Search CTL/CD8+ T-Cell Epitope Database

Found 20 matching records:

Displaying record number 59558

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HXB2 Location	Vpr(30-38) DNA(5646..5672)	Vpr Epitope Map
Author Location	Vpr(30-38)
Epitope	`AVRHFPRIW`	Epitope Alignment
Epitope Name	AW9
Species (MHC/HLA)	human(B*18)
Immunogen	HIV-1 infection
Experimental methods	CD8 T-cell Elispot - IFNγ, Flow cytometric T-cell cytokine assay
Keywords	rate of progression, optimal epitope, chronic infection

Notes

Correlation between HLA class I and spontaneous control of HIV-1 was significant for 7-8 epitopes when 341 chronic, HIV-infected subjects, divided into controllers and non-controllers, were tested for EliSpot responses to 257 optimally defined epitopes. 21 epitopes were associated with viral progression. Protective epitopes tend to cluster in regions of critical stability for the protein, therefore constraining escape.
AVRHFPRIW had a significantly positive association with HLA B*18; it was recognized by 7/19 B*18-positive subjects and 17/207 B*18-negative subjects.

References

Pereyra2014 Florencia Pereyra, David Heckerman, Jonathan M. Carlson, Carl Kadie, Damien Z. Soghoian, Daniel Karel, Ariel Goldenthal, Oliver B. Davis, Charles E. DeZiel, Tienho Lin, Jian Peng, Alicja Piechocka, Mary Carrington, and Bruce D. Walker. HIV Control Is Mediated in Part by CD8+ T-Cell Targeting of Specific Epitopes. J. Virol., 88(22):12937-12948, Nov 2014. PubMed ID: 25165115. Show all entries for this paper.

Displaying record number 55618

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HXB2 Location	Vpr(30-38) DNA(5646..5672)	Vpr Epitope Map
Author Location	Vpr
Epitope	`AVRHFPRIW`	Epitope Alignment
Epitope Name	AW9
Subtype	B
Species (MHC/HLA)	human(B27)
Immunogen	HIV-1 infection
Country	Netherlands
Experimental methods	CD8 T-cell Elispot - IFNγ
Keywords	computational epitope prediction

Notes

Peptide prediction programs based on MHC binding, proteasomal cleavage and TAP transport were applied to select novel epitopes absent from the Los Alamos HIV database. 22 novel epitopes were tested by IFN-gamma ELISpot and 19 (11 HLA-B27 restricted, 8 HLA-B57 restricted) induced strong positive responses.
Magnitude of response generated was similar to that of previously identified epitopes, but the number of individuals responding was lower. This could be explained by less stringent HLA-typing of subjects and perhaps high sequence variability within these novel epitopes.
AW9, AVRHFPRIW, is a known HLA-B27-restricted epitope used as a positive control for eliciting CTL IFN-gamma response.

References

Schellens2008 Ingrid M. M. Schellens, Can Kesmir, Frank Miedema, Debbie van Baarle, and José A. M. Borghans. An Unanticipated Lack of Consensus Cytotoxic T Lymphocyte Epitopes in HIV-1 Databases: The Contribution of Prediction Programs. AIDS, 22(1):33-37, 2 Jan 2008. PubMed ID: 18090389. Show all entries for this paper.

Displaying record number 62551

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HXB2 Location	Vpr(30-38) DNA(5646..5672)	Vpr Epitope Map
Author Location	Vpr(30-38)
Epitope	`AVRHFPRIW`	Epitope Alignment
Epitope Name	AW9
Subtype	B
Species (MHC/HLA)	human(B*57)
Immunogen	HIV-1 infection
Patient MHC/HLA	S00052: A01, A25, B18, B57, C06, C12
Country	United States
Experimental methods	CD8 T-cell Elispot - IFNγ, Other
Keywords	dynamics, chronic infection

Notes

This report analyzed 29 CTL responses against 23 HIV-1 epitopes in 9 untreated chronically infected "controllers" and identified inverse correlations between epitope variability and CTL clonal stability over time and between epitope variability and CTL clonal breadth.
Over 161 weeks, the AVRHFPRIW-specific CTL clonal response in individual S00052 demonstrated a 0.68 Sorenson similarity index and a mean breadth of 2.0.
Based on all HIV-1 subtype B sequences in LANL HIV Sequence Database at time of analysis, AVRHFPRIW had a Simpson diversity index of 0.86.

