Viral and Cellular mRNA Translation in Coronavirus-Infected Cells

K. Nakagawa, K. G. Lokugamage, S. Makino

Research output: Chapter in Book/Report/Conference proceedingChapter

25 Scopus citations

Abstract

Coronaviruses have large positive-strand RNA genomes that are 5′ capped and 3′ polyadenylated. The 5′-terminal two-thirds of the genome contain two open reading frames (ORFs), 1a and 1b, that together make up the viral replicase gene and encode two large polyproteins that are processed by viral proteases into 15–16 nonstructural proteins, most of them being involved in viral RNA synthesis. ORFs located in the 3′-terminal one-third of the genome encode structural and accessory proteins and are expressed from a set of 5′ leader-containing subgenomic mRNAs that are synthesized by a process called discontinuous transcription. Coronavirus protein synthesis not only involves cap-dependent translation mechanisms but also employs regulatory mechanisms, such as ribosomal frameshifting. Coronavirus replication is known to affect cellular translation, involving activation of stress-induced signaling pathways, and employing viral proteins that affect cellular mRNA translation and RNA stability. This chapter describes our current understanding of the mechanisms involved in coronavirus mRNA translation and changes in host mRNA translation observed in coronavirus-infected cells.

Original languageEnglish (US)
Title of host publicationAdvances in Virus Research
PublisherAcademic Press Inc.
Pages165-192
Number of pages28
DOIs
StatePublished - Dec 1 2016

Publication series

NameAdvances in Virus Research
Volume96
ISSN (Print)0065-3527
ISSN (Electronic)1557-8399

Keywords

  • Coronaviruses
  • Host gene expression
  • Host shutoff
  • Ribosomal frameshift
  • Stress response
  • Translation
  • Viral gene expression

ASJC Scopus subject areas

  • Virology
  • Infectious Diseases

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