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 

机构地区：[1]State Key Laboratory of Virology,Modem Virology Research Center,College of Life Sciences,Wuhan University,Wuhan 430072,China

出　　处：《Virologica Sinica》2021年第3期438-448,共11页中国病毒学（英文版）

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)。

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 replication.Sumoylation 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 bodies.Finally, 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.

关 键 词：Human parainfluenza virus type 3(HPIV3) PHOSPHOPROTEIN SUMOYLATION REPLICATION Viral replication 

分 类 号：R373.13[医药卫生—病原生物学]