References

Balamurugan2017 Arumugam Balamurugan, Deon Claiborne, Hwee L. Ng, and Otto O. Yang. HIV-1 Epitope Variability Is Associated with T Cell Receptor Repertoire Instability and Breadth. J. Virol., 91(16), 15 Aug 2017. PubMed ID: 28592539. Show all entries for this paper.

Displaying record number 2008

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HXB2 Location	Vpr(30-38) DNA(5646..5672)	Vpr Epitope Map
Author Location	Vpr
Epitope	`AVRHFPRIW`	Epitope Alignment
Epitope Name	Vpr-AW9
Subtype	B
Species (MHC/HLA)	human(B*57)
Immunogen	HIV-1 infection
Country	United States
Experimental methods	CD8 T-cell Elispot - IFNγ
Keywords	HAART, ART

Notes

Among HIV+ individuals who carried HLA B*57, 1/7 (14%) recognized this epitope.

References

Sabbaj2003 Steffanie Sabbaj, Anju Bansal, G. Douglas Ritter, Christopher Perkins, Bradley H. Edwards, Ethan Gough, Jianming Tang, James J. Szinger, Bette Korber, Craig M. Wilson, Richard A. Kaslow, Mark J. Mulligan, and Paul A. Goepfert. Cross-Reactive CD8+ T Cell Epitopes Identified in US Adolescent Minorities. J. Acquir. Immune Defic. Syndr., 33(4):426-438, 1 Aug 2003. PubMed ID: 12869831. Show all entries for this paper.

Displaying record number 54384

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HXB2 Location	Vpr(30-38) DNA(5646..5672)	Vpr Epitope Map
Author Location
Epitope	`AVRHFPRIW`	Epitope Alignment
Epitope Name	AW9
Species (MHC/HLA)	human(B*57)
Immunogen	HIV-1 infection
Experimental methods	CD8 T-cell Elispot - IFNγ
Keywords	escape

Notes

Impact of CTL escape mutations in HLA-B57 positive elite supressors was examined. Escape mutations in B57-restricted Gag epitopes were present in all viruses derived from plasma but were lacking in proviruses, suggesting a strong selective pressure acting upon virus in plasma. IFN-gamma responses were detected to both wild-type epitopes and mutant plasma virus epitopes. In some individuals, CD8 IL-2 secretion, rather than IFN-gamma responses, showed better correlation with the plasma viral variants.
HLA-B*57-restricted optimal epitope AVRHFPRIW was tested for immune response.

References

Bailey2006 Justin R. Bailey, Thomas M. Williams, Robert F. Siliciano, and Joel N. Blankson. Maintenance of Viral Suppression in HIV-1-Infected HLA-B*57+ Elite Suppressors Despite CTL Escape Mutations. J. Exp. Med., 203(5):1357-1369, 15 May 2006. PubMed ID: 16682496. Show all entries for this paper.

Displaying record number 54824

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HXB2 Location	Vpr(30-38) DNA(5646..5672)	Vpr Epitope Map
Author Location	Vpr(30-38)
Epitope	`AVRHFPRIW`	Epitope Alignment
Epitope Name	vprAV9
Species (MHC/HLA)	human(B*57)
Immunogen	HIV-1 infection
Country	Kenya, United Kingdom
Experimental methods	CD8 T-cell Elispot - IFNγ
Keywords	TCR usage, structure, characterizing CD8+ T cells

Notes

CD8+ T cell repertoire recognizing KAFSPEVIPMF [KF11] and variants and the structure of individual B*57-peptide complexes were studied.
In addition, immunodominance of the previously mapped B*57 epitopes during chronic infection was assessed. KGFNPEVIPMF and ISPRTLNAW were immunodominant both in frequency and magnitude of recognition.

