Simian virus 40 large-T bypasses the translational block imposed by the phosphorylation of elF-2α

Sathyamangalam Swaminathan, Prithi Rajan, Olga Savinova, Rosemary Jagus, Bayar Thimmapaya*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

17 Scopus citations

Abstract

One of the cellular defense mechanisms against virus infection is mediated by activating the interferon-induced, double-stranded-RNA-activated protein kinase, PKR. Upon activation, PKR phosphorylates and thereby inactivates the protein synthesis initiation factor, elF-2, leading to cessation of protein synthesis. Viruses have evolved diverse strategies to counteract this cellular antiviral response. A majority of these strategies target PKR to prevent its activation. Recently, we showed that simian virus40 (SV40) large-T antigen reverses PKR-mediated translational inhibition at a step downstream of PKR activation (Rajan et al., J. Virol. 69, 785-795, 1995). In this paper, we present evidence showing that SV40 can restore efficient translation in cells despite the elevated levels of phosphorylated elF-2α resulting from PKR activation. Thus, SV40 large-T-mediated translational rescue occurs at a step downstream of elF-2α phosphorylation.

Original languageEnglish (US)
Pages (from-to)321-323
Number of pages3
JournalVirology
Volume219
Issue number1
DOIs
StatePublished - May 1 1996

Funding

This work was supported by NIH Grants AI18029 and 20156 (B.T.) and NSF MCB 9317264 (R.J.). We thank Dr. Lynn O’Brien from the laboratory of the late Dr. Henshaw for providing monoclonal antibody to eIF-2α.

ASJC Scopus subject areas

  • Virology

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