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Journal of Virology, September 1999, p. 7853-7859, Vol. 73, No. 9
Department of Microbiology and Institute for
Cellular and Molecular Biology, The University of Texas at Austin,
Austin, Texas 787121; Department of
Microbiology and Immunology, The University of Texas Medical Branch
at Galveston, Galveston, Texas 77555-10192; and
Department of Pathology and Laboratory Medicine, Texas A&M
University Health Science Center, College Station, Texas
77843-11143
Received 10 February 1999/Accepted 26 May 1999
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.
0022-538X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
Induction of Apoptosis in Murine Coronavirus-Infected
Cultured Cells and Demonstration of E Protein as an Apoptosis
Inducer


*
Corresponding author. Mailing address: Department of
Microbiology and Immunology, The University of Texas Medical Branch at Galveston, Galveston, TX 77555-1019. Phone: (409) 772-2323. Fax: (409)
772-5065. E-mail: shmakino{at}utmb.edu.
Present address: Department of Microbiology and Immunology,
Stanford University, Stanford, CA 94305.
Present address: Department of Biology, California Institute of
Technology, Pasadena, CA 91125.
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