References

Gillespie2006 Geraldine M. A. Gillespie, Guillaume Stewart-Jones, Jaya Rengasamy, Tara Beattie, Job J. Bwayo, Francis A. Plummer, Rupert Kaul, Andrew J. McMichael, Philippa Easterbrook, Tao Dong, E. Yvonne Jones, and Sarah L. Rowland-Jones. Strong TCR Conservation and Altered T Cell Cross-Reactivity Characterize a B*57-Restricted Immune Response in HIV-1 Infection. J. Immunol., 177(6):3893-3902, 15 Sep 2006. PubMed ID: 16951352. Show all entries for this paper.

Displaying record number 57279

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HXB2 Location	Vpr(30-38) DNA(5646..5672)	Vpr Epitope Map
Author Location	Vpr
Epitope	`AVRHFPRIW`	Epitope Alignment
Epitope Name	AW9
Subtype	B
Species (MHC/HLA)	human(B*57)
Immunogen	HIV-1 infection
Country	Barbados, Haiti, Jamaica
Experimental methods	CD8 T-cell Elispot - IFNγ, Other
Keywords	mother-to-infant transmission, elite controllers

Notes

To dissect whether the protective effect of HLA-B*57 in HIV-1 infection is due to CTL that recognize HLA-B*57-restricted epitopes or by the presence of viral-fitness attenuating mutations in such B*57 epitopes, 13 mother-infant pairs were studied. The B57 advantage is primarily through the maintenance of a fitness-attenuating mutation in p24-Gag, T242N in epitope TW10 (TSTLQEQIGW).
Regardless of parental inheritance, HLA-B57 controls VL even in infancy and even when escape mutations from B*57 positive mothers are transmitted. Mutations in p24-Gag are predominant in mismatched-HLA subject pairs and arise after vertical transmission, impacting viral fitness.
Epitope AW9-Vpr, AVRHFPRIW, though outside of Gag did develop a mutation in one subject. It was not recognized by any B57-positive infants.

References

Schneidewind2009 Arne Schneidewind, Yanhua Tang, Mark A. Brockman, Elizabeth G. Ryland, Jacqueline Dunkley-Thompson, Julianne C. Steel-Duncan, M. Anne St. John, Joseph A. Conrad, Spyros A. Kalams, Francine Noel, Todd M. Allen, Celia D. Christie, and Margaret E. Feeney. Maternal Transmission of Human Immunodeficiency Virus Escape Mutations Subverts HLA-B57 Immunodominance but Facilitates Viral Control in the Haploidentical Infant. J. Virol., 83(17):8616-8627, Sep 2009. PubMed ID: 19515764. Show all entries for this paper.

Displaying record number 57402

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HXB2 Location	Vpr(30-38) DNA(5646..5672)	Vpr Epitope Map
Author Location	Vpr(30-38)
Epitope	`AVRHFPRIW`	Epitope Alignment
Epitope Name	AW9
Subtype	B
Species (MHC/HLA)	human(B*57)
Immunogen	in vitro stimulation or selection, HIV-1 infection
Country	United States
Experimental methods	CD8 T-cell Elispot - IFNγ, Other
Keywords	TCR usage, assay or method development, chronic infection

Notes

By using a modified spectratyping (immunoscoping) method, epitope-specific TCR breadth and sequences were quantitated rapidly. Overall magnitude of HIV-1 specific CTL responses to chronic infection were limited by the clonal breadth of TCR generated against HIV-1 epitopes tested in 12 patients with chronic, untreated infection.
CTL response specific to epitope AW9 was studied, TCR usage was BV06a in patient 00052.

References

Balamurugan2010 Arumugam Balamurugan, Hwee L. Ng, and Otto O. Yang. Rapid T Cell Receptor Delineation Reveals Clonal Expansion Limitation of the Magnitude of the HIV-1-Specific CD8+ T Cell Response. J. Immunol., 185(10):5935-5942, 15 Nov 2010. PubMed ID: 20944001. Show all entries for this paper.

