A mechanism for the control of protein synthesis by adenovirus VA RNAI

Robert P. O'Malley, Thomas M. Mariano, John Siekierka, Michael B. Mathews

Research output: Contribution to journalArticlepeer-review

200 Scopus citations


In the absence of VA RNAI, protein synthesis in adenovirus-infected HeLa cells fails because of defective initiation. Earlier work showed that the defect results from phosphorylation of the initiation factor elF-2 on its α subunit. We have identified the protein kinase responsible as the dsRNA-activated inhibitor of protein synthesis (DAI). DAI is present in uninfected HeLa cells at a basal level and in a largely inactive state. It is activated in cells infected with the adenovirus mutant Ad5 dl331, which produces no VA RNAI, but not in cells infected with wild-type virus. Activation occurs during the late phase of infection with the mutant virus, and the activator appears to be dsRNA produced by symmetrical transcription of the viral genome. VA RNAI antagonizes the activation of DAI by dsRNA, but it cannot inhibit the activity of DAI once activated. We propose a mechanism for VA RNAI action based on its partially double-stranded nature.

Original languageEnglish
Pages (from-to)391-400
Number of pages10
Issue number3
StatePublished - 14 Feb 1986


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