Identifying structural features of viral RNA recognized by host helicases

病毒劫持宿主细胞机器并募集宿主蛋白质以帮助病毒复制。已经做出相当大的努力来鉴定与病毒RNA/蛋白质相互作用的宿主蛋白质。然而，支持病毒复制的DEAD盒家族成员识别病毒RNA的生化和结构基础知之甚少。我的长期研究目标是研究这些被许多病毒利用的关键宿主解旋酶，以便详细了解广谱宿主解旋酶和病毒RNA相互作用背后的分子机制。尽管ATP依赖的核酸解旋是DEAD盒解旋酶的既定作用，但最近的研究表明，解旋酶影响RNA代谢的所有主要方面，并且通常在病毒复制中起重要作用。特别地，解旋酶DDX 3X和DDX 5与日本脑炎病毒、丙型肝炎病毒和SARS冠状病毒的病毒3'非翻译区（3' UTR）相互作用，并支持它们的复制。我的实验室将研究DDX 3X/DDX 5与黄病毒属成员的3'UTR相互作用的结构基础（

Viruses hijack the host cell machinery and recruit host proteins to aid viral replication. Considerable effort has been made to identify host proteins that interact with viral RNA/proteins. However, the biochemical and structural basis of viral RNA recognition by the members of the DEAD-box family, which support viral replication, is poorly understood. My long-term research goal is to study these key host helicases that are exploited by many viruses in order to gain detailed insights into the molecular mechanisms behind a broad spectrum of host helicases and viral RNA interactions. Despite the ATP-dependent unwinding of nucleic acids being the established role of DEAD-box helicases, recent studies demonstrate that helicases influence all major aspects of RNA metabolism and often play significant roles in viral replication. Particularly, the helicases DDX3X and DDX5 interact with the viral 3' untranslated region (3' UTR) of Japanese encephalitis virus, hepatitis C virus, and SARS coronavirus, and support their replication. My laboratory will investigate the structural basis of the interactions of DDX3X/DDX5 with 3' UTRs of members of the Flavivirus genus (