Displaying record number 58499

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HXB2 Location	Vpr(30-38) DNA(5646..5672)	Vpr Epitope Map
Author Location	Vpr(30-38)
Epitope	`AVRHFPRIW`	Epitope Alignment
Subtype	B
Species (MHC/HLA)	human(B*57)
Immunogen	HIV-1 infection
Country	Canada
Experimental methods	Other
Keywords	characterizing CD8+ T cells, elite controllers

Notes

Dual color EliSpot testing for IL-2 and IFN-γ was used to determine whether CTL restricted by MHC Class I alleles associated with slow progression to disease, viz. B*57 and B*27, had a more poly-functional profile than other CD8+ cells in a treatment-naive cohort from Montreal. B*57/B*27-restricted CTL producing IL-2 or IFN-γ or IL-2/IFN-γ, were similar in both slow progressors (SP) and progressors. Other non-protective MHC-I-restricted CTL producing both IL-2/IFN-γ, were greater in number in SP than progressors.
Within SP, peptides restricted by both protective and non-protective MHC-I alleles elicited CTL with the same functional profile. For progressors, peptides and epitopes restricted by protective B*57/B*27 alleles stimulated a higher proportion of dual-(IL-2/IFN-γ)secreting CTL.
HLA-B*57-restricted Vpr optimal epitope AVRHFPRIW was tested in a dual color EliSpot and was found to elicit CTL that could produce IL-2 and/or IFN-γ.

References

Peretz2011 Yoav Peretz, Olivia Marra, Réjean Thomas, Danielle Legault, Pierre Côté, Mohamed-Rachid Boulassel, Danielle Rouleau, Jean-Pierre Routy, Rafick-Pierre Sékaly, Christos M Tsoukas, Cécile Tremblay, and Nicole F. Bernard. Relative Contribution of HIV-Specific Functional Lymphocyte Subsets Restricted by Protective and Non-Protective HLA Alleles. Viral Immunol, 24(3):189-198, Jun 2011. PubMed ID: 21668360. Show all entries for this paper.

Displaying record number 59141

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HXB2 Location	Vpr(30-38) DNA(5646..5672)	Vpr Epitope Map
Author Location	Vpr
Epitope	`AVRHFPRIW`	Epitope Alignment
		Show epitope variants
Epitope Name	AW9
Subtype	B
Species (MHC/HLA)	human(B*57)
Immunogen	HIV-1 infection
Country	Germany
Experimental methods	CD8 T-cell Elispot - IFNγ
Keywords	elite controllers

Notes

In a follow-up on the anonymous 1999 Berlin patient (not Timothy Brown of 2008), viral replication suppression was seen after 15 years of absence of ART. Half the HIV-specific CTL responses in this patient were restricted by HLA-B*57, with the most immunodominant being against Nef HW9, HTQGYFPDW.
B*57-restricted Vpr AW9, AVRHFPRIW, elicited a CTL response of >500 sfu/10⁶ PBMC when tested by EliSpot. Patient autologous sequence was AVRHFPRvW.

References

Jessen2014 Heiko Jessen, Todd M. Allen, and Hendrik Streeck. How a Single Patient Influenced HIV Research — 15-Year Follow-Up. N. Engl. J. Med., 370(7):682-683, 13 Feb 2014. PubMed ID: 24521131. Show all entries for this paper.

Displaying record number 59559

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HXB2 Location	Vpr(30-38) DNA(5646..5672)	Vpr Epitope Map
Author Location	Vpr(30-38)
Epitope	`AVRHFPRIW`	Epitope Alignment
Epitope Name	AW9
Species (MHC/HLA)	human(B*57)
Immunogen	HIV-1 infection
Experimental methods	CD8 T-cell Elispot - IFNγ, Flow cytometric T-cell cytokine assay
Keywords	rate of progression, optimal epitope, chronic infection

Notes

Correlation between HLA class I and spontaneous control of HIV-1 was significant for 7-8 epitopes when 341 chronic, HIV-infected subjects, divided into controllers and non-controllers, were tested for EliSpot responses to 257 optimally defined epitopes. 21 epitopes were associated with viral progression. Protective epitopes tend to cluster in regions of critical stability for the protein, therefore constraining escape.
AVRHFPRIW had a significantly positive association with HLA B*57; it was recognized by 24/98 B*57-positive subjects and 24/226 B*57-negative subjects.

