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

Patrick T.W. Law(Chinese University of Hong Kong), Chi Hang Wong(Chinese University of Hong Kong), Thomas Chi Chuen Au(Chinese University of Hong Kong), Chi-Pang Chuck(Chinese University of Hong Kong), Siu‐Kai Kong(Chinese University of Hong Kong), Paul K.S. Chan(Chinese University of Hong Kong), Ka‐Fai To(Chinese University of Hong Kong), Anthony W.I. Lo(Chinese University of Hong Kong), Judy Yuet‐Wa Chan(Chinese University of Hong Kong), Yick-Keung Suen(Chinese University of Hong Kong), Ho Yin Edwin Chan(Chinese University of Hong Kong), Kwok‐Pui Fung(Chinese University of Hong Kong), Mary Miu Yee Waye(Chinese University of Hong Kong), Joseph J.�Y. Sung(Chinese University of Hong Kong), Yuk Ming Dennis Lo(Chinese University of Hong Kong), Stephen Kwok‐Wing Tsui(Chinese University of Hong Kong)
Journal of General Virology
June 15, 2005
Cited by 168

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.


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