DOWNREGULATION OF AUTOPHAGY BY HERPESVIRUS BCL-2 HOMOLOGS

疱疹病毒 BCL-2 同源物下调自噬

• 批准号: 7715511
• 负责人: Chang-Seng Liang
• 金额: $ 3.24万
• 依托单位: HARVARD MEDICAL SCHOOL
• 依托单位国家: 美国
• 财政年份: 2008
• 资助国家: 美国
• 起止时间: 2008-06-05 至 2009-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7715511
• 关键词: Acquired Immunodeficiency Syndrome; Apoptosis; Autophagocytosis; Cells; Computer Retrieval of Information on Scientific Projects Database; Down-Regulation; Funding; Grant; Herpesviridae; Homologous Gene; Institution; Pathogenesis; Pathway interactions; Proteins; Research; Research Personnel; Resources; Role; Satellite Viruses; Simplexvirus; Source; Staging; United States National Institutes of Health; Viral; Virus; Virus Diseases; response

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.

该副本是利用众多研究子项目之一 由NIH/NCRR资助的中心赠款提供的资源。子弹和 调查员（PI）可能已经从其他NIH来源获得了主要资金， 因此可以在其他清晰的条目中代表。列出的机构是 对于中心，这不一定是调查员的机构。 细胞自噬途径在病毒感染和发病机理中的关键作用变得越来越明显。越来越多的证据表明，病毒已经开发出不同的策略来对其自身的利益进行精心调节自噬，从而促进有效的病毒复制或促进病毒持久性。尽管我们对这些策略的理解仍处于起步阶段，但最近的进步表明，γ疱疹病毒Bcl-2同源物（VBCL-2）保护病毒感染的细胞免受凋亡的侵蚀，还通过与自噬蛋白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已演变为具有增强的抗自助噬活性，这表明细胞自噬在响应病毒感染和与病毒相关的发病机理中起着重要作用。与艾滋病有关。