	1666.34	1894.94	pass	91.7	67.0	Y
	137	[M + 2H ]2+	585.3	[M + 3H]3+	1753.94	1930.94	pass	97.0	66.0	Y
	138	[M + 2H ]2+	587.8	[M + 3H]3+	1781.01	2103.01	pass	99.3	67.0	Y
	139	[M + 2H ]2+	—	—	1806.09	2148.09	pass	89.1	69.0	Y
	140	[M + 2H ]2+	588.5	[M + 3H]3+	1763.06	2109.06	pass	92.0	66.0	Y
	141	[M + 2H ]2+	—	—	1787.14	2103.14	pass	90.1	66.0	Y
	142	[M + 2H ]2+	561.8	[M + 3H]3+	1652.03	2024.03	pass	93.6	66.0	Y
	143	[M + 2H ]2+	601.0	[M + 3H]3+	1806.18	2256.18	pass	90.7	66.0	Y
	144	[M + 2H ]2+	676.8	[M + 3H]3+	1817.08	2273.08	pass	94.8	69.0	Y
	145	[M + 2H ]2+	587.2	[M + 3H]3+	1759.08	2101.08	pass	93.6	70.0	Y
	146	[M + 2H ]2+	—	—	1780.08	2322.08	pass	91.6	70.0	Y
	147	[M + 2H ]2+	544.5	[M + 3H]3+	1630.92	1858.92	pass	87.8	70.0	Y
	148	[M + 2H ]2+	—	—	1552.89	1780.85	pass	82.6	73.0	Y
	149	[M + 2H ]2+	—	—	1579.83	1807.83	pass	82.4	71.0	Y
	150	[M + 2H ]2+	—	—	1706.96	1934.96	pass	81.8	67.0	Y
	151	[M + 2H ]2+	—	—	1681.84	1913.84	pass	85.6	67.0	Y
	152	[M + 2H ]2+	—	—	1832.98	2050.98	pass	83.0	68.0	Y
	153	[M + 2H ]2+	—	—	1825.95	2053.95	pass	81.9	67.0	Y
	154	[M + 2H ]2+	—	—	1984.20	2222.20	pass	84.8	68.0	Y
	155	[M + 2H ]2+	—	—	2068.27	2298.27	pass	83.9	68.0	Y
	156	[M + 2H ]2+	679.4	[M + 3H]3+	2018.17	2246.17	pass	81.6	66.0	Y
	157	[M + 2H ]2+	664.8	[M + 3H]3+	1962.15	2190.15	pass	87.8	69.0	Y
	158	[M + 2H ]2+	—	—	1843.06	2071.06	pass	92.8	67.0	Y
	159	[M + 2H ]2+	—	—	1787.93	1901.93	pass	81.4	67.0	Y
	160	[M + 2H ]2+	612.9	[M + 3H]3+	1836.01	1054.01	pass	85.8	69.0	Y
	161	[M + 2H ]2+	616.3	[M + 3H]3+	1849.86	2073.85	pass	88.2	68.0	Y
	162	[M + 2H ]2+	610.8	[M + 3H]3+	1829.91	2057.91	pass	90.9	70.0	Y
	163	[M + 2H ]2+	625.3	[M + 3H]3+	1873.02	2216.02	pass	93.4	68.0	Y
	164	[M + 2H ]2+	—	—	1874.06	2307.06	pass	91.1	71.0	Y
	165	[M + 2H ]2+	—	—	1936.19	2164.19	pass	80.8	71.0	Y
	166	[M + 2H ]2+	—	—	1980.24	2205.24	pass	89.9	71.0	Y
	167	[M + 2H ]2+	700.5	[M + 3H]3+	2098.42	2328.42	pass	93.3	70.0	Y
	168	[M + 2H ]2+	660.8	[M + 3H]3+	2002.43	2231.42	pass	83.2	70.0	Y
	169	—	—	—	1853.29	2081.29	pass	approx. 20-80	68.0	Y	2)
	170	[M + 2H]2+	1672.77	[M + Na]+	1650.14	1878.14	pass	approx. 80	68.0	Y	1)
	171	[M + 2H]2+	1648.75	[M + H]+	1648.13	1879.13	pass	approx. 80)	67.0	Y	1)
	172	[M + 2H]2+	1514.30	[M + H]+	1513.89	1741.89	pass	approx. 80	68.0	Y	1)
	173	[M + 2H]2+	—	—	1670.08	2012.08	pass	85.3	67.0	Y	3)
	174	[M + 2H]2+	558.0	[M + 3H]3+	1671.02	2013.02	pass	95.5	66.0	Y
	175	[M + 2H]2+	567.9	[M + 3H]3+	1701.01	2043.01	pass	89.8	65.0	Y
