The 3a protein of severe acute respiratory syndrome-associated coronavirus induces apoptosis in Vero E6 cells

J Gen Virol. 2005 Jul;86(Pt 7):1921-1930. doi: 10.1099/vir.0.80813-0.

Abstract

An outbreak of severe acute respiratory syndrome (SARS) occurred in China and the first case emerged in mid-November 2002. The aetiological agent of this disease was found to be a previously unknown coronavirus, SARS-associated coronavirus (SARS-CoV). The detailed pathology of SARS-CoV infection and the host response to the viral infection are still not known. The 3a gene encodes a non-structural viral protein, which is predicted to be a transmembrane protein. In this study, it was shown that the 3a protein was expressed in the lungs and intestinal tissues of SARS patients and that the protein localized to the endoplasmic reticulum in 3a-transfected monkey kidney Vero E6 cells. In vitro experiments of chromatin condensation and DNA fragmentation suggested that the 3a protein may trigger apoptosis. These data showed that overexpression of a single SARS-CoV protein can induce apoptosis in vitro.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis*
  • Chlorocebus aethiops
  • Endoplasmic Reticulum / metabolism
  • Endoplasmic Reticulum / virology
  • Humans
  • Intestinal Mucosa / metabolism
  • Intestines / virology
  • Lung / metabolism
  • Lung / virology
  • Severe Acute Respiratory Syndrome / virology
  • Severe acute respiratory syndrome-related coronavirus / metabolism
  • Severe acute respiratory syndrome-related coronavirus / pathogenicity*
  • Vero Cells
  • Viral Envelope Proteins
  • Viral Proteins / metabolism*
  • Viroporin Proteins

Substances

  • 3a protein, SARS-CoV
  • Viral Envelope Proteins
  • Viral Proteins
  • Viroporin Proteins