Department of Microbiology & Immunology and Emory Vaccine Center, 1462 Clifton Road, Emory University School of Medicine, Atlanta, Georgia 30322, USA.
J Virol. 2011 May;85(10):5125-35. doi: 10.1128/JVI.01682-10. Epub 2011 Feb 23.
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.
人类巨细胞病毒 UL103 编码一种被膜蛋白，在疱疹病毒亚群中保守。缺乏该基因产物的突变病毒表现出细胞游离病毒产物积累显著减少和细胞间传播不良。鉴于感染突变病毒的细胞中病毒蛋白和病毒 DNA 以正常动力学积累，UL103 似乎在复制的晚期发挥作用，在无衣壳致密体和病毒粒子的出芽中起关键作用。在存在或不存在 DNA 包装抑制剂 2-溴-5,6-二氯-1-（β-D-核糖呋喃基）苯并咪唑的情况下，突变病毒感染的细胞中，在细胞外空间中观察到很少的致密体。在逆转包装抑制后，UL103 对细胞游离病毒的积累有显著影响，但对细胞相关病毒的积累没有影响。因此，UL103 在成熟过程中发挥了新的重要作用，调节感染细胞中病毒颗粒和致密体的出芽。
