Goodwin D J, Walters M S, Smith P G, Thurau M, Fickenscher H, Whitehouse A
Molecular Medicine Unit, St. James's University Hospital, University of Leeds, Leeds LS9 7TF, United Kingdom.
J Virol. 2001 Apr;75(8):4008-13. doi: 10.1128/JVI.75.8.4008-4013.2001.
Herpesviruses occur in two distinct forms of infection, lytic replication and latent persistence. In this study, we investigated the molecular mechanisms that govern the latent-lytic switch in the prototype gamma-2 herpesvirus, herpesvirus saimiri (HVS). We utilized a persistently HVS-infected A549 cell line, in which HVS DNA is stably maintained as nonintegrated circular episomes, to assess the role of the open reading frame 50 (ORF 50) (Rta) proteins in the latent-lytic switch. Northern blot analysis and virus recovery assays determined that the ORF 50a gene product, when expressed under the control of a constitutively active promoter, was sufficient to reactivate the entire lytic replication cycle, producing infectious virus particles. Furthermore, although the ORF 50 proteins of HVS strains A11 and C488 are structurally divergent, they were both capable of inducing the lytic replication cycle in this model of HVS latency.
疱疹病毒以两种不同形式的感染存在，即裂解复制和潜伏持续。在本研究中，我们调查了控制原型γ-2疱疹病毒——赛米利疱疹病毒（HVS）潜伏-裂解转换的分子机制。我们利用持续感染HVS的A549细胞系（其中HVS DNA作为非整合环状附加体稳定维持）来评估开放阅读框50（ORF 50）（Rta）蛋白在潜伏-裂解转换中的作用。Northern印迹分析和病毒回收试验确定，当在组成型活性启动子的控制下表达时，ORF 50a基因产物足以重新激活整个裂解复制周期，产生感染性病毒颗粒。此外，尽管HVS毒株A11和C488的ORF 50蛋白在结构上存在差异，但它们在这种HVS潜伏模型中均能够诱导裂解复制周期。
