1. Academic Validation
  2. Zebrafish maoc1 Attenuates Spring Viremia of Carp Virus Propagation by Promoting Autophagy-Lysosome-Dependent Degradation of Viral Phosphoprotein

Zebrafish maoc1 Attenuates Spring Viremia of Carp Virus Propagation by Promoting Autophagy-Lysosome-Dependent Degradation of Viral Phosphoprotein

  • J Virol. 2023 Feb 6;e0133822. doi: 10.1128/jvi.01338-22.
Yanan Song # 1 2 Sijia Fan # 2 Dawei Zhang 2 Jun Li 2 Zhi Li 2 Ziyi Li 2 Wuhan Xiao 2 3 4 5 Jing Wang 2 3 4
Affiliations

Affiliations

  • 1 College of Fisheries and Life Science, Dalian Ocean University, Dalian, People's Republic of China.
  • 2 State Key Laboratory of Freshwater Ecology and Biotechnology, Institute of Hydrobiology, Chinese Academy of Sciences, Wuhan, People's Republic of China.
  • 3 The Innovation Academy of Seed Design, Chinese Academy of Sciences, Wuhan, People's Republic of China.
  • 4 University of Chinese Academy of Sciences, Beijing, People's Republic of China.
  • 5 Hubei Hongshan Laboratory, Wuhan, People's Republic of China.
  • # Contributed equally.
Abstract

Spring viremia of carp virus (SVCV) is the causative agent of spring viremia of carp (SVC), an important infectious disease that causes high mortality in aquaculture cyprinids. How the host defends against SVCV Infection and the underlying mechanisms are still elusive. In this study, we identify that a novel gene named maoc1 is induced by SVCV Infection. maoc1-deficient zebrafish are more susceptible to SVCV Infection, with higher virus replication and Antiviral gene induction. Further assays indicate that maoc1 interacts with the P protein of SVCV to trigger P protein degradation through the autophagy-lysosomal pathway, leading to the restriction of SVCV propagation. These findings reveal a unique zebrafish defense machinery in response to SVCV Infection. IMPORTANCE SVCV P protein plays an essential role in the virus replication and viral immune evasion process. Here, we identify maoc1 as a novel SVCV-inducible gene and demonstrate its Antiviral capacity through attenuating SVCV replication, by directly binding to P protein and mediating its degradation via the autophagy-lysosomal pathway. Therefore, this study not only reveals an essential role of maoc1 in fighting against SVCV Infection but also demonstrates an unusual host defense mechanism in response to invading viruses.

Keywords

SVCV; autophagy; maoc1; phosphoprotein; propagation.

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