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Journal of Virology, August 2009, p. 7449-7456, Vol. 83, No. 15
0022-538X/09/$08.00+0     doi:10.1128/JVI.00325-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Murine Cytomegalovirus Capsid Assembly Is Dependent on US22 Family Gene M140 in Infected Macrophages{triangledown}

Laura K. Hanson,1,{dagger} Jacquelyn S. Slater,1 Victoria J. Cavanaugh,1 William W. Newcomb,2 Lisa L. Bolin,1 Christine N. Nelson,1 Lisa D. Fetters,1 Qiyi Tang,3,{ddagger} Jay C. Brown,2 Gerd G. Maul,3 and Ann E. Campbell1*

Department of Microbiology and Molecular Cell Biology, Eastern Virginia Medical School, Norfolk, Virginia 23507,1 Department of Microbiology and Cancer Center, University of Virginia Health System, Charlottesville, Virginia 22908,2 The Wistar Institute, Philadelphia, Pennsylvania 191043

Received 13 February 2009/ Accepted 8 May 2009

Macrophages are an important target cell for infection with cytomegalovirus (CMV). A number of viral genes that either are expressed specifically in this cell type or function to optimize CMV replication in this host cell have now been identified. Among these is the murine CMV (MCMV) US22 gene family member M140, a nonessential early gene whose deletion (RV{Delta}140) leads to significant impairment in virus replication in differentiated macrophages. We have now determined that the defect in replication is at the stage of viral DNA encapsidation. Although the rate of RV{Delta}140 genome replication and extent of DNA cleavage were comparable to those for revertant virus, deletion of M140 resulted in a significant reduction in the number of viral capsids in the nucleus, and the viral DNA remained sensitive to DNase treatment. These data are indicative of incomplete virion assembly. Steady-state levels of both the major capsid protein (M86) and tegument protein M25 were reduced in the absence of the M140 protein (pM140). This effect may be related to the localization of pM140 to an aggresome-like, microtubule organizing center-associated structure that is known to target misfolded and overexpressed proteins for degradation. It appears, therefore, that pM140 indirectly influences MCMV capsid formation in differentiated macrophages by regulating the stability of viral structural proteins.

* Corresponding author. Mailing address: Department of Microbiology and Molecular Cell Biology, Eastern Virginia Medical School, P.O. Box 1980, 700 W. Olney Rd., Norfolk, VA 23501. Phone: (757) 446-5667. Fax: (757) 624-2255. E-mail: campbeae{at}evms.edu

{triangledown} Published ahead of print on 20 May 2009.

{dagger} Present address: Department of Biology, Texas Woman's University, Denton, TX.

{ddagger} Present address: Department of Microbiology/AIDS Program, Ponce School of Medicine, Ponce, PR.

Journal of Virology, August 2009, p. 7449-7456, Vol. 83, No. 15
0022-538X/09/$08.00+0     doi:10.1128/JVI.00325-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





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