期刊
JOURNAL OF VIROLOGY
卷 79, 期 13, 页码 8614-8619出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.79.13.8614-8619.2005
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资金
- NINDS NIH HHS [R0I-NS33506, R01 NS033506] Funding Source: Medline
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.
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