Cellular mRNA translation is blocked at both initiation and elongation after infection by influenza virus or adenovirus Journal Article


Authors: Katze, M. G.; DeCorato, D.; Krug, R. M.
Article Title: Cellular mRNA translation is blocked at both initiation and elongation after infection by influenza virus or adenovirus
Abstract: During influenza virus infection, protein synthesis is maintained at high levels and a dramatic switch from cellular to viral protein synthesis occurs despite the presence of high levels of functional cellular mRNAs in the cytoplasm of infected cells (M.G. Katze and R.M. Krug, Mol. Cell. Biol. 4:2198-2206, 1984). To determine the step at which the block in cellular mRNA translation occurs, we compared the polysome association of several representative cellular mRNAs (actin, glyceraldehyde-3-phosphate dehydrogenase, and pHe7 mRNAs) in infected and uninfected HeLa cells. We showed that most of these cellular mRNAs remained polysome associated after influenza viral infection, indicating that the elongation of the proteins encoded by these cellular mRNAs was severely inhibited. Because the polysomes containing these cellular mRNAs did not increase in size but either remained the same size or decreased in size, the initiation step in cellular protein synthesis must also have been defective. Several control experiments established that the cellular mRNAs sedimenting in the polysome region of sucrose gradients were in fact associated with polyribosomes. Most definitively, puromycin treatment of infected cells caused the dissociation of polysomes and the release of cellular, as well as viral, mRNAs from the polysomes, indicating that the cellular mRNAs were associated with polysomes that were capable of forming at least a single peptide bond. A similar analysis was performed with HeLa cells infected by adenovirus, which also dramatically shuts down cellular protein synthesis. Again, it was found that most of the cellular mRNAs, which were translatable in reticulocyte extracts, remained associated with polysomes and that there was a combined initiation-elongation block to cellular protein synthesis. In cells infected by both adenovirus and influenza virus, influenza viral mRNAs were on larger polysomes than were several late adenoviral mRNAs with comparably sized coding regions. In addition, after influenza virus superinfection of cells infected by the adenovirus mutant dl331, a situation in which there is a limiation in the amount of functional initiation factor eIF-2 (M.G. Katze, B.M. Detjen, B. Safer, and R.M. Krug, Mol. Cell. Biol. 6:1741-1750, 1986), influenzae viral mRNAs, but not late adenoviral mRNAs, were on polysomes. These results indicate that influenza viral mRNAs are better initiators of translation than are late adenoviral mRNAs.
Keywords: human cell; heredity; in vitro study; cell culture; messenger rna; rna translation; virus infection; radioisotope; influenza virus; human; priority journal; human adenovirus
Journal Title: Journal of Virology
Volume: 60
Issue: 3
ISSN: 0022-538X
Publisher: American Society for Microbiology  
Date Published: 1986-12-01
Start Page: 1027
End Page: 1039
Language: English
DOI: 10.1128/jvi.60.3.1027-1039.1986
PUBMED: 3023655
PROVIDER: scopus
PMCID: PMC253342
DOI/URL:
Notes: Article -- Export Date: 18 August 2021 -- Source: Scopus
Altmetric
Citation Impact
BMJ Impact Analytics
MSK Authors
  1. Robert M. Krug
    18 Krug