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文献详情 >Nonmuscle myosin IIA promotes ... 收藏

Nonmuscle myosin IIA promotes the internalization of influenza A virus and regulates viral polymerase activity through interacting with nucleoprotein in human pulmonary cells

作     者:Jian Chen Jian Liu Zhilu Chen Daobin Feng Cuisong Zhu Jun Fan Shuye Zhang Xiaoyan Zhang Jianqing Xu Jian Chen;Jian Liu;Zhilu Chen;Daobin Feng;Cuisong Zhu;Jun Fan;Shuye Zhang;Xiaoyan Zhang;Jianqing Xu

作者机构:Clinical Center for Bio-TherapyZhongshan HospitalFudan University(Xiamen Branch)Shanghai200032China Center for Infectious Disease ResearchScience of Life SciencesWestlake UniversityHangzhou310024China Shanghai Public Health Clinical Center&Institutes of Biomedical SciencesShanghai Medical CollegeFudan UniversityShanghai201508China 

出 版 物:《Virologica Sinica》 (中国病毒学(英文版))

年 卷 期:2023年第38卷第1期

页      面:128-141页

核心收录:

学科分类:0710[理学-生物学] 090601[农学-基础兽医学] 09[农学] 0906[农学-兽医学] 

基  金:supported by the National Natural Science Foundation of China(82071788,81901598,81771704,and 82041015) National Key R&D Program of China(2022YFC2604100) 

主  题:Myosin IIA(MYH9) Influenza A virus(IAV) vRNP activity Virus-host interactions Virus entry 

摘      要:Influenza A virus(IAV),responsible for seasonal epidemics and recurring pandemics,represents a global threat to public *** the risk of a potential IAV pandemic,it is increasingly important to better understand virushost interactions and develop new anti-viral ***,we reported nonmuscle myosin IIA(MYH9)-mediated regulation of IAV ***9 depletion caused a profound inhibition of IAV infection by reducing viral attachment and internalization in human lung epithelial ***,overexpression of MYH9 also led to a significant reduction in viral productive ***,overexpression of MYH9 retained viral attachment,internalization,or uncoating,but suppressed the viral ribonucleoprotein(vRNP)activity in a minigenome *** analyses found that excess MYH9 might interrupt the formation of vRNP by interacting with the viral nucleoprotein(NP)and result in the reduction of the completed vRNP in the nucleus,thereby inhibiting subsequent viral RNA transcription and ***,we discovered that MYH9 can interact with IAV NP protein and engage in the regulation of vRNP complexes,thereby involving viral *** findings enlighten new mechanistic insights into the complicated interface of host-IAV interactions,ultimately making it an attractive target for the generation of antiviral drugs.

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