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Background The ability of HIV-1 to rapidly accumulate mutations provides the virus with an effective means of escaping CD8+ cytotoxic T lymphocyte (CTL) responses. Here we describe how subtle alterations in CTL epitopes expressed by naturally occurring HIV-1 variants can result in an incomplete escape from pre-existing CTL recognition to create a pro-inflammatory environment, providing the virus with a selective advantage.

HIV-1 selectively exploits cross-reactive CTL “help” to promote dysfunctional programming of pro-inflammatory dendritic cells