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Journal of Virology, January 2003, p. 631-641, Vol. 77, No. 1
0022-538X/03/$08.00+0     DOI: 10.1128/JVI.77.1.631-641.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Disruption of Mitochondrial Networks by the Human Cytomegalovirus UL37 Gene Product Viral Mitochondrion-Localized Inhibitor of Apoptosis

A. Louise McCormick, Vanessa L. Smith, Dar Chow, and Edward S. Mocarski*

Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, California 94305-5124

Received 17 June 2002/ Accepted 26 September 2002

By 24 h after infection with human cytomegalovirus, the reticular mitochondrial network characteristic of uninfected fibroblasts was disrupted as mitochondria became punctate and dispersed. These alterations were associated with expression of the immediate-early ({alpha}) antiapoptotic UL37x1 gene product viral mitochondrion-localized inhibitor of apoptosis (vMIA). Similar alterations in mitochondrial morphology were induced directly by vMIA in transfected cells. A 68-amino-acid antiapoptotic derivative of vMIA containing the mitochondrial localization and antiapoptotic domains also induced disruption, whereas a mutant lacking the antiapoptotic domain failed to cause disruption. These data suggest that the fission and/or fusion process that normally controls mitochondrial networks is altered by vMIA. Mitochondrial fission has been implicated in the induction of apoptosis and vMIA-mediated inhibition of apoptosis may occur subsequent to this event.

* Corresponding author. Mailing address: Department of Microbiology & Immunology, Fairchild Science Building, Stanford University School of Medicine, Stanford, CA 94305-5124. Phone: (650) 723-6435. Fax: (650) 723-1606. E-mail: mocarski{at}stanford.edu.

Journal of Virology, January 2003, p. 631-641, Vol. 77, No. 1
0022-538X/03/$08.00+0     DOI: 10.1128/JVI.77.1.631-641.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.





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