Abstract
A major aim in the study of immune responses to AIDS-associated retroviruses is to define how viral replication is controlled during the long course of infection. In early studies of HIV immunity, virus-specific CD8+ cytotoxic T lymphocyte (CTL) responses were readily detected1,2. Over the past decade, increasing evidence has been generated to suggest that these lymphocytes play a crucial role in containing HIV replication. Activated HIV-specific CTLs emerge early in infection, coincident with a decline in the initial viraemia, and remain abundant throughout chronic infection until the rapid rise in viral load at the onset of AIDS (Ref. 3). The central role of CTLs in virus control is illustrated by the simian model of AIDS, in which total CD8+-T-cell depletion results in a clear rise in viraemia, whereas the return of antigen-specific CTLs is closely followed by suppression of viraemia4,5. Furthermore, in cross-sectional human studies, levels of HIV-specific CTLs are negatively correlated with viraemia6. These studies imply that viruses that persist in the presence of ongoing CTL activity must have immune evasion properties.
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