References

Displaying record number 61567

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HXB2 Location	Vpr(30-38) DNA(5646..5672)	Vpr Epitope Map
Author Location	Vpr
Epitope	`AVRHFPRIW`	Epitope Alignment
Epitope Name	B57-AW9(vpr)
Species (MHC/HLA)	human(B*57)
Immunogen	HIV-1 infection
Patient MHC/HLA	AC-108: A02, B57, B61, C03, C*06
Country	United States
Experimental methods	CD8 T-cell Elispot - IFNγ, Intracellular cytokine staining
Keywords	acute/early infection, protective allele

Notes

HLA-B*57-restricted CTL responses were relatively immunodominant in breadth and strength during acute early infection of HIV-1. 6/9 HLA-B*57 patients controlled viremia to <5000 copies/ml for up to 29 months post-infection.
Epitope B57-AW9(vpr), AVRHFPRIW, elicited CTL response in 1/9 acute early HIV-1-infected subjects; AC-108 = 230 SFC/10⁶ PBMC.

References

Altfeld2003a Marcus Altfeld, Marylyn M. Addo, Eric S. Rosenberg, Frederick M. Hecht, Paul K. Lee, Martin Vogel, Xu G. Yu, Rika Draenert, Mary N. Johnston, Daryld Strick, Todd M. Allen, Margaret E. Feeney, James O. Kahn, Rafick P. Sekaly, Jay A. Levy, Jürgen K. Rockstroh, Philip J. Goulder, and Bruce D. Walker. Influence of HLA-B57 on Clinical Presentation and Viral Control during Acute HIV-1 Infection. AIDS, 17(18):2581-2591, 5 Dec 2003. PubMed ID: 14685052. Show all entries for this paper.

Displaying record number 55603

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HXB2 Location	Vpr(30-38) DNA(5646..5672)	Vpr Epitope Map
Author Location	Vpr
Epitope	`AVRHFPRIW`	Epitope Alignment
Epitope Name	AW9
Subtype	B
Species (MHC/HLA)	human(B57)
Immunogen	HIV-1 infection
Country	Netherlands
Experimental methods	CD8 T-cell Elispot - IFNγ
Keywords	computational epitope prediction

Notes

Peptide prediction programs based on MHC binding, proteasomal cleavage and TAP transport were applied to select novel epitopes absent from the Los Alamos HIV database. 22 novel epitopes were tested by IFN-gamma ELISpot and 19 (11 HLA-B27 restricted, 8 HLA-B57 restricted) induced strong positive responses.
Magnitude of response generated was similar to that of previously identified epitopes, but the number of individuals responding was lower. This could be explained by less stringent HLA-typing of subjects and perhaps high sequence variability within these novel epitopes.
AW9(Vpr), AVRHFPRIW, is a known HLA-B57-restricted epitope used as a positive control for eliciting CTL IFN-gamma response.

References

Displaying record number 53554

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HXB2 Location	Vpr(30-38) DNA(5646..5672)	Vpr Epitope Map
Author Location	Vpr(30-38)
Epitope	`AVRHFPRIW`	Epitope Alignment
Subtype	B
Species (MHC/HLA)	human(B57)
Immunogen	HIV-1 infection
Patient MHC/HLA	A1, A3, B57, B7, Cw6, Cw7
Country	United States
Experimental methods	CD8 T-cell Elispot - IFNγ
Keywords

Notes

Two-thirds of all mutations arising in non-envelope proteins during the transition from acute to chronic infection were found to be due to either CD8 T-cell-associated selective pressures or reversion of HLA-I-associated mutations selected in a previous host.The predominance of escape mutations at highly polymorphic sites was observed across different HIV-1 clades.
This epitope was reactive, but escape mutations did not accrue in it over time.

References

Allen2005a Todd M. Allen, Marcus Altfeld, Shaun C. Geer, Elizabeth T. Kalife, Corey Moore, Kristin M. O'Sullivan, Ivna DeSouza, Margaret E. Feeney, Robert L. Eldridge, Erica L. Maier, Daniel E. Kaufmann, Matthew P. Lahaie, Laura Reyor, Giancarlo Tanzi, Mary N. Johnston, Christian Brander, Rika Draenert, Jurgen K. Rockstroh, Heiko Jessen, Eric S. Rosenberg, Simon A. Mallal, and Bruce D. Walker. Selective Escape from CD8+ T-Cell Responses Represents a Major Driving Force of Human Immunodeficiency Virus Type 1 (HIV-1) Sequence Diversity and Reveals Constraints on HIV-1 Evolution. J. Virol., 79(21):13239-13249, Nov 2005. PubMed ID: 16227247. Show all entries for this paper.