	176	[M + 2H]2+	584.8	[M + 3H]3+	1751.97	2093.97	pass	88.3	67.0	Y
	177	[M + 2H]2+	—	—	1720.97	2062.97	pass	87.9	68.0	Y
	178	[M + 2H]2+	543.3	[M + 3H]3+	2623.90	1985.90	pass	95.4	68.0	Y
	179	[M + 2H]2+	550.0	[M + 3H]3+	1736.97	2192.97	pass	90.0	68.0	Y
	180	[M + 2H]2+	545.2	[M + 3H]3+	1632.80	1974.80	pass	91.1	68.0	Y
	181	[M + 2H]2+	543.1	[M + 3H]3+	1626.64	1965.64	pass	88.5	69.0	Y
	182	[M + 2H]2+	562.2	[M + 3H]3+	1743.75	2193.75	pass	90.4	67.0	Y
	183	[M + 2H]2+	587.8	[M + 3H]3+	1780.79	2330.79	pass	9085.4	67.0	Y
	184	[M + 2H]2+	549.2	[M + 3H]3+	1646.73	2214.73	pass	97.1	67.0	Y
	185	[M + 2H]2+	564.3	[M + 3H]3+	1689.91	7145.91	pass	89.2	67.0	Y
	186	[M + 2H]2+	—	—	1676.90	1904.90	pass	85.0	68.0	Y
	187	[M + 2H]2+	578.5	[M + 3H]3+	1743.04	1961.01	pass	88.9	68.0	Y
	188	[M + 2H]2+	—	—	1765.12	1993.12	pass	83.7	69.0	Y
	189	[M + 2H]2+	642.3	[M + 3H]3+	1924.23	2380.23	pass	91.7	70.0	Y
	190	[M + 2H]2+	631.6	[M + 3H]3+	2892.28	2462.28	pass	86.1	67.0	Y
	191	[M + 2H]2+	620.7	[M + 3H]3+	1855.26	2315.26	pass	87.6	66.0	Y
	192	[M + 2H]2+	616.3	[M + 3H]3+	1846.25	2416.25	pass	82.7	65.0	Y
	193	[M + 2H]2+	—	—	1723.13	2065.13	pass	94.0	66.0	Y
	194	[M + 2H]2+	600.0	[M + 3H]3+	1787.12	2253.12	pass	85.9	86.0	Y
	195	[M + 2H]2+	611.4	[M + 3H]3+	1831.18	2287.18	pass	87.8	68.0	Y
	196	[M + 2H]2+	659.7	[M + 3H]3+	1976.30	2432.30	pass	90.3	66.0	Y
	197	[M + 2H]2+	—	—	2054.39	2312.39	pass	93.9	66.0	Y
	198	[M + 2H]2+	—	—	2070.37	2298.37	pass	84.2	66.0	Y
	199	[M + 2H]2+	627.5	[M + 3H]3+	1880.08	2108.08	pass	92.0	66.0	Y
	200	[M + 2H]2+	589.5	[M + 3H]3+	1769.98	1933.98	pass	91.4	66.0	Y
	201	[M + 2H]2+	—	—	1556.74	1786.74	pass	84.9	6SXI	Y
	202	[M + 2H]2+	—	—	1414.62	1528.62	pass	80.4	66.0	Y
	203	[M + 2H]2+	—	—	1445.58	1559.58	pass	83.7	67.0	Y	3)
	204	[M + 2H]2+	—	—	1515.67	1743.67	pass	90.0	67.0	Y
	205	[M + 2H]2+	548.3	[M + 3H]3+	1641.83	1983.83	pass	88.2	66.0	Y
	206	[M + 2H]2+	558.6	[M + 3H]3+	1672.92	2325.92	pass	87.6	66.0	Y
	207	[M + 2H]2+	574.2	[M + 3H]3+	1720.11	2176.11	pass	89.1	68.0	Y
	208	[M + 2H]2+	601.7	[M + 3H]3+	1802.24	2486.24	pass	82.0	67.0	Y
	209	[M + 2H]2+	601.7	[M + 3H]3+	1800.24	7436.24	pass	82.3	67.0	Y
	210	[M + 2H]2+	610.3	[M + 3H]3+	1828.21	2512.21	pass	91.3	66.0	Y
	211	[M + 2H]2+	494.5	[M + 3H]3+	1480.79	2050.79	pass	97.3	68.0	Y
	Comments:
	1) estimated on ESI/MAID:
	2) estimated on MALD:
	3) dissolved in ACN/H2O
	4) dissolved in TFA/H2O
	5) dissolved in DMSO

