Actin is a component of the compensation mechanism in pseudorabies virus virions lacking the major tegument protein VP22.
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.
del Rio
T
T
Department of Molecular Biology, Princeton University, Princeton, New Jersey 08544-1014, USA.
DeCoste
C J
CJ
Enquist
L W
LW
D000199:Actins / Q000378:metabolism*; D000818:Animals; D002460:Cell Line; D017930:Genes, Reporter; D049452:Green Fluorescent Proteins / Q000032:analysis / Q000235:genetics; D011558:Herpesvirus 1, Suid / Q000235:genetics* / Q000378:metabolism* / Q000472:pathogenicity; D014764:Viral Proteins / Q000235:genetics* / Q000378:metabolism; D015678:Viral Structural Proteins / Q000235:genetics* / Q000378:metabolism; D014771:Virion / Q000235:genetics; D014774:Virulence; D014779:Virus Replication
D000199:Actins; C502892:VP22 protein, Pseudorabies virus; D014764:Viral Proteins; D015678:Viral Structural Proteins; D049452:Green Fluorescent Proteins