Nuclear-cytoplasmic transport and VAI RNA-independent translation of influenza viral messenger RNAs in late adenovirus-infected cells. Academic Article uri icon

Overview

abstract

  • Influenza virus-specific proteins are synthesized at essentially the same levels in late adenovirus-infected HeLa cells as in cells not infected with adenovirus, indicating that influenza viral mRNA escapes the blocks exerted by adenovirus against host-cell mRNA expression-transport from the nucleus and translation. A significant proportion of the influenza viral mRNAs synthesized in these cells possesses the 5' ends of the major late adenovirus transcripts, resulting from capped RNA-primed initiation of influenza viral mRNA synthesis. We determined whether the ability of influenza viral mRNA to escape from the adenovirus-imposed blocks is due to utilization of the adenovirus-specific transport and translational systems because of the adenovirus 5' ends on the influenza viral mRNAs, or to establishment of influenza virus-specific transport and translational systems. Our results indicate that the second mechanism is operating, as the transport of influenza viral mRNAs from the nucleus and their translation is independent of the presence of adenovirus 5' ends. Furthermore, efficient translation of influenza viral mRNAs, but not of either adenovirus or host mRNAs, occurs in cells infected by the adenovirus deletion mutant dl331 , which does not synthesize VAI RNA ( Thimmappaya et al., 1982). Consequently, utilizing the translational machinery that had been inactivated by adenovirus, influenza virus establishes a system that selectively translates influenza viral mRNAs.

publication date

  • June 1, 1984

Research

keywords

  • Adenoviruses, Human
  • Cell Nucleus
  • Cell Transformation, Viral
  • Influenza A virus
  • Polyribosomes
  • Protein Biosynthesis
  • RNA, Messenger
  • Viral Proteins

Identity

Scopus Document Identifier

  • 0021173699

Digital Object Identifier (DOI)

  • 10.1016/0092-8674(84)90378-7

PubMed ID

  • 6327069

Additional Document Info

volume

  • 37

issue

  • 2