Sumoylation of Human Parainfluenza Virus Type 3 Phosphoprotein Correlates with A Reduction in Viral Replication

作     者：Qi Cheng Wenjing Huai Xiaoyan Wu Mingzhou Chen Qi Cheng;Wenjing Huai;Xiaoyan Wu;Mingzhou Chen

作者机构：State Key Laboratory of VirologyModem Virology Research CenterCollege of Life SciencesWuhan UniversityWuhan 430072China 

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

年 卷 期：2021年第36卷第3期

页      面：438-448页

核心收录：

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] 

基　　金：supported by grants from National Key R&D Program of China (2017YFA0505801) the National Natural Science Foundation of China (81825015, 81871650 and 31630086) National Science and Technology Major Project (2018ZX10101004) the Natural Science Foundation of Hubei Province Innovation Group (2017CFA022) Advanced Customer Cultivation Project of Wuhan National Biosafety Laboratory (2019ACCP-MS06) 

主　　题：Human parainfluenza virus type 3(HPIV3) Phosphoprotein Sumoylation Replication Viral replication 

摘      要：Human parainfluenza virus type 3(HPIV3), a member of the Paramyxoviridae family, can cause lower respiratory disease in infants and young children. The phosphoprotein(P) of HPIV3 is an essential cofactor of the viral RNA-dependent RNA polymerase large protein(L). P connects nucleocapsid protein(N) with L to initiate genome transcription and *** influences many important pathways of the target proteins, and many viral proteins are also themselves sumoylated. In this study, we found that the P of HPIV3 could be sumoylated, and mutation of K492 and K532 to arginine(PK492 R/K532 R) failed to be sumoylated within P, which enhances HPIV3 minigenome activity. Biochemical studies showed that PK492 R/K532 Rhad no effect on its interactions with N, formation of homo-tetramers and formation of inclusion ***, we found that incorporation of K492 R/K532 R into a recombinant HPIV3(rHPIV3-PK492 R/K532 R) increased viral production in culture cells, suggesting that sumoylation attenuates functions of P and down-regulates viral replication.