Human immunodeficiency virus type 1 (
HIV-1)-specific
cytotoxic T lymphocytes (CTLs)
play a critical
role in the control of
HIV-1 infection and replication.
HIV-1 evades CTL mediated
pressure through viral escape
mutations within targeted CTLs
epitopes or flanking regions, but this process is usually associated with a viral fitness
cost. The mutated
epitopes may weaken the level of the original CTL responses, however, the
immune system holds potential to mount denovo responses towards those newly emerged
epitopes. This article briefly summarizes recent
research progress regarding the competition between
HIV-1's escape
mutations and host CTL responses.