Actin is a component of the compensation mechanism in pseudorabies virus virions lacking the major tegument protein VP22

T. Del Rio, C. J. DeCoste, L. W. Enquist

Research output: Contribution to journalArticle

32 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)8614-8619
Number of pages6
JournalJournal of virology
Volume79
Issue number13
DOIs
StatePublished - Jul 2005

All Science Journal Classification (ASJC) codes

  • Microbiology
  • Immunology
  • Insect Science
  • Virology

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