An, Sungwhan and Chen, Chun-Jen and Yu, Xin and Leibowitz, Julian L. and Makino, Shinji (1999) Induction of Apoptosis in Murine Coronavirus-Infected Cultured Cells and Demonstration of E Protein as an Apoptosis Inducer. Journal of Virology, 73 (9). pp. 7853-7859. ISSN 0022-538X. http://resolver.caltech.edu/CaltechAUTHORS:ANSjvir99
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We 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.
|Additional Information:||Copyright © 1999, American Society for Microbiology. Received 10 February 1999/Accepted 26 May 1999 The first two authors contributed equally to this study. We thank Fumihiro Taguchi, National Institute of Neuroscience, Japan, for RVV t(+), Stephen A. Stohlman, University of Southern California, for vJN, vJM, and vJHE, J. Marie Hardwick, Johns Hopkins University, for plasmids pZIPneo and pZIPbcl-2, and Bernard Moss, NIH Laboratory of Viral Disease, for pSC11ss and pMJ601. We also thank John F. Repass and Sangeeta Banerjee for proofreading of the manuscript. This work was supported by Public Health Service grant AI29984 from the National Institutes for Health (to S.M.) and grants from the National Multiple Sclerosis Society and the Stearman family (to J.L.L.).|
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|Deposited On:||20 Feb 2006|
|Last Modified:||26 Dec 2012 08:46|
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