TABLE 7
HIV-1 Consensus B Tat (NIH AIDS Reagent 5138)
DATA SHEET
HIV-1 Consensus 8 Tat (15-mer) peptides - Complete Set (Cat# 5138, Lot# 11)
	Solubility Data
				Molecular		Peptide			10%
				Weight	Purity	Content			Acetic
CAT #	Peptide Name	SEQUENCE	LOT #	g/mol	[%]	[%]	Water	PBS	Acid	DMSO
5113	HIV-1 Clade B consensus tat	MEPVDPRLEPWKHPG	070034	1786.85	>80%	90%	−	−	−	+
5114	HIV-1 Clade B consensus tat	DPRLEPWKHPGSQPK	070035	1770.88	>80%	90%	−	−	+	+
5115	HIV-1 Clade B consensus tat	EPWKHPGSQPKTACT	070036	1665.77	>80%	90%	−	−	+	+
5116	HIV-1 Clade B consensus tat	HPGSQPKTACTNCYC	070037	1608.63	>80%	90%	−	−	+	+
5117	HIV-1 Clade B consensus tat	QPKTACTNCYCKKCC	070038	1692.67	>80%	80%	−	−	−	+
5118	HIV-1 Clade B consensus tat	ACINCYCKKCCFHCQ	070039	1753.62	>80%	80%	−	+	+	+
5119	HIV-1 Clade B consensus tat	CYCKKCCFHCQVCFI	070040	1826.71	>80%	85%	−	+	+	+
5120	HIV-1 Clade B consensus tat	KCCFHCQVCFITKGL	070041	1728.78	>80%	90%	−	+	+	+
5121	HIV-1 Clade B consensus tat	HCQVCFITKGLGISY	070042	1667.79	>80%	95%	−	+	+	+
5122	HIV-1 Clade B consensus tat	CFITKGLGISYGRKK	070043	1669.89	>80%	80%	−	+	+	+
5123	HIV-1 Clade B consensus tat	KGLGISYGRKKRRQR	070044	1802.04	>80%	70%	−	+	+	+
5124	HIV-1 Clade B consensus tat	ISYGRKKRRQRRRAP	070045	1927.12	>80%	75%	−	−	−	+
5125	HIV-1 Clade B consensus tat	RKKRRQRRRAPQDSQ	070046	1965.11	>80%	85%	−	+	+	+
5126	HIV-1 Clade B consensus tat	RQRRRAPQDSQTHQV	070047	1861.97	>80%	90%	−	+	+	+
5127	HIV-1 Clade B consensus tat	RAPQDSGTHQVSLSK	070048	1680.84	>80%	90%	−	+	+	+
5128	HIV-1 Clade B consensus tat	DSQTHQVSLSKQPAS	070049	1611.77	>80%	85%	−	+	+	+
5129	HIV-1 Clade B consensus tat	HQVSLSKQPASGPRG	070050	1618.83	>80%	70%	−	+	+	+
5130	HIV-1 Clade B consensus tat	LSKQPASQPRGDPTG	070050	1618.83	>80%	70%	−	+	+	+
5131	HIV-1 Clade B consensus tat	PASQPRGDPTGPKES	070052	1522.71	>80%	85%	−	+	+	+
5132	HIV-1 Clade B consensus tat	PRGDPTGPKESKKKV	070053	1622.87	>80%	70%	−	−	+	+
5133	HIV-1 Clade B consensus tat	PTGPKESKKKVERET	070054	1712.90	>80%	75%	−	−	+	+
5134	HIV-1 Clade B consensus tat	KESKKKVERETETDP	070055	1802.90	>80%	85%	−	−	+	+
5135	HIV-1 Clade B consensus tat	KKVERETETDPVDQ	070056	1544.75	>80%	95%	−	−	+	+
Determination of solubility: appr. 0.25 mg of the respective peptide was incubcted with 1 ml of solvent.
Solubility was assessed by visual inspection of the resulting solution/suspension.
“+”: complete dissolution
“−”: incomplete dissolution
NOTE:
Peptides that are difficult to solubilize can almost always be dissolved in DMSO. Once a peptide is in solution, the DMSO can be slowly diluted witn aqueous medium. Care must be taken to ensure that the peptide does not begin to precipitate out of solution.

