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Journal of Virology, July 2005, p. 8614-8619, Vol. 79, No. 13
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.13.8614-8619.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Actin Is a Component of the Compensation Mechanism in Pseudorabies Virus Virions Lacking the Major Tegument Protein VP22

T. del Rio,{dagger} C. J. DeCoste, and L.W. Enquist*

Department of Molecular Biology, Princeton University, Princeton, New Jersey 08540

Received 19 January 2005/ Accepted 24 March 2005

Despite being a major component of the pseudorabies virus tegument, VP22 is not required for PRV replication, virulence, or neuroinvasion (T. del Rio, H. C. Werner, and L. W. Enquist, J. Virol. 76:774-782, 2002). In the absence of VP22, tegument assembly compensates in a limited fashion with increased incorporation of cellular actin. Infection of epithelial cell lines expressing fluorescent actin fusion proteins resulted in the incorporation of filamentous and nonfilamentous actin into individual virions that were predominately light, noninfectious particles. We conclude that cellular actin is incorporated in the tegument of wild-type virions and is part of a compensation mechanism for VP22-null virions.

* Corresponding author. Mailing address: Schultz Laboratory, Department of Molecular Biology, Princeton University, Princeton, NJ 08544-1014. Phone: (609) 258-2664. Fax: (609) 258-1035. E-mail: lenquist{at}princeton.edu.

{dagger} Present address: Neurobiology Section, Division of Biological Sciences, UCSD, 9500 Gilman Drive, La Jolla, CA 92093-0357.

Journal of Virology, July 2005, p. 8614-8619, Vol. 79, No. 13
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.13.8614-8619.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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