RT Journal Article SR Electronic(1) A1 Law, Patrick T. W. A1 Wong, Chi-Hang A1 Au, Thomas C. C. A1 Chuck, Chi-Pang A1 Kong, Siu-Kai A1 Chan, Paul K. S. A1 To, Ka-Fai A1 Lo, Anthony W. I. A1 Chan, Judy Y. W. A1 Suen, Yick-Keung A1 Chan, H. Y. Edwin A1 Fung, Kwok-Pui A1 Waye, Mary M. Y. A1 Sung, Joseph J. Y. A1 Lo, Y. M. Dennis A1 Tsui, Stephen K. W.YR 2005 T1 The 3a protein of severe acute respiratory syndrome-associated coronavirus induces apoptosis in Vero E6 cells JF Journal of General Virology, VO 86 IS 7 SP 1921 OP 1930 DO https://doi.org/10.1099/vir.0.80813-0 PB Microbiology Society, SN 1465-2099, AB 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., UL https://www.microbiologyresearch.org/content/journal/jgv/10.1099/vir.0.80813-0