Search CTL/CD8+ T-Cell Epitope Database

Found 4 matching records:

Displaying record number 58403

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HXB2 Location	Nef(186-194) DNA(9352..9378)	Nef Epitope Map
Author Location	( IIIB, MN)
Epitope	`DSRLAFHHV`	Epitope Alignment
Subtype	B
Species (MHC/HLA)	human(B*51)
Immunogen	HIV-1 infection
Country	China
Experimental methods	CD8 T-cell Elispot - IFNγ, CTL suppression of replication
Keywords	rate of progression, HLA associated polymorphism, elite controllers

Notes

To study the beneficial effects of HLA-B*51 without confounding founder effects, 22 HLA-B*51+ subjects selected from a Chinese cohort of plasma-route HIV-infected individuals, without ART for 10 years, were studied. Progression to AIDS was associated with sequential mutation selection and subsequent CTL response within 3 immunodominant epitopes, in order - Pol LPPVVAKEI (LI9), followed by Gag NANPDCKTI (NI9) and then Pol TAFTIPSI (TI8). Thus a multi-layered response is suggested to be beneficial for control in B*51-carrying controllers.
The order of mutations in HIV-1 appears to be the L743I mutation at position 1 of the LI9 epitope followed by the V289L mutation at position 8 of TV8 epitope and then the A328S mutation in position 2 of the NI9 epitope.
Epitope DSRLAFHHV had a <20% frequency of recognition and a mean magnitude of ∼100 SFU/million PBMC when CTL response is measured by ex vivo EliSpot in HLA-B51+ subjects.

References

Zhang2011 YongHong Zhang, YanChun Peng, HuiPing Yan, Keyi Xu, Masumichi Saito, Hao Wu, XinYue Chen, Srinika Ranasinghe, Nozomi Kuse, Tim Powell, Yan Zhao, WeiHua Li, Xin Zhang, Xia Feng, Ning Li, Aleksandra Leligdowicz, XiaoNing Xu, Mina John, Masafumi Takiguchi, Andrew McMichael, Sarah Rowland-Jones, and Tao Dong. Multilayered Defense in HLA-B51-Associated HIV Viral Control. J. Immunol., 187(2):684-691, 15 Jul 2011. PubMed ID: 21670313. Show all entries for this paper.

Displaying record number 1092

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HXB2 Location	Nef(186-194) DNA(9352..9378)	Nef Epitope Map
Author Location	Nef(186-194 BRU)
Epitope	`DSRLAFHHV`	Epitope Alignment
Species (MHC/HLA)	human(B51)
Immunogen
Experimental methods
Keywords

Notes

Resulted in the assembly of HLA-B51.

References

Connan1994 F. Connan, F. Hlavac, J. Hoebeke, J. G. Guillet, and J. Choppin. A Simple Assay for Detection of Peptides Promoting the Assembly of HLA Class I Molecules. Eur. J. Immunol., 24:777-780, 1994. Peptides from influenza and HIV-1 were tested for their ability to promote the assembly of HLA-A2 and HLA-B51 molecules in T2 cell lysates. HIV Pol 476-484 allowed significant assembly of HLA-A2, and is a target for CTL. Nef peptide 186-194 produced significant assembly of HLA-B51. A hydrophobic anchor residue (V, L, I) at position 9 could occupy pocket F, and a hydrophobic residue (V, L) at position 3 or 4 may anchor to hydrophobic pocket D of HLA-B51. Proline at position 2 increases HLA-B51 anchoring. PubMed ID: 8125145. Show all entries for this paper.

Displaying record number 52992

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HXB2 Location	Nef(186-194) DNA(9352..9378)	Nef Epitope Map
Author Location	Nef(186-194)
Epitope	`DSRLAFHHV`	Epitope Alignment
		Show epitope variants
Species (MHC/HLA)	human(B51)
Immunogen	HIV-1 infection
Patient MHC/HLA	A3, A32, B15, B51, C*03, Cw6, DQ7, DR4, DR8
Country	Netherlands
Experimental methods	CD8 T-cell Elispot - IFNγ, Flow cytometric T-cell cytokine assay
Keywords	rate of progression, escape

Notes

Both stable potential epitopes and epitopes with escape mutations were found in a patient with increasing viral load over a time period of 4 years. Fixation of escape mutations occurred sequentially and correlated with the rise in viral load and with the increased number of productively infected cells.
This is one of 7 epitopes from this individual that varied over time, although the internal mutations did not become fixed. The dsLlaLRhM variant residues arose at early time points, and the dsrlaVhhv variant residue arose at intermediate time points.

References

Geels2003 Mark J. Geels, Marion Cornelissen, Hanneke Schuitemaker, Kiersten Anderson, David Kwa, Jolanda Maas, John T. Dekker, Elly Baan, Fokla Zorgdrager, Remco van den Burg, Martijn van Beelen, Vladimir V. Lukashov, Tong-Ming Fu, William A. Paxton, Lia van der Hoek, Sheri A. Dubey, John W. Shiver, and Jaap Goudsmit. Identification of Sequential Viral Escape Mutants Associated with Altered T-Cell Responses in a Human Immunodeficiency Virus Type 1-Infected Individual. J. Virol., 77(23):12430-12440, Dec 2003. PubMed ID: 14610167. Show all entries for this paper.

Displaying record number 53541

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HXB2 Location	Nef(186-194) DNA(9352..9378)	Nef Epitope Map
Author Location	Nef
Epitope	`DSRLAFHHV`	Epitope Alignment
Epitope Name	DV9
Subtype	B
Species (MHC/HLA)	human
Immunogen	HIV-1 infection
Patient MHC/HLA	A28, A29, B14, B44, Cw8
Country	United States
Experimental methods	CD8 T-cell Elispot - IFNγ
Keywords	subtype comparisons, escape, characterizing CD8+ T cells, viral fitness and reversion

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.
An escape mutation at position 7, DSRLAFqHV, was found not to correspond to the most polymorphic residue in the epitope. This is a novel unmapped epitope.

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.