Coronavirus papain-like proteases induce autophagy but block autophagosome fusion with lysosomes through interacting with Beclin 1
作者单位：军事医学科学院放射与辐射医学研究所 Beijing Institute of Radiation Medicine
会议名称：《第八届全国医学生物化学与分子生物学第五届全国临床应用生物化学与分子生物学2013华东六省一市生物化学与分子生物学联合学术研讨会》
会议日期：2013年
学科分类：1007[医学-药学(可授医学、理学学位)] 100705[医学-微生物与生化药学] 1001[医学-基础医学(可授医学、理学学位)] 100103[医学-病原生物学] 10[医学]
关 键 词：Coronavirus NL63 Papain-like protease Autophagy Beclinl STING
摘 要：Autophagy is a cellular catabolic process that sequesters cargo in double-membraned autophagosome and delivers the cargo to lysosomes to be degraded for recycling resource for *** plays important roles in modulating viral replication and antiviral innate and adaptive immune *** studies demonstrated that coronavirus infection is associated with the autophagic process,however,the underlying mechanisms for autophagy induction are largely ***,we show that the papain-like proteases(PLP) of human coronavirus(HCoV) NL63 induce *** found that the transmembrane(TM) form of the papain-like protease PLP2(PLP2-TM) acts as a novel autophagy-inducing protein encoded by ***,PLP2-TM induces incomplete autophagy process,as PLP2-TM increases the accumulation of autophagosomes but blocks the fusion of autophagosomes with lysosomes,leading to prevention of the degradation of the autophagic substrate,***,PLP2-TM colocalizes and interacts with autophagy marker protein ***,PLP2-TM interacts and deubiquitinates Beclinl to upregulate Beclinl expression and promote Beclinl interaction with STING,the key regulator for antiviral IFN ***,these results suggested that the coronavirus papain-like proteases induce incomplete autophagy by interacting with Beclin 1,which in turn may modulate coronavirus replication and antiviral innate immunity.