Search CTL/CD8+ T-Cell Epitope Database

Found 23 matching records:

Displaying record number 57290

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HXB2 Location	Gag(20-28) p17(20-28) DNA(847..873)	Gag Epitope Map
Author Location
Epitope	`RLRPGGKKK`	Epitope Alignment
Epitope Name	RK9
Subtype	B
Species (MHC/HLA)	human(A*03)
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.
Non-B57-epitope RK9-p17, RLRPGGKKK restricted by A*03, was recognized by an infant with maternally-inherited B57.

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 57280

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HXB2 Location	Gag(77-85) p17(77-85) DNA(1018..1044)	Gag Epitope Map
Author Location
Epitope	`SLYNTVATL`	Epitope Alignment
Epitope Name	SL9
Subtype	B
Species (MHC/HLA)	human(A*02)
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.
Non-B57-epitope SL9-Gag, SLYNTVATL restricted by A*02, was recognized by one paternally inherited B57-positive infant.

References

Displaying record number 57285

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HXB2 Location	Gag(127-135) p17(127)-p24(3) DNA(1168..1194)	Gag Epitope Map
Author Location
Epitope	`QVSQNYPIV`	Epitope Alignment
Epitope Name	QV9
Subtype	B
Species (MHC/HLA)	human(A*68)
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.
Non-B57-epitope QV9-p17-p24, QVSQNYPIV restricted by A*68, was recognized by an infant with maternally-inherited B57.

References

Displaying record number 57245

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HXB2 Location	Gag(147-155) p24(15-23) DNA(1228..1254)	Gag Epitope Map
Author Location	p24
Epitope	`ISPRTLNAW`	Epitope Alignment
Epitope Name	ISW9
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 ISW9, ISPRTLNAW, gained a previously described mutation I147L, lSPRTLNAW as well as a flanking processing mutation A146P, p|lSPRTLNAW. Other variants seen were p|ltPRTLNAW, t|mSPRTLNAW and s|mSPRTLNAW. 2 of 4 infants with paternally inherited B57 and 1 of 4 with maternally inherited B57 recognized this epitope.

References

Displaying record number 57247

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HXB2 Location	Gag(162-172) p24(30-40) DNA(1273..1305)	Gag Epitope Map
Author Location	p24
Epitope	`KAFSPEVIPMF`	Epitope Alignment
Epitope Name	KF11
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 KF11, KAFSPEVIPMF, rarely escapes in Clade B and no stable mutation was seen in these subject pairs. The A163G mutation, KgFSPEVIPMF, likely affects viral fitness. Other variants seen were KsFSPEVIPMF, KnFSPEVIPMF, KgFnPEVIPMF and KqFSPEVIPMF. 3 of 4 infants with paternally inherited B57 and 2 of 4 with maternally inherited B57 recognized this epitope.

References

Displaying record number 57281

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HXB2 Location	Gag(180-188) p24(48-56) DNA(1327..1353)	Gag Epitope Map
Author Location
Epitope	`TPQDLNTML`	Epitope Alignment
Epitope Name	TL9
Subtype	B
Species (MHC/HLA)	human(B*42)
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.
Non-B57-epitope TL9-Gag, TPQDLNTML restricted by B*42, was recognized by an infant with one paternally inherited B57.

References

Displaying record number 57283

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HXB2 Location	Gag(180-188) p24(48-56) DNA(1327..1353)	Gag Epitope Map
Author Location
Epitope	`TPQDLNTML`	Epitope Alignment
Epitope Name	TL9
Subtype	B
Species (MHC/HLA)	human(C*08)
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.
Non-B57-epitope TL9-Gag, TPQDLNTML restricted by Cw*08, was recognized by an infant with maternally-inherited B57.

References

Displaying record number 57244

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HXB2 Location	Gag(240-249) p24(108-117) DNA(1507..1536)	Gag Epitope Map
Author Location	p24
Epitope	`TSTLQEQIGW`	Epitope Alignment
Epitope Name	TW10
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.
In this epitope, TSTLQEQIGW, the transmitted T242N mutation, TSnLQEQIGW persisted in all HLA-B*57 positive infants with B57-negative or -positive mothers. In Infant2, a B57-positive infant with B57-negative mother, mutations at H219Q and M228I emerged to offset fitness cost of the T242N escape.
1 of 5 B57-negative infants with B-57 positive mothers did not have a reversion at T242N, though this mutation was transmitted and reverted in all other infants of this group. In this Infant7 compensatory capsid stabilization mutations had emerged, viz. H219Q and M228I, as well as changes at I223, G248 and N252 which correlated with a relative infectivty better than that of the wild type virus. Infant13 viral sequence with only I223V displayed a much lower replication capacity in assays.
Other mutations at this epitope were TSTLQEQIaW, TSnLQEQIaW, TSnLQEQItW, TSTLQEQItW and TSnLQEQvaW.
B57-positive Infant4 inherited T242N compensatory mutations from his B57-negative mother, but T242N was lacking in the mother, so not transmitted. By 2 years of age Infant4 had a predominance of T242N, but high VL suggesting that the protective effect of HLA-B57 is contingent on infecting viral sequence. Also, populations high in B57 may lose their protection by transmission of viruses containing compensatory mutations.

References

Displaying record number 57286

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HXB2 Location	Gag(305-313) p24(173-181) DNA(1702..1728)	Gag Epitope Map
Author Location
Epitope	`RAEQASQEV`	Epitope Alignment
Epitope Name	RV9
Subtype	B
Species (MHC/HLA)	human(C*08)
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.
Non-B57-epitope RV9-p24, RAEQASQEV restricted by Cw*08, was recognized by an infant with maternally-inherited B57.

