Attenuating innate immunity and facilitating β-coronavirus infection by NSP1 of SARS-CoV-2 through specific redistributing hnRNP A2/B1 cellular localization  

作　　者：Fanghang Zhou Qianya Wan Sheng Chen Ying Chen Pui-Hui Wang Xi Yao Ming-liang He 

机构地区：[1]Department of Biomedical Sciences,City University of Hong Kong,Kowloon,Hong Kong SAR,China [2]Advanced Medical Research Institute,Cheeloo College of Medicine,Shandong University,250012,Jinan,Shandong,China [3]CityU Shenzhen Research Institute,Nanshan,Shenzhen,China

出　　处：《Signal Transduction and Targeted Therapy》2021年第11期3174-3176,共3页信号转导与靶向治疗（英文）

基　　金：The work was partially supported by grants from The Science Technology and Innovation Committee of Shenzhen Municipality[JCYJ20180507181627057];RGC General Research Fund of Hong Kong Special Administrative Region[11104020];Strategic funds from City University of Hong Kong to M.L.H.

摘　　要：Dear Editor,Evidence shows the NSP1’s crucial roles of theβ-coronavirus SARS-CoV-2 in promoting cellular mRNA degradation,inhibiting host cell translation,innate immunity,and inducing inflammatory cytokine storm in the pathogenesis of COVID-19.1,2 More interestingly,NSP1 deletion in infectious clones prevents virus infection.3 However,little is known how NSP1 interacts with host factors to disrupt the host’s innate immunity for facilitating virus infection and reproduction.As a(+)ssRNA virus,SARS-CoV-2 completes its life cycle in the cytosol;viral RNA processing is the key for controlling and regulating the virus reproduction and pathogenesis.The ribonucleoproteins hnRNPs are the main factors responsible for RNA processing,including RNA splicing,maturation,decay,and translation,and even innate immunity in some cases.

关 键 词：NSP1 IMMUNITY INFECTION 

分 类 号：R373[医药卫生—病原生物学]