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Rev regulates translation of human immunodeficiency virus type 1 RNAs

¹ Department of Medicine, Addenbrooke's Hospital, Cambridge CB2 2QQ, UK
² Department of Biological Sciences, University of Warwick, Warwick CV4 7AL, UK
³ Christian Doppler Laboratory for Gene Therapeutic Vectors, Research Institute of Virology and Biomedicine, University for Veterinary Sciences, Vienna, Austria

Correspondence
Andrew M. L. Lever
amll1{at}mole.bio.cam.ac.uk

Full-length human immunodeficiency virus type 1 (HIV-1) RNA acts as both mRNA, encoding Gag and Gag–Pol polyproteins, and genomic RNA. Translation of this RNA must be tightly controlled to allow sufficient protein synthesis prior to a switch to particle production. The viral protein Rev stimulates nuclear export of unspliced HIV-1 RNAs containing the Rev response element, but may also stimulate translation of these RNAs. We previously identified an additional Rev binding site in the 5' untranslated region of the HIV-1 RNA. We show that Rev inhibits translation non-specifically at high concentrations and stimulates translation of HIV-1 RNAs at intermediate concentrations in vitro. Stimulation is dependent on the presence of the Rev binding site within the 5' untranslated region and not on the Rev response element. In COS-1 cells, translation from an HIV-1 reporter is specifically increased by coexpression of Rev.

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