Mechanisms of HIV-1 escape from immune responses and antiretroviral drugs

Abstract

Despite the fact that HIV-1 induces vigorous antiviral immune responses, viral replication is never completely controlled in infected individuals. Recent studies have provided insight into the mechanisms by which focused immune pressure directed at particular B or T cell epitopes leads to the rapid appearance of escape mutations. Even if anti-HIV-1 immune responses could be enhanced to the point where they inhibit viral replication to the same extent as certain combinations of antiretroviral drugs, eradication would be unlikely because of the persistence of the virus in an extremely stable latent reservoir in resting memory CD4(+) T cells.