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1 Centre for Emerging Infectious Diseases, The Chinese University of Hong Kong, Shatin, NT, Hong Kong SAR, China
2 Department of Biochemistry, The Chinese University of Hong Kong, Shatin, NT, Hong Kong SAR, China
3 Department of Microbiology, The Chinese University of Hong Kong, Shatin, NT, Hong Kong SAR, China
4 Department of Anatomical and Cellular Pathology, The Chinese University of Hong Kong, Shatin, NT, Hong Kong SAR, China
5 The Croucher Laboratory for Human Genomics, The Chinese University of Hong Kong, Shatin, NT, Hong Kong SAR, China
6 Department of Medicine and Therapeutics, The Chinese University of Hong Kong, Shatin, NT, Hong Kong SAR, China
7 Department of Chemical Pathology, The Chinese University of Hong Kong, Shatin, NT, Hong Kong SAR, China
Correspondence
Stephen K. W. Tsui
kwtsui{at}cuhk.edu.hk
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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