Search CTL/CD8+ T-Cell Epitope Database

Found 17 matching records:

Displaying record number 55285

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HXB2 Location	Gag(219-233) p24(87-101) DNA(1444..1488)	Gag Epitope Map
Author Location	Gag
Epitope	`HAGPIAPGQMREPRG`	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 restricted epitope, HAGPIAPGQMREPRG was mutated to qAGPIAPGQMREPRG 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.

Displaying record number 55286

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HXB2 Location	Pol(188-196) RT(33-41) DNA(2646..2672)	Pol Epitope Map
Author Location	Pol
Epitope	`ALVEICTEM`	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 restricted epitope, ALVEICTEM was mutated to ALiEICTEM in the daughter D2 isolate.

References

Displaying record number 55288

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HXB2 Location	Pol(334-342) RT(179-187) DNA(3084..3110)	Pol Epitope Map
Author Location	Pol
Epitope	`VIYQYMDDL`	Epitope Alignment
		Show epitope variants
Subtype	B
Species (MHC/HLA)	human(A*02:01, 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/A*0201 restricted epitope, VIYQYMDDL was mutated to cIYQYMDDL in the daughter D2 isolate.

References

Displaying record number 55284

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HXB2 Location	Vpr(59-67) DNA(5733..5759)	Vpr Epitope Map
Author Location	Vpr
Epitope	`AIIRILQQL`	Epitope Alignment
		Show epitope variants
Subtype	B
Species (MHC/HLA)	human(A*02:01)
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-A*0201 restricted epitope, AIIRILQQL, was mutated to AI(L)RILQQL in the daughter D2 isolate.

References

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

Displaying record number 55287

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HXB2 Location	gp160(34-55) gp120(34-55) DNA(6324..6389)	gp160 Epitope Map
Author Location	Env
Epitope	`LWVTVYYGVPVWKEATTTLFCA`	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 restricted epitope, LWVTVYYGVPVWKEATTTLFCA was mutated to wWVTVYYGVPVWKEATnTLFCA in the daughter D2 isolate.

References

Displaying record number 55294

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HXB2 Location	gp160(239-247) gp120(239-247) DNA(6939..6965)	gp160 Epitope Map
Author Location	Env
Epitope	`CTNVSTVQC`	Epitope Alignment
		Show epitope variants
Subtype	B
Species (MHC/HLA)	human(Cw8)
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-Cw8 restricted epitope, CTNVSTVQC was mutated to CqNVSTVQC in the daughter D2 isolate.

References

Displaying record number 55291

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HXB2 Location	gp160(583-592) gp41(72-81) DNA(7971..8000)	gp160 Epitope Map
Author Location	Env
Epitope	`VERYLKDQQL`	Epitope Alignment
		Show epitope variants
Subtype	B
Species (MHC/HLA)	human(B14)
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-B14 restricted epitope, VERYLKDQQL was mutated to VERYLrDQQL in the daughter D2 isolate.

References

Displaying record number 55292

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HXB2 Location	gp160(584-592) gp41(73-81) DNA(7974..8000)	gp160 Epitope Map
Author Location	Env
Epitope	`ERYLKDQQL`	Epitope Alignment
		Show epitope variants
Subtype	B
Species (MHC/HLA)	human(B*14:02, B14)
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-B14/B*1402 restricted epitope, ERYLKDQQL was mutated to ERYLrDQQL in the daughter D2 isolate.

References

Displaying record number 55295

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HXB2 Location	gp160(678-686) gp41(167-175) DNA(8256..8282)	gp160 Epitope Map
Author Location	Env
Epitope	`WLWYIKIFI`	Epitope Alignment
		Show epitope variants
Subtype	B
Species (MHC/HLA)	human(A*02:01)
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.
Epitope WLWYIKIFI was the only one mutated, to WLWYIrIFI in the mother M2 isolate. WLWYIKIFI was designated as being restricted to A2.1, a known alias for HLA-A*0201 which is expressed by daughter.

References

Displaying record number 55289

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HXB2 Location	gp160(814-822) gp41(303-311) DNA(8664..8690)	gp160 Epitope Map
Author Location	Env
Epitope	`LLNATAIAV`	Epitope Alignment
		Show epitope variants
Subtype	B
Species (MHC/HLA)	human(A*02:01, 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/A*0201 restricted epitope, LLNATAIAV was mutated to LLNAiAIAV in the daughter D2 isolate.

References

Displaying record number 55298

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HXB2 Location	Nef(9-23) DNA(8821..8865)	Nef Epitope Map
Author Location	Nef
Epitope	`SVVGWPTVRERMRRA`	Epitope Alignment
		Show epitope variants
Epitope Name	nef-5141
Subtype	B
Species (MHC/HLA)	human
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 Nef overlapping peptide, SVVGWPTVRERMRRA was mutated in the daughter D2 isolate to SiVGWPaVRdRMRRA.

References

Displaying record number 55299

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HXB2 Location	Nef(13-27) DNA(8833..8877)	Nef Epitope Map
Author Location	Nef
Epitope	`WPTVRERMRRAEPAA`	Epitope Alignment
		Show epitope variants
Epitope Name	nef-5142
Subtype	B
Species (MHC/HLA)	human
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 Nef overlapping peptide, WPTVRERMRRAEPAA was mutated in the daughter D2 isolate to WPaVRdRMRRAEPAA.

References

Displaying record number 55317

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HXB2 Location	Nef(69-83) DNA(9001..9045)	Nef Epitope Map
Author Location	Nef
Epitope	`PVRPQVPLRPMTYKA`	Epitope Alignment
		Show epitope variants
Epitope Name	nef-5156
Subtype	B
Species (MHC/HLA)	human
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 Nef overlapping peptide, PVRPQVPLRPMTYKA was mutated in the daughter D2 isolate to PVRPQVPLRPMTfKA.

References

Displaying record number 55316

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HXB2 Location	Nef(73-87) DNA(9013..9057)	Nef Epitope Map
Author Location	Nef
Epitope	`QVPLRPMTYKAAVDL`	Epitope Alignment
		Show epitope variants
Epitope Name	nef-5157
Subtype	B
Species (MHC/HLA)	human
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 Nef overlapping peptide, QVPLRPMTYKAAVDL was mutated in the daughter D2 isolate to QVPLRPMTfKAAVDL.

References

Displaying record number 55300

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HXB2 Location	Nef(77-91) DNA(9025..9069)	Nef Epitope Map
Author Location	Nef
Epitope	`RPMTYKAAVDLSHFL`	Epitope Alignment
		Show epitope variants
Epitope Name	nef-5158
Subtype	B
Species (MHC/HLA)	human
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 Nef overlapping peptide, RPMTYKAAVDLSHFL was mutated in the daughter D2 isolate to RPMTfKAAVDLSHFL.

References

Displaying record number 55303

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HXB2 Location	Nef(129-143) DNA(9181..9225)	Nef Epitope Map
Author Location	Nef
Epitope	`PGPGIRYPLTFGWCF`	Epitope Alignment
		Show epitope variants
Epitope Name	nef-5171
Subtype	B
Species (MHC/HLA)	human
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 Nef overlapping peptide, PGPGIRYPLTFGWCF was mutated in the daughter D2 isolate to PGPGtRfPLTFGWCF.