Displaying record number 53649

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HXB2 Location	Vpr(30-38) DNA(5646..5672)	Vpr Epitope Map
Author Location
Epitope	`AVRHFPRIW`	Epitope Alignment
Species (MHC/HLA)	human(B*58:01, B57)
Immunogen	HIV-1 infection
Experimental methods	CD8 T-cell Elispot - IFNγ, Chromium-release assay
Keywords	responses in children, mother-to-infant transmission, escape

Notes

Escape mutations in TW10 and other B57-restricted epitopes were shown to arise early in infants following perinatal infection. Some escape variants were likely to have been transmitted vertically, from HLA-B57/5801 positive HIV-1 infected mothers, while others arose during infancy in cases where the children inherited the B57/5801 allele paternally. In contrast to adults, the majority of children showed a robust response to the escape variants, suggesting that infants are able to mount functional immune responses and drive immune escape and that a developing immune system may exhibit greater plasticity in recognizing viral variants.

References

Feeney2005a Margaret E. Feeney, Yanhua Tang, Katja Pfafferott, Kathleen A. Roosevelt, Rika Draenert, Alicja Trocha, Xu G. Yu, Cori Verrill, Todd Allen, Corey Moore, Simon Mallal, Sandra Burchett, Kenneth McIntosh, Stephen I. Pelton, M. Anne St. John, Rohan Hazra, Paul Klenerman, Marcus Altfeld, Bruce D. Walker, and Philip J. R. Goulder. HIV-1 Viral Escape in Infancy Followed by Emergence of a Variant-Specific CTL Response. J. Immunol., 174(12):7524-7530, 15 Jun 2005. PubMed ID: 15944251. Show all entries for this paper.

Displaying record number 53660

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HXB2 Location	Vpr(30-38) DNA(5646..5672)	Vpr Epitope Map
Author Location	Vpr
Epitope	`AVRHFPRIW`	Epitope Alignment
Subtype	B, C
Species (MHC/HLA)	human(B57, B63)
Immunogen	HIV-1 infection
Experimental methods	CD8 T-cell Elispot - IFNγ
Keywords	rate of progression, HLA cross-presentation, optimal epitope, novel epitope

Notes

HLA-B63-positive subjects were shown to be able to generate CTL responses early in acute HIV infection and to control HIV replication in the absence of antiretroviral treatment. Since HLA-B63 shares the epitope binding motif of HLA-B57 and -B58, it was shown that HLA-B63-positive individuals mounted CTL responses to previously identified B57-restricted epitopes, as well as novel, B63-restricted epitopes. Moreover, these novel B63-restricted epitopes can also be presented by HLA-B57 and -B58.
This epitope was recognized by 30% of B63-positive subjects and 14% of B57/58-positive subjects. B63-AVRHFPRIW is a novel epitope.

References

Frahm2005a Nicole Frahm, Sharon Adams, Photini Kiepiela, Caitlyn H. Linde, Hannah S. Hewitt, Mathias Lichterfeld, Kaori Sango, Nancy V. Brown, Eunice Pae, Alysse G. Wurcel, Marcus Altfeld, Margaret E. Feeney, Todd M. Allen, Timothy Roach, M. Anne St. John, Eric S. Daar, Eric Rosenberg, Bette Korber, Francesco Marincola, Bruce D. Walker, Philip J. R. Goulder, and Christian Brander. HLA-B63 Presents HLA-B57/B58-Restricted Cytotoxic T-Lymphocyte Epitopes and Is Associated with Low Human Immunodeficiency Virus Load. J. Virol., 79(16):10218-10225, Aug 2005. PubMed ID: 16051815. Show all entries for this paper.

