Cytomegalovirus UL103 Controls Virion and Dense Body Egress▿

• Authors: Jenny Ahlqvist, Emory University; Edward S Mocarski, Emory University
• Journal Title: Journal of Virology
• Volume: Volume 85, Number 10
• Publisher: American Society for Microbiology | 2011-05, Pages 5125-5135
• Type of Work: Article | Final Publisher PDF
• Publisher DOI: http://doi.org/10.1128/JVI.01682-10
• Subjects: Biology, Virology; Health Sciences, Immunology; Biology, Microbiology

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.