2021-01-012024-05-13https://scholars.lib.ntu.edu.tw/handle/123456789/651656Enteroviruses represent a global health threat. Enteroviruses recognize intracellular Golgi membranes in replication organelles to escape host innate immune system and amplify their genomes. The functionality of these replication organelles depends on the activities of both the viral nonstructural proteins and the co-opted host proteins. 3A protein of enteroviruses plays an important role to form replication complex for viral RNA replication, but this mechanism is still unclear. To elucidate this mechanism, enterovirus A71 (EV-A71) is used herein as a virus model to investigate how these replication organelles are formed and to identify the cellular components that are critical in this process. Immunoprecipitation assay is combined with LC-MS/MS analysis to identify 172 cellular proteins and four viral proteins interacting with EV-A71 3A protein. Rab7a is one of the host proteins that selected for further investigation. Rab7a is the key regulator in endo-lysosomal trafficking. This project has the following goals. Aim I. To investigate the interaction of viral proteins with Rab7a Aim II. To investigate the role of Rab7a in viral replication Aim III. To investigate the role of Rab7a in other enteroviruses replication Understanding how viral proteins hijack the regulatory mechanisms of membrane metabolism to form replication organelles will provide a new perspective on various areas of cell biology and virology and will be indispensable for the development of a new generation of anti-viral control strategies.enteroviruses, replication organelles, enterovirus A71 3A protein, Rab7a