Claims

1. A method of preventing or treating a HIV infection comprising administering to a mammal in need thereof, a therapeutically effective amount of a CD8+ T cell vaccine composition, wherein the CD8+ T cell has been pre-stimulated with at least one HIV epitope, to thereby enhance a CD8+ T cell immune response against HIV.

2. The method of claim 1, wherein the pre-stimulation occurs ex-vivo.

3. The method of claim 1, wherein the CD8+ T cell has been pre-stimulated with at least two, three, four, five, six, seven, eight, nine, or ten HIV epitopes, alone or in combination, with at least one cytokine.

4. The method of claim 1, wherein the at least one HIV epitope is a subdominant, dominant epitope, or combination thereof.

5-7. (canceled)

8. The method of claim 4, wherein the at least one HIV epitope is selected from an epitope in the HIV-1 Gag, HIV-1 Nef, HIV-1 Rev, HIV-1 Tat, or HIV-1 Env, or combination thereof; or in a pool or mixture of HIV epitopes.

9-10. (canceled)

11. The method of claim 8, wherein the pool or mixture of HIV epitope is selected from the group consisting of (i) a pool or mixture of HIV-1 Gag represented by the peptide sequences set forth in Table 2, Table 4, or both; (ii) a pool or mixture of HIV-1 Nef represented by the peptide sequences set forth in Table 3; (iii) a pool or mixture of HIV-1 Rev represented by the peptide sequences set forth in Table 5; (iv) a pool or mixture of HIV-1 Tat represented by the peptide sequences set forth in Table 7; and (v) a pool or mixture of HIV-1 Env represented by the peptide sequences set forth in Table 6.

12-16. (canceled)

17. The method of claim 8, wherein the epitope in the HIV-1 Gag is selected from any one of SEQ ID NOs: 1-17, or combination thereof, and wherein said HIV-1 Gag is from proviral HIV-1 DNA in resting CD4+ T cells from mammals during the acute phase or chronic phase of infection.

18. (canceled)

19. The method of claim 1, wherein the at least one HIV epitope is synthetic, unmutated, or mutated.

20-22. (canceled)

23. The method of claim 1, wherein the CD8+ T cell is from CP36 or CP39.

24. The method of claim 1, wherein the CD8+ T cell is autologous.

25. (canceled)

26. The method of claim 3, wherein the at least one cytokine is interleukin-2 (IL-2).

27. The method of claim 1, wherein the CD8+ T cell to CD4+ T cell ratio is enhanced.

28. The method of claim 1, wherein the CD8+ T cell response targets latent or reactivated HIV-1 infected cells.

29. The method of claim 1, wherein the CD8+ T cell immune response is greater in magnitude than a CD8+ T cell immune response induced by administration of an unstimulated CD8+ T cell composition or by administration of the HIV epitope alone.

30. (canceled)

31. The method of claim 1, wherein the efficacy of the immune response against HIV results in aa reduction of the levels of HIV viral replication, wherein said reduction is a decreased in logio reductions of about 2-logs, 3-logs, 4-logs, 5-logs, 6-logs, 7-logs, 8-logs, or 9-logs; (ii) a reduction of levels of plasma HIV-1 RNA wherein said reduction of the levels of plasma HIV-1 RNA is in log10 reductions of about 2-logs, 3-logs, 4-logs, 5-logs, 6-logs, 7-logs, 8-logs, or 9-logs; (iii) a reduction of levels of proviral HIV-1 DNA, wherein said reduction is a decrease of 100-, 200-, 300-, 400-, 500-, 600-, 700-, 800-, 900-, 1000-, 1500-, or 2000-fold; (iv) a reduction of the HIV-1 latent reservoir, wherein said reduction is a decrease of 100-, 200-, 300-, 400-, 500-, 600-, 700-, 800-, 900-, 1000-, 1500-, or 2000-fold when compared to the resting CD4+ T cell population of about 1012 cells in any healthy or infected individual or total latently infected resting CD4+ T cell population of about 106 to about 107 cells; or (v) a delay in rebound of HIV viremia after cessation of antiretroviral therapy measured in months of about 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, or 11 months, or combination thereof.

32-42. (canceled)

43. The method of claim 1, wherein the mammal is a human, and said human is afflicted with HIV-1, chronically infected with HIV-1, or acutely infected with HIV-1.

44-46. (canceled)

47. The method of claim 1, wherein the CD8+ T cell vaccine composition is administered to (i) a human on suppressive antiretroviral therapy; (ii) to the antiretroviral-treated human followed by antiretroviral treatment interruption; (iii) the antiretroviral-treated human in combination with latency reversing therapy.

48-49. (canceled)

50. The method of claim 1, wherein the composition is administered to the mammal more than one time over the course of treating or preventing.

51. The method of claim 1, wherein the composition is administered to the mammal in need thereof at about weeks two, three, four, five, six, seven, eight, nine, ten, eleven, twelve, thirteen, fourteen, fifteen, and sixteen post-HIV infection.

52. The method of claim 1, wherein the therapeutically effective amount is about 102, 103, 104, 105, 106, 107, 108, 109, 1010, 1011, or 1012 prestimulated CD8+ T cells per infusion into a patient.

53. (canceled)