References

Displaying record number 57246

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HXB2 Location	Gag(308-316) p24(176-184) DNA(1711..1737)	Gag Epitope Map
Author Location	p24
Epitope	`QASQEVKNW`	Epitope Alignment
Epitope Name	QW9
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.
No stable mutations were seen within epitope QW9, QASQEVKNW though common variants were transmitted vertically. Other variants seen were QAtQEVKNW, QASQdVKNW and QASQEVKgW. 2 of 4 infants with paternally inherited B57 and 1 of 4 with maternally inherited B57 recognized this epitope.

References

Displaying record number 57289

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HXB2 Location	Gag(433-442) p2p7p1p6(70-79) DNA(2086..2115)	Gag Epitope Map
Author Location
Epitope	`FLGKIWPSHK`	Epitope Alignment
Epitope Name	FK10
Subtype	B
Species (MHC/HLA)	human(A*02)
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.
Non-B57-epitope FK10-p2p7p1p6, FLGKIWPSHK restricted by A*02, was recognized by an infant with maternally-inherited B57.

References

Displaying record number 57288

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HXB2 Location	Pol(464-472) RT(309-317) DNA(3474..3500)	Pol Epitope Map
Author Location
Epitope	`ILKEPVHGV`	Epitope Alignment
Epitope Name	IV9
Subtype	B
Species (MHC/HLA)	human(A*02)
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.
Non-B57-epitope IV9-RT, ILKEPVHGV restricted by A*02, was recognized by an infant with maternally-inherited B57.

References

Displaying record number 57278

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HXB2 Location	Pol(530-538) RT(375-383) DNA(3672..3698)	Pol Epitope Map
Author Location	RT
Epitope	`IATESIVIW`	Epitope Alignment
Epitope Name	IAW9
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 IAW9-RT, IATESIVIW, was recognized by 3 of 4 infants with paternally- and 1 of 4 maternally-inherited B57.

References

Displaying record number 57277

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HXB2 Location	Pol(562-571) RT(407-416) DNA(3768..3797)	Pol Epitope Map
Author Location	RT
Epitope	`QATWIPEWEF`	Epitope Alignment
Epitope Name	QF10
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 QF10-RT, QATWIPEWEF, was recognized by 2 of 4 infants with paternally inherited B57.

References

Displaying record number 57292

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HXB2 Location	Vif(17-26) DNA(5089..5118)	Vif Epitope Map
Author Location
Epitope	`RIRTWKSLVK`	Epitope Alignment
Epitope Name	RK10
Subtype	B
Species (MHC/HLA)	human(A*03)
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.
Non-B57-epitope RK10-Vif, RIRTWKSLVK restricted by A*03, was recognized by an infant with maternally-inherited B57.

References

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

Displaying record number 57284

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HXB2 Location	Tat(39-49) DNA(5945..5977)	Tat Epitope Map
Author Location
Epitope	`ITKGLGISYGR`	Epitope Alignment
Epitope Name	IR11
Subtype	B
Species (MHC/HLA)	human(A*68)
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.
Non-B57-epitope IR11-Tat, ITKGLGISYGR restricted by A*68, was recognized by an infant with maternally-inherited B57.

References

Displaying record number 57293

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HXB2 Location	gp160(770-780) gp41(259-269) DNA(8532..8564)	gp160 Epitope Map
Author Location
Epitope	`RLRDLLLIVTR`	Epitope Alignment
Epitope Name	RR11
Subtype	B
Species (MHC/HLA)	human(A*03)
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.
Non-B57-epitope RR11-gp160, RLRDLLLIVTR restricted by A*03, was recognized by an infant with maternally-inherited B57.

References

Displaying record number 57291

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HXB2 Location	Nef(73-82) DNA(9013..9042)	Nef Epitope Map
Author Location
Epitope	`QVPLRPMTYK`	Epitope Alignment
Epitope Name	QK10
Subtype	B
Species (MHC/HLA)	human(A*03)
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.
Non-B57-epitope QK10-Nef, QVPLRPMTYK restricted by A*03, was recognized by an infant with maternally-inherited B57.

References

Displaying record number 57251

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HXB2 Location	Nef(82-90) DNA(9040..9066)	Nef Epitope Map
Author Location	Nef
Epitope	`KAAVDLSHF`	Epitope Alignment
Epitope Name	KAF9
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 KAF9-Nef, KAAVDLSHF, though outside of Gag did develop a mutation in two subjects. No B57-positive infants recognized this epitope.

References

Displaying record number 57287

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HXB2 Location	Nef(105-115) DNA(9109..9141)	Nef Epitope Map
Author Location
Epitope	`RRQDILDLWVY`	Epitope Alignment
Epitope Name	RY11
Subtype	B
Species (MHC/HLA)	human(C*07)
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.
Non-B57-epitope RY11-Nef, RRQDILDLWVY restricted by Cw*07, was recognized by an infant with maternally-inherited B57.

References

Displaying record number 57253

Download this epitope record as JSON.

HXB2 Location	Nef(116-124) DNA(9142..9168)	Nef Epitope Map
Author Location	Nef
Epitope	`HTQGYFPDW`	Epitope Alignment
Epitope Name	HW9
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 HW9-Nef, HTQGYFPDW, though outside of Gag did develop a mutation in two subjects. 1 of 4 infants with paternally inherited B57 recognized this epitope.

References

Displaying record number 57276

Download this epitope record as JSON.

HXB2 Location	Nef(120-127) DNA(9154..9177)	Nef Epitope Map
Author Location	Nef
Epitope	`YFPDWQNY`	Epitope Alignment
Epitope Name	YY8
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 YY8-Nef, YFPDWQNY, was recognized by 1 of 4 infants with maternally inherited B57.