Your browser doesn't support javascript.
loading
Flavivirus prM interacts with MDA5 and MAVS to inhibit RLR antiviral signaling.
Sui, Liyan; Zhao, Yinghua; Wang, Wenfang; Chi, Hongmiao; Tian, Tian; Wu, Ping; Zhang, Jinlong; Zhao, Yicheng; Wei, Zheng-Kai; Hou, Zhijun; Zhou, Guoqiang; Wang, Guoqing; Wang, Zedong; Liu, Quan.
Afiliação
  • Sui L; Department of Infectious Diseases and Center of Infectious diseases and Pathogen Biology, Key Laboratory of Organ Regeneration and Transplantation of the Ministry of Education, Key Laboratory of Zoonotic Diseases, The First Hospital of Jilin University, Changchun, China.
  • Zhao Y; Department of Infectious Diseases and Center of Infectious diseases and Pathogen Biology, Key Laboratory of Organ Regeneration and Transplantation of the Ministry of Education, Key Laboratory of Zoonotic Diseases, The First Hospital of Jilin University, Changchun, China.
  • Wang W; College of Basic Medical Science, Jilin University, Changchun, China.
  • Chi H; College of Basic Medical Science, Jilin University, Changchun, China.
  • Tian T; College of Basic Medical Science, Jilin University, Changchun, China.
  • Wu P; College of Wildlife and Protected Area, Northeast Forestry University, Harbin, China.
  • Zhang J; Department of Infectious Diseases and Center of Infectious diseases and Pathogen Biology, Key Laboratory of Organ Regeneration and Transplantation of the Ministry of Education, Key Laboratory of Zoonotic Diseases, The First Hospital of Jilin University, Changchun, China.
  • Zhao Y; Department of Infectious Diseases and Center of Infectious diseases and Pathogen Biology, Key Laboratory of Organ Regeneration and Transplantation of the Ministry of Education, Key Laboratory of Zoonotic Diseases, The First Hospital of Jilin University, Changchun, China.
  • Wei ZK; School of Life Sciences and Engineering, Foshan University, Foshan, China.
  • Hou Z; College of Wildlife and Protected Area, Northeast Forestry University, Harbin, China.
  • Zhou G; The Biological safety level-3 Laboratory, Changchun Institute of Biological Products Co., Ltd, Changchun, China.
  • Wang G; College of Basic Medical Science, Jilin University, Changchun, China.
  • Wang Z; Department of Infectious Diseases and Center of Infectious diseases and Pathogen Biology, Key Laboratory of Organ Regeneration and Transplantation of the Ministry of Education, Key Laboratory of Zoonotic Diseases, The First Hospital of Jilin University, Changchun, China. wangzedong@jlu.edu.cn.
  • Liu Q; Department of Infectious Diseases and Center of Infectious diseases and Pathogen Biology, Key Laboratory of Organ Regeneration and Transplantation of the Ministry of Education, Key Laboratory of Zoonotic Diseases, The First Hospital of Jilin University, Changchun, China. liuquan1973@hotmail.com.
Cell Biosci ; 13(1): 9, 2023 Jan 13.
Article em En | MEDLINE | ID: mdl-36639652
ABSTRACT

BACKGROUND:

Vector-borne flaviviruses, including tick-borne encephalitis virus (TBEV), Zika virus (ZIKV), West Nile virus (WNV), yellow fever virus (YFV), dengue virus (DENV), and Japanese encephalitis virus (JEV), pose a growing threat to public health worldwide, and have evolved complex mechanisms to overcome host antiviral innate immunity. However, the underlying mechanisms of flavivirus structural proteins to evade host immune response remain elusive.

RESULTS:

We showed that TBEV structural protein, pre-membrane (prM) protein, could inhibit type I interferon (IFN-I) production. Mechanically, TBEV prM interacted with both MDA5 and MAVS and interfered with the formation of MDA5-MAVS complex, thereby impeding the nuclear translocation and dimerization of IRF3 to inhibit RLR antiviral signaling. ZIKV and WNV prM was also demonstrated to interact with both MDA5 and MAVS, while dengue virus serotype 2 (DENV2) and YFV prM associated only with MDA5 or MAVS to suppress IFN-I production. In contrast, JEV prM could not suppress IFN-I production. Overexpression of TBEV and ZIKV prM significantly promoted the replication of TBEV and Sendai virus.

CONCLUSION:

Our findings reveal the immune evasion mechanisms of flavivirus prM, which may contribute to understanding flavivirus pathogenicity, therapeutic intervention and vaccine development.
Palavras-chave

Texto completo: 1 Base de dados: MEDLINE Idioma: En Ano de publicação: 2023 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Idioma: En Ano de publicação: 2023 Tipo de documento: Article