DOWNREGULATION OF AUTOPHAGY BY HERPESVIRUS BCL-2 HOMOLOGS

这个子项目是许多研究子项目中利用 资源由NIH/NCRR资助的中心拨款提供。子项目和 调查员(PI)可能从NIH的另一个来源获得了主要资金， 并因此可以在其他清晰的条目中表示。列出的机构是 该中心不一定是调查人员的机构。 细胞自噬途径在病毒感染和发病机制中的关键作用日益明显。越来越多的证据表明，病毒已经发展出不同的策略，为了自己的利益而精心调节细胞内的自噬，从而促进病毒的有效复制或促进病毒的持续。虽然我们对这些策略的了解还处于初级阶段，但最近的研究表明，伽马疱疹病毒Bcl2同源基因(VBcl2)可以保护感染病毒的细胞免受凋亡，也可以通过与自噬蛋白Beclin1的直接相互作用来抑制细胞自噬途径。有趣的是，与宿主相比，vBcl-2已经进化到具有增强的抗自噬活性，这表明细胞自噬在应对病毒感染和病毒相关的致病机制中发挥着重要作用。与艾滋病有关。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The critical role of the cellular autophagy pathway in viral infection and pathogenesis has become increasingly apparent. Mounting evidences suggest that viruses have developed different strategies to meticulously modulate intracellular autophagy for their own benefits, thereby either promoting efficient viral replication or facilitating viral persistence. While our understanding of these strategies is still in its incipient stage, recent advances demonstrate that gamma herpesvirus Bcl-2 homolog (vBcl-2), which protects virus-infected cells from apoptosis, also suppresses cellular autophagy pathway through its direct interaction with autophagy protein Beclin1. Intriguingly, vBcl-2 has evolved to harbor the enhanced anti-autophagic activity compared to its host counterpart, suggesting an important role of cellular autophagy in response to viral infection and virus-associated pathogenesis. AIDS related.