Mechanisms of coronavirus nsp1-mediated control of host and viral gene expression

Keisuke Nakagawa, Shinji Makino

Research output: Contribution to journalReview articlepeer-review

42 Scopus citations


Many viruses disrupt host gene expression by degrading host mRNAs and/or manipu-lating translation activities to create a cellular environment favorable for viral replication. Often, virus-induced suppression of host gene expression, including those involved in antiviral responses, contributes to viral pathogenicity. Accordingly, clarifying the mechanisms of virus-induced dis-ruption of host gene expression is important for understanding virus–host cell interactions and virus pathogenesis. Three highly pathogenic human coronaviruses (CoVs), including severe acute respiratory syndrome (SARS)-CoV, Middle East respiratory syndrome (MERS)-CoV, and SARS-CoV-2, have emerged in the past two decades. All of them encode nonstructural protein 1 (nsp1) in their genomes. Nsp1 of SARS-CoV and MERS-CoV exhibit common biological functions for inducing endonucleolytic cleavage of host mRNAs and inhibition of host translation, while viral mRNAs evade the nsp1-induced mRNA cleavage. SARS-CoV nsp1 is a major pathogenic determinant for this virus, supporting the notion that a viral protein that suppresses host gene expression can be a virulence factor, and further suggesting the possibility that SARS-CoV-2 nsp1, which has high amino acid identity with SARS-CoV nsp1, may serve as a major virulence factor. This review summarizes the gene expression suppression functions of nsp1 of CoVs, with a primary focus on SARS-CoV nsp1 and MERS-CoV nsp1.

Original languageEnglish (US)
Article number300
Pages (from-to)1-18
Number of pages18
Issue number2
StatePublished - Feb 2021


  • Coronaviruses
  • Host gene expression suppression
  • MRNA degradation
  • Nsp1
  • Translational suppression
  • Virulence factor

ASJC Scopus subject areas

  • Medicine(all)


Dive into the research topics of 'Mechanisms of coronavirus nsp1-mediated control of host and viral gene expression'. Together they form a unique fingerprint.

Cite this