Apobec3A maintains HIV-1 latency through recruitment of epigenetic silencing machinery to the long terminal repeat

Significance Human immunodeficiency virus 1 (HIV-1) infection causes a life-long disease, due to the ability of the virus to integrate into the host genome and establish latent infection. While research has revealed a number of host restriction factors that block primary infection, much less is understood with regard to the host factors that promote or block reactivation of the integrated proviral HIV-1. In this study, we show that a member of the Apobec3A (apolipoprotein B MRNA editing enzyme catalytic subunit 3A) family, A3A, suppresses HIV-1 reactivation by recruiting chromatin-modifying enzymes to impose repressive marks around the long terminal repeat promoter region. Identification of host factors that control HIV-1 latency may provide clues for therapeutic interventions needed to remove the viral reservoir from the infected individual.