Abstract:
: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.
journal_name
FEBS Lettjournal_title
FEBS lettersauthors
Wang R,Zhang X,Ding H,Qiao Y,Han X,Geng W,Guan G,Cui H,Zhao B,Wu Y,Liang G,Shang Hdoi
10.1002/1873-3468.12954subject
Has Abstractpub_date
2018-01-01 00:00:00pages
284-294issue
2eissn
0014-5793issn
1873-3468journal_volume
592pub_type
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