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Updated: Aug 17, 2026

A Restriction Enzyme Based Cloning Method to Assess the In vitro Replication Capacity of HIV-1 Subtype C Gag-MJ4 Chimeric Viruses
Published on: August 31, 2014
A therapy-related point mutation changes the HLA restriction of an HIV-1 Pol epitope from A2 to B57 and enhances its
Rosemarie D Mason1, Michael D Grant
1Immunology Program, Division of Basic Medical Sciences, Faculty of Medicine, Memorial University of Newfoundland, St John's, NL, Canada A1B 3V6.
In this study, we investigated CD8 T-cell recognition of wild-type HIV-1 Pol (RT 210-220) peptide LRWGFTTPDKK and of several variants incorporating common antiretroviral therapy-associated mutations (L210W, T215Y, Y215C). LRWGFTTPDKK was weakly and infrequently recognized in the context of HLA-A2. However, the 215C mutation created a strong, commonly recognized HLA-B57-restricted epitope. An antiretroviral therapy-associated mutation thus alters the HLA restriction of a weak Pol epitope, potentially enhancing CD8 T-cell recognition of HIV.
In this study, we investigated CD8 T-cell recognition of wild-type HIV-1 Pol (RT 210-220) peptide LRWGFTTPDKK and of several variants incorporating common antiretroviral therapy-associated mutations (L210W, T215Y, Y215C). LRWGFTTPDKK was weakly and infrequently recognized in the context of HLA-A2. However, the 215C mutation created a strong, commonly recognized HLA-B57-restricted epitope. An antiretroviral therapy-associated mutation thus alters the HLA restriction of a weak Pol epitope, potentially enhancing CD8 T-cell recognition of HIV.
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