IFITM proteins inhibit HIV-1 protein synthesis.

Autor: Lee WJ; Blizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, E1 2AT, United Kingdom., Fu RM; Division of Infection and Pathway Medicine, School of Biomedical Sciences, University of Edinburgh, Edinburgh, EH16 4SB, United Kingdom., Liang C; McGill University AIDS Centre, Lady Davis Institute, Montreal, Quebec, H3T 1E2, Canada., Sloan RD; Blizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, E1 2AT, United Kingdom. richard.sloan@ed.ac.uk.; Division of Infection and Pathway Medicine, School of Biomedical Sciences, University of Edinburgh, Edinburgh, EH16 4SB, United Kingdom. richard.sloan@ed.ac.uk.; ZJU-UoE Institute, Zhejiang University, Haining, Zhejiang, 314400, P.R. China. richard.sloan@ed.ac.uk.
Jazyk: angličtina
Zdroj: Scientific reports [Sci Rep] 2018 Sep 28; Vol. 8 (1), pp. 14551. Date of Electronic Publication: 2018 Sep 28.
DOI: 10.1038/s41598-018-32785-5
Abstrakt: Interferon induced transmembrane proteins (IFITMs) inhibit the cellular entry of a broad range of viruses, but it has been suspected that for HIV-1 IFITMs may also inhibit a post-integration replicative step. We show that IFITM expression reduces HIV-1 viral protein synthesis by preferentially excluding viral mRNA transcripts from translation and thereby restricts viral production. Codon-optimization of proviral DNA rescues viral translation, implying that IFITM-mediated restriction requires recognition of viral RNA elements. In addition, we find that expression of the viral accessory protein Nef can help overcome the IFITM-mediated inhibition of virus production. Our studies identify a novel role for IFITMs in inhibiting HIV replication at the level of translation, but show that the effects can be overcome by the lentiviral protein Nef.
Databáze: MEDLINE
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