Search CTL/CD8+ T-Cell Epitope Database

Found 4 matching records:

Displaying record number 627

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HXB2 Location	gp160(33-42) gp120(33-42) DNA(6321..6350)	gp160 Epitope Map
Author Location	Env(32-41 LAI)
Epitope	`KLWVTVYYGV`	Epitope Alignment
Epitope Name	Env32-41
Subtype	B
Species (MHC/HLA)	human(A*02:01)
Immunogen	vaccine
Country	United States
Experimental methods	Chromium-release assay
Keywords	dendritic cells, enhancing activity

Vaccine Details

Vaccine type	protein
Vaccine strain	B clade MN
Vaccine component	gp160

Notes

Conserved HLA-A*0201-restricted CTL epitopes in HIV-Env were defined and characterized. In 5 HIV-1-infected subjects, 4 epitopes could bind HLA-A*0201 and elicit CTL responses and 2 of these, KLTPLCVTL and SLLNATDIAV, were found to be processed in vivo.
Peptide 1, KLWVTVYYGV, was recognized by CTL from 1/5 HIV-1-infected patients.

References

Dupuis1995 M. Dupuis, S. K. Kundu, and T. C. Merigan. Characterization of HLA-A*0201-Restricted Cytotoxic T Cell Epitopes in Conserved Regions of the HIV Type 1 gp160 Protein. J. Immunol., 155:2232-2239, 1995. Five HLA-A2 HIV-1 seropositive HIV-1 MN rec gp160 vaccinees had their CTL activity assessed using peptides known to bind with high affinity to HLA-A*0201. Four of the patients had specific CTL activity for a minimum of at least three epitopes, thus the response appears heterogeneous. One of the four peptides was confirmed to be HLA A2 restricted. Epitopes were highly conserved. PubMed ID: 7543542. Show all entries for this paper.

Displaying record number 628

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HXB2 Location	gp160(33-42) gp120(33-42) DNA(6321..6350)	gp160 Epitope Map
Author Location	Env(32-41 subtype B)
Epitope	`KLWVTVYYGV`	Epitope Alignment
Subtype	B
Species (MHC/HLA)	human(A*02:01)
Immunogen	HIV-1 infection, vaccine
Experimental methods
Keywords	binding affinity

Vaccine Details

Vaccine type	protein
Vaccine strain	B clade MN
Vaccine component	gp160

Notes

Ten HIV-1+ HLA A2 asymptomatic individuals were given two courses of HIV-1 MN rgp160 vaccine over a 2 year period.
Two hundred and fifty three HIV-1 peptides of 9 or 10 aa possessing the HLA-A2.1 binding motif (Leu at position 2, Val at the C terminus) were identified in gp160, of which 25 had a high or intermediate binding affinity.
Eleven peptides were studied that had high HLA-A2 binding affinity -- a CTL response was detected to 9/11 peptides in at least 1 individual.
CTL responses after reimmunization may include recall responses -- only individuals with vaccine cross-reactive sequences prior to vaccination showed detectable CTL responses.

References

Kundu1998a S. K. Kundu, M. Dupuis, A. Sette, E. Celis, F. Dorner, M. Eibl, and T. C. Merigan. Role of preimmunization virus sequences in cellular immunity in HIV- infected patients during HIV type 1 MN recombinant gp160 immunization. AIDS Res. Hum. Retroviruses, 14:1669-78, 1998. PubMed ID: 9870321. Show all entries for this paper.

Displaying record number 57079

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HXB2 Location	gp160(33-42) gp120(33-42) DNA(6321..6350)	gp160 Epitope Map
Author Location	gp120(33-42 DU422)
Epitope	`KLWVTVYYGV`	Epitope Alignment
Subtype	B
Species (MHC/HLA)	human(A*02:01)
Immunogen	in vitro stimulation or selection
Experimental methods	CD8 T-cell Elispot - IFNγ, Chromium-release assay, Tetramer binding
Keywords	dendritic cells

Notes

Three types of myeloid dendritic cells - monocytic dendritic cells, Langerhans cells, and interstitial dermal-intestinal dendritic cells - were shown to be able to prime CD8+ T-cell responses to HIV-1. Primed monocytic dendritic cells from 2 uninfected adult donors had broad primary T-cell reactivity, reacting with 15mers containing 42 known epitopes in Gag, Env, and Nef.
One of the reactive 15mers contained optimal epitope KLWVTVYYGV, which was restricted by HLA A*0201.

References

Colleton2009 Bonnie A. Colleton, Xiao-Li Huang, Nada M. Melhem, Zheng Fan, Luann Borowski, Giovanna Rappocciolo, and Charles R. Rinaldo. Primary Human Immunodeficiency Virus Type 1-Specific CD8+ T-Cell Responses Induced by Myeloid Dendritic Cells. J. Virol., 83(12):6288-6299, Jun 2009. PubMed ID: 19357176. Show all entries for this paper.

Displaying record number 55290

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HXB2 Location	gp160(33-42) gp120(33-42) DNA(6321..6350)	gp160 Epitope Map
Author Location	Env
Epitope	`KLWVTVYYGV`	Epitope Alignment
		Show epitope variants
Subtype	B
Species (MHC/HLA)	human(A2)
Immunogen	HIV-1 infection
Patient MHC/HLA	A1, A19, B35:01, B44, C16, Cw7; A02:01, A19, B14, B44, C16, Cw8
Country	United States
Experimental methods	CD8 T-cell Elispot - IFNγ
Keywords	HAART, ART, mother-to-infant transmission, rate of progression, escape, co-receptor, mutation acquisition, HLA associated polymorphism

Notes

HIV-1 mother-to-child transmission is studied for LTNPs by comparing entire genomes from 2 mother (M1, M2) and 2 daughter (D1, D2) RNA samples of a mother-child pair over 11 years. Genetic distance was 94% between subjects' strains. Divergence in sequences was attributed to distinct HLA selection pressures as ds/dn was larger for intra- rather than inter-person sequences. 10 new mutations in D2 were found related to unique daughter HLA alleles.
Functional ELISpot studies using D2 and Nef peptides reveal strong associations between CTL responses and escape variants, contributing to delayed progression.
LTNP status was not related to defective virus since all viral genes were intact and CTL response did not effectively control viral load. It is supposed that genetic HLA background and HIV-1 epitope-immune response interaction account for nonprogression of disease.
All isolates contained R77Q in Vpr, a variation associated with reduction of cellular apoptosis.
This HLA-A2/A2.1 restricted epitope, KLWVTVYYGV was mutated to nwWVTVYYGV in the daughter D2 isolate.

References

Reinis2007 Milan Reinis, Barbara Weiser, Carla Kuiken, Tao Dong, Dorothy Lang, Sharon Nachman, Yonghong Zhang, Sarah Rowland-Jones, and Harold Burger. Genomic Analysis of HIV Type 1 Strains Derived from a Mother and Child Pair of Long-Term Nonprogressors. AIDS Res. Hum. Retroviruses, 23(2):309-315, Feb 2007. PubMed ID: 17331038. Show all entries for this paper.