Abstract：
:In mammals, one of the most pronounced consequences of viral infection is the induction of type I interferons, cytokines with potent antiviral activity. Schlafen (Slfn) genes are a subset of interferon-stimulated early response genes (ISGs) that are also induced directly by pathogens via the interferon regulatory factor 3 (IRF3) pathway. However, many ISGs are of unknown or incompletely understood function. Here we show that human SLFN11 potently and specifically abrogates the production of retroviruses such as human immunodeficiency virus 1 (HIV-1). Our study revealed that SLFN11 has no effect on the early steps of the retroviral infection cycle, including reverse transcription, integration and transcription. Rather, SLFN11 acts at the late stage of virus production by selectively inhibiting the expression of viral proteins in a codon-usage-dependent manner. We further find that SLFN11 binds transfer RNA, and counteracts changes in the tRNA pool elicited by the presence of HIV. Our studies identified a novel antiviral mechanism within the innate immune response, in which SLFN11 selectively inhibits viral protein synthesis in HIV-infected cells by means of codon-bias discrimination.
journal_name
Naturejournal_title
Natureauthors
Li M,Kao E,Gao X,Sandig H,Limmer K,Pavon-Eternod M,Jones TE,Landry S,Pan T,Weitzman MD,David Mdoi
10.1038/nature11433subject
Has Abstractpub_date
2012-11-01 00:00:00pages
125-8issue
7422eissn
0028-0836issn
1476-4687pii
nature11433journal_volume
491pub_type
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