CHUN-JEN CHEN2018-09-102018-09-1019990022538Xhttp://scholars.lib.ntu.edu.tw/handle/123456789/346538https://www.scopus.com/inward/record.uri?eid=2-s2.0-0032816080&doi=10.1128%2fjvi.73.9.7853-7859.1999&partnerID=40&md5=a63e9fa840a725e55bbd500423e177fdWe demonstrated that infection of 17Cl-1 cells with the murine coronavirus mouse hepatitis virus (MHV) induced caspase-dependent apoptosis. MHV-infected DBT cells did not show apoptotic changes, indicating that apoptosis was not a universal mechanism of cell death in MHV-infected cells. Expression of MHV structural proteins by recombinant vaccinia viruses showed that expression of MHV E protein induced apoptosis in DBT cells, whereas expression of other MHV structural proteins, including S protein, M protein, N protein, and hemagglutinin-esterase protein, failed to induce apoptosis. MHV E protein-mediated apoptosis was suppressed by a high level of Bcl-2 oncogene expression. Our data showed that MHV E protein is a multifunctional protein; in addition to its known function in coronavirus envelope formation, it also induces apoptosis.protein bcl 2; virus protein; animal cell; apoptosis; article; controlled study; gene expression; Murine hepatitis coronavirus; nonhuman; oncogene; priority journal; protein expression; RNA virus infection; virus expressionjournal article104388792-s2.0-0032816080