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J Virol. 2011 May;85(10):5125-35. doi: 10.1128/JVI.01682-10. Epub 2011 Feb 23.

Cytomegalovirus UL103 controls virion and dense body egress.

Author information

  • 1Department of Microbiology & Immunology and Emory Vaccine Center, 1462 Clifton Road, Emory University School of Medicine, Atlanta, Georgia 30322, USA.

Abstract

Human cytomegalovirus UL103 encodes a tegument protein that is conserved across herpesvirus subgroups. Mutant viruses lacking this gene product exhibit dramatically reduced accumulation of cell-free virus progeny and poor cell-to-cell spread. Given that viral proteins and viral DNA accumulate with normal kinetics in cells infected with mutant virus, UL103 appears to function during the late phase of replication, playing a critical role in egress of capsidless dense bodies and virions. Few dense bodies were observed in the extracellular space in mutant virus-infected cells in the presence or absence of the DNA encapsidation inhibitor 2-bromo-5,6-dichloro-1-(β-d-ribofuranosyl)benzimidazole. Upon reversal of encapsidation inhibition, UL103 had a striking impact on accumulation of cell-free virus, but not on accumulation of cell-associated virus. Thus, UL103 plays a novel and important role during maturation, regulating virus particle and dense body egress from infected cells.

PMID:
21345947
[PubMed - indexed for MEDLINE]
PMCID:
PMC3126192
Free PMC Article

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