Author: ["A J Leslie","K J Pfafferott","P Chetty","R Draenert","M M Addo","M Feeney","Y Tang","E C Holmes","T Allen","J G Prado","M Altfeld","C Brander","C Dixon","D Ramduth","P Jeena","S A Thomas","A St John","T A Roach","B Kupfer","G Luzzi","A Edwards","G Taylor","H Lyall","G Tudor-Williams","V Novelli","J Martinez-Picado","P Kiepiela","B D Walker","P J R Goulder"]
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Abstract
Within-patient HIV evolution reflects the strong selection pressure driving viral escape from cytotoxic T-lymphocyte (CTL) recognition. Whether this intrapatient accumulation of escape mutations translates into HIV evolution at the population level has not been evaluated. We studied over 300 patients drawn from the B- and C-clade epidemics, focusing on human leukocyte antigen (HLA) alleles HLA-B57 and HLA-B5801, which are associated with long-term HIV control and are therefore likely to exert strong selection pressure on the virus. The CTL response dominating acute infection in HLA-B57/5801-positive subjects drove positive selection of an escape mutation that reverted to wild-type after transmission to HLA-B57/5801-negative individuals. A second escape mutation within the epitope, by contrast, was maintained after transmission. These data show that the process of accumulation of escape mutations within HIV is not inevitable. Complex epitope- and residue-specific selection forces, including CTL-mediated positive selection pressure and virus-mediated purifying selection, operate in tandem to shape HIV evolution at the population level.Cite this article
Leslie, A., Pfafferott, K., Chetty, P. et al. HIV evolution: CTL escape mutation and reversion after transmission. Nat Med 10, 282–289 (2004). https://doi.org/10.1038/nm992 