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

• DOI: 10.1099/vir.0.80813-0
• Publication Date: 2005-06-15T18:02:57Z
• Authors: Patrick T. W. Law; Chi-Hang Wong; Thomas C. C. Au; Chi-Pang Chuck; Siu-Kai Kong; Paul K. S. Chan; Ka-Fai To; Anthony W. I. Lo; Judy Y. W. Chan; Yick-Keung Suen; H. Y. Edwin Chan; Kwok-Pui Fung; Mary M. Y. Waye; Joseph J. Y. Sung; Y. M. Dennis Lo; Stephen K. W. Tsui
• Keywords: 0303 health sciences; Apoptosis; Endoplasmic Reticulum; Severe Acute Respiratory Syndrome; Viroporin Proteins; 3. Good health; Intestines; Viral Proteins; 03 medical and health sciences; Severe acute respiratory syndrome-related coronavirus; Viral Envelope Proteins; Chlorocebus aethiops; Animals; Humans; Intestinal Mucosa; Lung; Vero Cells

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.