| Literature DB >> 15958670 |
Patrick T W Law1,2, Chi-Hang Wong2, Thomas C C Au2, Chi-Pang Chuck1, Siu-Kai Kong1, Paul K S Chan3, Ka-Fai To4, Anthony W I Lo4, Judy Y W Chan1, Yick-Keung Suen1, H Y Edwin Chan1, Kwok-Pui Fung5,1, Mary M Y Waye5,1, Joseph J Y Sung6,2, Y M Dennis Lo7,2, Stephen K W Tsui5,1,2.
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.Entities:
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Year: 2005 PMID: 15958670 DOI: 10.1099/vir.0.80813-0
Source DB: PubMed Journal: J Gen Virol ISSN: 0022-1317 Impact factor: 3.891