Inhibition of 40S--Met--tRNAfMet ribosomal initiation complex formation by vaccinia virus.
Infection with vaccinia virus (a poxvirus) quickly and efficiently shuts off host protein synthesis in the presence of actinomycin D (refs 3--5) or cycloheximide. The cellular messenger RNA apparently remains stable in the infected cells exposed to inhibitors of viral gene transcription. In some cases vaccinia viral RNA or poly(A) synthesis have been implicated in the establishment of this effect. However, in the presence of cordycepin (3-deoxyadenosine) which blocks viral gene transcription and cytoplasmic poly(A) synthesis, cellular protein synthesis is still efficiently inhibited in vaccinia virus-infected cells. This shutoff is also observed in vitro, in the corresponding cell-free extracts, and in a reticulocyte lysate. Therefore the shutoff of host protein synthesis is probably mediated by a factor associated with vaccinia virions. We now report that the formation of the 40S--Met-tRNAfMet initiation complex is inhibited in cytoplasmic extracts derived from vaccinia virus-infected cells exposed to cordycepin to block viral gene expression. A similar inhibition is found in reticulocyte lysates incubated with purified vaccinia cores, confirming the hypothesis that the factor associated with the viral cores is responsible for the inhibition observed in vaccinia virus-infected cells exposed to inhibitors of transcription.[1]References
- Inhibition of 40S--Met--tRNAfMet ribosomal initiation complex formation by vaccinia virus. Person, A., Ben-Hamida, F., Beaud, G. Nature (1980) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg
