Activation-induced cytidine deaminase (AID), a member of the APOBEC family that induces antibody diversification, has been shown to inhibit the replication of hepatitis B virus, Kaposi's sarcoma-associated herpesvirus, and retro-transposons. However, whether AID can inhibit human immunodeficiency virus 1 (HIV-1) replication remains unclear. Here, we report that AID impairs the synthesis of HIV-1 components by interacting with the complex of Tat. This interaction recruits the RNA exosome to degrade the nascent HIV-1 transcript. AID also targets the HIV-1-integrated genome via the Tat-P-TEFb-TAR complex. Thus, we propose a novel function for AID as an adaptor protein that represses viral transcription. Our findings provide insights into developing anti-HIV therapeutics and understanding how host cells restrict integrated virus replication.
Keywords: AICDA; HIV-1; RNA exosome.
© 2017 Federation of European Biochemical Societies.