Abstract
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.
Highlights
The ability of HIV-1 to rapidly accumulate mutations provides the virus with an effective means of escaping CD8+ cytotoxic T lymphocyte (CTL) responses
We developed a dendritic cell (DC)-based in vitro model to induce primary CTLs specific against naturally occuring HIV-1 Gag epitope variants identified through sequencing of virus obtained in a longitudunal study from a subject with chronic HIV-1 infection
Instead of eliminating variant antigen-expressing immature DC as a negative immune feedback mechanism, the cross-reactive CTLs promoted the differentiation of DC into highly reactive mature DC capable of producing enhanced levels of IL-12 and IL-6, as well as the T cell chemoattractants CXCL10 and CCL5
Summary
The ability of HIV-1 to rapidly accumulate mutations provides the virus with an effective means of escaping CD8+ cytotoxic T lymphocyte (CTL) responses. 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
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