HIV evolution: CTL escape mutation and reversion after transmission

AJ Leslie, KJ Pfafferott, P Chetty, R Draenert… - Nature medicine, 2004 - nature.com
AJ Leslie, KJ Pfafferott, P Chetty, R Draenert, MM Addo, M Feeney, Y Tang, EC Holmes
Nature medicine, 2004nature.com
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 …
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.
nature.com