Displaying record number 1263

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HXB2 Location	Vpr(30-38) DNA(5646..5672)	Vpr Epitope Map
Author Location	Vpr(29-38 SF2)
Epitope	`AVRHFPRIW`	Epitope Alignment
Species (MHC/HLA)	human(B*57:01)
Immunogen	HIV-1 infection
Experimental methods
Keywords	acute/early infection

Notes

CTL responses against HIV-1 Vpr, Vpu, and Vif were analyzed in multiple HIV-1-infected individuals.
This epitope was recognized by 4/6 individuals expressing B*5701 allele.
Individuals with long-term nonprogressive and treated chronic HIV-1 infection targeted Vpr more frequently than individuals with treated acute infection.
Vpr is a frequent target of HIV-1 specific CD8+ T-cells -- a response was detected in 45% of individuals tested and Vpr and p17 were the most preferentially targeted proteins per unit length by CD8+ T-cells.

References

Altfeld2001c M. Altfeld, M. M. Addo, R. L. Eldridge, X. G. Yu, S. Thomas, A. Khatri, D. Strick, M. N. Phillips, G. B. Cohen, S. A. Islam, S. A. Kalams, C. Brander, P. J. Goulder, E. S. Rosenberg, B. D. Walker, and The HIV Study Collaboration.. Vpr is preferentially targeted by CTL during HIV-1 infection. J. Immunol., 167(5):2743-52, 1 Sep 2001. URL: http://www.jimmunol.org/cgi/content/full/167/5/2743. PubMed ID: 11509618. Show all entries for this paper.

Displaying record number 52406

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HXB2 Location	Vpr(30-38) DNA(5646..5672)	Vpr Epitope Map
Author Location	Vpr(29-38)
Epitope	`AVRHFPRIW`	Epitope Alignment
Subtype	B
Species (MHC/HLA)	human(B*57:01)
Immunogen	HIV-1 infection
Experimental methods
Keywords	early-expressed proteins

Notes

CTL responses against regulatory and accessory proteins in 70 HIV-1 infected patients were studied using overlapping peptides and Elispot.
28% targeted one or more overlapping Tat peptides; 36%, Rev peptides; 33%, Vif peptides; 40%, Vpr peptides; and 2%, Vpu peptides.
All known optimally defined epitopes were summarized for the five proteins.

References

Addo2002a M. M. Addo, X. G. Yu, E. S. Rosenberg, B. D. Walker, and M. Altfeld. Cytotoxic T-Lymphocyte (CTL) Responses Directed against Regulatory and Accessory Proteins in HIV-1 Infection. DNA Cell Biol., 21(9):671-678, Sep 2002. PubMed ID: 12396610. Show all entries for this paper.

Displaying record number 52598

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HXB2 Location	Vpr(30-38) DNA(5646..5672)	Vpr Epitope Map
Author Location	Vpr(30-38)
Epitope	`AVRHFPRIW`	Epitope Alignment
Species (MHC/HLA)	human(B*57:01)
Immunogen
Experimental methods
Keywords	optimal epitope, A-list

References

Llano2019 Anuska Llano, Samandhy Cedeño, Sandra Silva Arrieta, and Christian Brander. The 2019 Optimal HIV CTL Epitopes Update: Growing Diversity in Epitope Length and HLA restriction. 2019. Show all entries for this paper.

Displaying record number 59557

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HXB2 Location	Vpr(30-38) DNA(5646..5672)	Vpr Epitope Map
Author Location	Vpr(30-38)
Epitope	`AVRHFPRIW`	Epitope Alignment
Epitope Name	AW9
Species (MHC/HLA)	human(C*14)
Immunogen	HIV-1 infection
Experimental methods	CD8 T-cell Elispot - IFNγ, Flow cytometric T-cell cytokine assay
Keywords	rate of progression, optimal epitope, chronic infection

Notes

Correlation between HLA class I and spontaneous control of HIV-1 was significant for 7-8 epitopes when 341 chronic, HIV-infected subjects, divided into controllers and non-controllers, were tested for EliSpot responses to 257 optimally defined epitopes. 21 epitopes were associated with viral progression. Protective epitopes tend to cluster in regions of critical stability for the protein, therefore constraining escape.
AVRHFPRIW had a significantly positive association with HLA C*14; it was recognized by 12/17 C*14-positive subjects and 48/324 C*14-negative subjects.