Deciphering the cell type specific control of HCMV tegument-delivered pp71 subcellular localization

疱疹病毒将病毒编码的转录激活蛋白包装到 它们的病毒粒子。人巨细胞病毒(HCMV)编码的被膜反式激活因子是pp71蛋白。 当细胞被生产性感染时，pp71被释放到细胞质中，移位到细胞核，并 激活病毒即刻早期(IE)转录。疱疹病毒也会造成潜伏的感染 产生期基因表达缺失或减弱。外皮交付的pp71仍在 原代CD34+细胞的细胞质，其中HCMV建立潜伏期。因此，细胞内的亚细胞定位 在溶血性感染期间，被膜传递的pp71与IE转录活性存在差异相关(pp71在 核内，IE转录开启)和潜伏期(pp71在胞浆内，IE转录关闭)。在这里，我们建议 为了确定被膜递送的pp71的亚细胞定位作为一种 开发一种人工控制它的方法并从而控制HCMV感染的命运的第一步 (裂解或潜伏)。

Herpesviruses package virally-encoded transcriptional activating proteins into the tegument layer of their virions. The tegument transactivator encoded by human cytomegalovirus (HCMV) is the pp71 protein. When cells are productively infected, pp71 is released into the cytoplasm, translocates to the nucleus, and activates viral immediate early (IE) transcription. Herpesviruses also establish latent infections where productive phase gene expression is absent or attenuated. Tegument-delivered pp71 remains in the cytoplasm of the primary CD34+ cells where HCMV establishes latency. Thus, the subcellular localization of tegument-delivered pp71 differentially correlates with IE transcriptional activity during lytic infection (pp71 in the nucleus, IE transcription on) and latency (pp71 in the cytoplasm, IE transcription off). Here, we propose to identify the natural way in which the subcellular localization of tegument-delivered pp71 is controlled as a first step toward developing a method to artificially control it, and thus control the fate of an HCMV infection (lytic or latent).