Search CTL/CD8+ T-Cell Epitope Database

Found 5 matching records:

Displaying record number 1796

HXB2 Location	gp160(2-10) gp120(2-10) DNA(6228..6254)	gp160 Epitope Map
Author Location	gp120(2-10)
Epitope	`RVKEKYQHL`	Epitope Alignment
Species (MHC/HLA)	human(B*08)
Immunogen	HIV-1 infection
Experimental methods
Keywords

Notes

B*08-restricted CTL accounted for about 1/3 of the total CTL response in one individual.

References

Day2001 C. L. Day, A. K. Shea, M. A. Altfeld, D. P. Olson, S. P. Buchbinder, F. M. Hecht, E. S. Rosenberg, B. D. Walker, and S. A. Kalams. Relative dominance of epitope-specific cytotoxic T-lymphocyte responses in human immunodeficiency virus type 1-infected persons with shared HLA alleles. J. Virol., 75(14):6279-91, Jul 2001. URL: http://jvi.asm.org/cgi/content/full/75/14/6279. PubMed ID: 11413294. Show all entries for this paper.

Displaying record number 621

HXB2 Location	gp160(2-10) gp120(2-10) DNA(6228..6254)	gp160 Epitope Map
Author Location	gp160(2-10 IIIB)
Epitope	`RVKEKYQHL`	Epitope Alignment
Species (MHC/HLA)	human(B*0801)
Immunogen	HIV-1 infection
Experimental methods
Keywords	optimal epitope

Notes

C. Brander notes this is a B*0801 epitope.

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 61997

HXB2 Location	gp160(2-10) gp120(2-10) DNA(6228..6254)	gp160 Epitope Map
Author Location	Env(2-10)
Epitope	`RVKEKYQHL`	Epitope Alignment
Species (MHC/HLA)	human(B*0801)
Immunogen	peptide-HLA interaction
Experimental methods	Intracellular cytokine staining, Other
Keywords	assay or method development, NK cells

Notes

Contamination of what were previously thought to be highly specific epitopes identified through HLA IP-based immunopeptidomics is exposed. A low-level of co-isolation of erroneously assigned Class I-restricted peptides is found viz. HLA class II peptides, extended peptides from HIV Gag, and peptides from the B lymphoblastoid cell line 721.221 previously thought to be Class I deficient but which actually does present HLA-Cw*0102.
9/64 C8166 cell lysate identified epitopes are actually known epitopes. RVKEKYQHL is one of them, restricted by B*0801.

References

Partridge2018 Thomas Partridge, Annalisa Nicastri, Anna E. Kliszczak, Louis-Marie Yindom, Benedikt M. Kessler, Nicola Ternette, and Persephone Borrow. Discrimination Between Human Leukocyte Antigen Class I-Bound and Co-Purified HIV-Derived Peptides in Immunopeptidomics Workflows. Front. Immunol., 9:912, 2018. PubMed ID: 29780384. Show all entries for this paper.

Displaying record number 620

HXB2 Location	gp160(2-10) gp120(2-10) DNA(6228..6254)	gp160 Epitope Map
Author Location	gp160(2-10 IIIB)
Epitope	`RVKEKYQHL`	Epitope Alignment
		Show epitope variants
Species (MHC/HLA)	human(B8)
Immunogen	HIV-1 infection
Experimental methods
Keywords	subtype comparisons

Notes

HIV IIIB proteins were used to define the range of CTL epitopes recognized by 3 lab workers accidentally infected with HIV-1 IIIB.
Type-specific epitope, unique to the LAI and IIIB because of a deletion of three amino acids that are present in all other subtype B HIV-1s.
RVKGIRKNYQHL, a variant found in JRCSF, was not recognized.
This epitope is in the signal sequence of gp120.

References

Sipsas1997 N. V. Sipsas, S. A. Kalams, A. Trocha, S. He, W. A. Blattner, B. D. Walker, and R. P. Johnson. Identification of Type-Specific Cytotoxic T Lymphocyte Responses to Homologous Viral Proteins in Laboratory Workers Accidentally Infected with HIV-1. J. Clin. Invest., 99:752-762, 1997. To examine a situation where the autologous strain and the reference reagents would be the same, the CTL response of three lab workers accidentally infected with HIV IIIB was studied. Both group specific and type specific epitopes were targets for CTL clones. One subject had a broadening of CTL response over time, using a broad range of restricting HLA class I alleles. Characterization of the cytotoxic T lymphocyte (CTL) response against HIV-1 has been limited by the use of target cells expressing viral proteins from laboratory isolates of HIV-1. This approach has favored identification of group-specific CTL responses and precluded assessment of the extent of type-specific CTL responses directed against HIV-1. Using cells expressing viral proteins from the HIV-1 IIIB strain, we performed a detailed characterization of HIV-1-specific CTL response in three laboratory workers accidentally infected with HIV-1 IIIB. Eight of the epitopes identified were group specific, lying in relatively conserved regions of Gag, reverse transcriptase, and envelope. Three type-specific epitopes were identified, two of them in highly variable regions of envelope. In longitudinal studies in one subject, seven different epitopes and five different restricting HLA class I alleles were identified, with a progressive increase in the number of CTL epitopes recognized by this subject over time. Our data demonstrate that type-specific CTL responses make up a significant proportion of the host cellular immune response against HIV-1 and that a broadening of epitope specificity may occur. PubMed ID: 9045880. Show all entries for this paper.

Displaying record number 54811

HXB2 Location	gp160(2-10) gp120(2-10) DNA(6228..6254)	gp160 Epitope Map
Author Location
Epitope	`RVKEKYQHL`	Epitope Alignment
Species (MHC/HLA)	(B8)
Immunogen
Experimental methods
Keywords	review, immunodominance, escape, vaccine antigen design

Notes

This review discusses current literature on particular CTL escape mutations that significantly impair viral fitness and argues for a concerted effort to identify these targets.
This epitope is discussed in the context of the hierarchy of recognized HLA-B8 epitopes during acute infection.

References

Altfeld2006a Marcus Altfeld and Todd M. Allen. Hitting HIV Where It Hurts: An Alternative Approach to HIV Vaccine Design. Trends Immunol., 27(11):504-510, Nov 2006. PubMed ID: 16997629. Show all entries for this paper.