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Background Post-integration latency is a critical barrier to achieving a complete cure for HIV. Epigenetic micro-environment alterations at the integrated HIV-1 LTR, coupled with modulations of the HIV-1 Tat feedback circuit, influence the onset and maintenance of latency. In this context, we have previously identified the epigenetic core pressor SIN3/HDAC complex as part of the in-vitro HIV-1 Tat nuclear interactome. Here we delineate the dynamics of their antagonistic functional relationship in the control of HIV-1 latency.

retrovirology

The reciprocal antagonistic interplay between HIV-1 Tat and SIN3A specifies the epigenetic switch between de-repression versus maintenance of HIV-1 gene silencing