Open AccessSevere acute respiratory syndrome coronavirus 3C‐like protease‐induced apoptosis
Author(s) -
Lin ChengWen,
Lin KuanHsun,
Hsieh TsungHan,
Shiu ShiYi,
Li JengYi
Publication year - 2006
Publication title -
fems immunology & medical microbiology
Language(s) - English
Resource type - Journals
eISSN - 1574-695X
pISSN - 0928-8244
DOI - 10.1111/j.1574-695x.2006.00045.x
Subject(s) - biology , apoptosis , coronavirus , betacoronavirus , virology , respiratory system , protease , covid-19 , pneumonia , immunology , microbiology and biotechnology , medicine , pathology , enzyme , genetics , outbreak , disease , infectious disease (medical specialty) , anatomy , biochemistry
The pathogenesis of severe acute respiratory syndrome‐associated coronavirus (SARS‐CoV) is an important issue for the treatment and prevention of severe acute respiratory syndrome. Recently, SARS‐CoV has been demonstrated to induce cell apoptosis in Vero‐E6 cells. The possible role of SARS‐CoV 3C‐like protease (3CL pro ) in virus‐induced apoptosis is characterized in this study. Growth arrest and apoptosis via caspase‐3 and caspase‐9 activities were demonstrated in SARS‐CoV 3CL pro ‐expressing human promonocyte cells. The fluorescence intensity of dihydrorhodamine 123 staining indicated that cellular reactive oxygen species were markedly increased in SARS‐CoV 3CL pro ‐expressing cells. Moreover, in vivo signalling pathway assay indicated that 3CL pro increased the activation of the nuclear factor‐kappa B‐dependent reporter, but inhibited activator protein‐1‐dependent transcription. This finding is likely to be responsible for virus‐induced apoptotic signalling.