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Displaying record number 62168
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- This review of HIV-1 adaptation to HLA uses CTL escape as a means to track HIV-1 host cellular immune interactions. Escape falls into 3 categories (1) mutations that act upon processes upstream of epitope-HLA binding like antigen processing mutations (2) mutations that compromise epitope-HLA binding and (3) escapes that act downstream of epitope-HLA binding like those that reduce or abrogate recognition due to TCR-complexing mutations. The categories need not be mutually exclusive!
- An example of an antigen-processing escape mutation is the B*5703-restricted Gag A146P substitution, selected at the residue immediately upstream of Gag IW9, which prevents N-terminal aminopeptidase-mediated trimming of the epitope [Draenert et al. J. Exp. Med. 199:905-915 (2004)].
References
Carlson2015
Jonathan M. Carlson, Anh Q. Le, Aniqa Shahid, and Zabrina L. Brumme. HIV-1 Adaptation to HLA: A Window into Virus-Host Immune Interactions. Trends Microbiol., 23(4):212-224, Apr 2015. PubMed ID: 25613992.
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Displaying record number 62167
Download this epitope
record as JSON.
Notes
- This review of HIV-1 adaptation to HLA uses CTL escape as a means to track HIV-1 host cellular immune interactions. Escape falls into 3 categories (1) mutations that act upon processes upstream of epitope-HLA binding like antigen processing mutations (2) mutations that compromise epitope-HLA binding and (3) escapes that act downstream of epitope-HLA binding like those that reduce or abrogate recognition due to TCR-complexing mutations. The categories need not be mutually exclusive!
- 3/4ths of HLA-B*57-expressing HIV-1 subtype B-infected persons select the Gag T242N substitution in the Gag TW10 epitope, TSTLQEQIGW, within 3 months of infection. 50% of infected subjects subsequently select G248A at thereby confer- ring complete escape from B*57-restricted, TW10-specific CTL. [Leslie et al. Nat. Med 10:282-289 (2004); Brumme et al. JVI 82: 9216-9227 (2008)]
References
Carlson2015
Jonathan M. Carlson, Anh Q. Le, Aniqa Shahid, and Zabrina L. Brumme. HIV-1 Adaptation to HLA: A Window into Virus-Host Immune Interactions. Trends Microbiol., 23(4):212-224, Apr 2015. PubMed ID: 25613992.
Show all entries for this paper.
Displaying record number 62169
Download this epitope
record as JSON.
Notes
- This review of HIV-1 adaptation to HLA uses CTL escape as a means to track HIV-1 host cellular immune interactions. Escape falls into 3 categories (1) mutations that act upon processes upstream of epitope-HLA binding like antigen processing mutations (2) mutations that compromise epitope-HLA binding and (3) escapes that act downstream of epitope-HLA binding like those that reduce or abrogate recognition due to TCR-complexing mutations. The categories need not be mutually exclusive!
- Of all the HLA-associated polymorphisms that occur within or near optimally described CTL epitopes, roughly 20% occur at anchor positions, a frequency that is approximately twofold higher than expected by chance and they are estimated to confer an average 10-fold reduction in predicted epitope–HLA binding affinity. An example is the B*27-restricted Gag R264K mutation, selected at position two of the B*27-restricted Gag KK10, KRWIILGLNK epitope, which abrogates epitope–HLA binding [Goulder et al. Nat. Med. 3:212-217 (1997)].
- ‘TCR escape mutations’ typically occur at central epitope positions. For example, the B*27-associated Gag L268M substitution of Gag KK10, retains B*27-binding ability but abrogates epitope recognition by many B*27-restricted TCR clonotypes in the repertoire.
References
Carlson2015
Jonathan M. Carlson, Anh Q. Le, Aniqa Shahid, and Zabrina L. Brumme. HIV-1 Adaptation to HLA: A Window into Virus-Host Immune Interactions. Trends Microbiol., 23(4):212-224, Apr 2015. PubMed ID: 25613992.
Show all entries for this paper.
Displaying record number 62170
Download this epitope
record as JSON.
Notes
- This review of HIV-1 adaptation to HLA uses CTL escape as a means to track HIV-1 host cellular immune interactions. Escape falls into 3 categories (1) mutations that act upon processes upstream of epitope-HLA binding like antigen processing mutations (2) mutations that compromise epitope-HLA binding and (3) escapes that act downstream of epitope-HLA binding like those that reduce or abrogate recognition due to TCR-complexing mutations. The categories need not be mutually exclusive!
- The frequency of an HLA allele in a given population largely determines the prevalence of its associated escape mutation(s) in circulation. The B*51- associated I135X mutation in HIV-1 RT at the C terminus of TI8, TAFTIPSI, in In Japan, however, where the combined prevalence of B*51 – and the related allele B*52 – exceeds 40%, the population consensus at RT codon 135 is not I as in other parts of the world, but rather 135T, the B*51/ B*52-associated escape form. [Yagita et al. JVI 87:2253-2263 (2013)].
References
Carlson2015
Jonathan M. Carlson, Anh Q. Le, Aniqa Shahid, and Zabrina L. Brumme. HIV-1 Adaptation to HLA: A Window into Virus-Host Immune Interactions. Trends Microbiol., 23(4):212-224, Apr 2015. PubMed ID: 25613992.
Show all entries for this paper.
