Human Herpesvirus 6B U26 Inhibits the Activation of the RLR/MAVS Signaling Pathway

Author:

Jiang Xuefeng1,Tang Tian1,Guo Jinfeng1,Wang Yuhang1,Li Peipei2,Chen Xiangjun2,Wang Lily2,Wen Yiqun2,Jia Junli1,Emanuela Garbarino1,Hu Benshun1,Chen Shuhua3,Yao Kun1,Li Linyun4,Tang Huaming156ORCID

Affiliation:

1. Department of Immunology, Nanjing Medical University, Nanjing, People’s Republic of China

2. Department of Women’s Hospital of Nanjing Medical University, Nanjing Medical University, Nanjing, People’s Republic of China

3. Department of Critical Care Medicine, Changzhou Cancer Hospital Affiliated to Soochow University, Changzhou, People’s Republic of China

4. Department of Medical Genetics, Nanjing Medical University, Nanjing, People’s Republic of China

5. Key Laboratory of Antibody Technique of Ministry of Health, Nanjing Medical University, Nanjing, People’s Republic of China

6. The Laboratory Center for Basic Medical Sciences, Nanjing Medical University, Nanjing, People’s Republic of China

Abstract

HHV-6B (human herpesvirus 6B) is well known to evade host antiviral responses and establish a lifelong latent infection. How HHV-6B evades RNA recognition is still poorly understood. Our results indicate that HHV-6 U26 plays a vital role in RLR/MAVS signaling pathway activity. Knockout of endogenous MAVS could facilitate HHV-6B replication. The findings in this study could provide new insights into host-virus interactions and help develop a new therapy against HHV-6B infection.

Publisher

American Society for Microbiology

Subject

Virology,Microbiology

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