The 3a protein of SARS-coronavirus induces apoptosis in Vero E6 cells

被引:8
|
作者
Waye, Mary M. Y. [1 ]
Law, Patrick T. W. [1 ]
Wong, Chi-Hang [1 ]
Au, Thomas C. C. [1 ]
Chuck, Chi-Pang [1 ]
Kong, Siu-Kai [1 ]
Chan, Paul K. S. [1 ]
To, Ka-Fai [1 ]
Lo, Anthony W. I. [1 ]
Chan, Judy Y. W. [1 ]
Suen, Yick-Keung [1 ]
Chan, H. Y. Edwin [1 ]
Fung, Kwok-Pui [1 ]
Sung, Joseph J. Y. [1 ]
Lo, Y. M. Dennis [1 ]
Tsui, Stephen K. W. [1 ]
机构
[1] Chinese Univ Hong Kong, Dept Biochem, Shatin, Hong Kong, Peoples R China
关键词
ACUTE RESPIRATORY SYNDROME; GENOME SEQUENCE; EPIDEMIOLOGY; VIRUSES;
D O I
10.1109/IEMBS.2005.1616242
中图分类号
R318 [生物医学工程];
学科分类号
0831 ;
摘要
An outbreak of severe acute respiratory syndrome (SARS) occurred in China and the first case emerged in mid November 2002. The etiologic agent of this disease was found to be a previously unknown 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, we showed that the 3a protein was localized to the endoplasmic reticulum (ER) in 3a-transfected monkey kidney Vero E6 cells. In vitro experiments of chromatin condensation and DNA fragmentation suggest that the 3a protein may trigger apoptosis. Our data show that over-expression of a single SARS-CoV protein can induce apoptosis in vitro. Thus GFP-3a fusion protein could also be used as a biosensor for monitoring the cytopathic features of SARS infection, e.g. lymphopenia, in animal model systems, similar to nucleocapsid and 7a proteins.
引用
收藏
页码:7482 / 7485
页数:4
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