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ZNF33B Promotes Japanese Encephalitis Virus Infection by Regulating the Stability of M6A-Modified Trim25 to Control
Jian Du1,2,3, Chunwei Li1,2,3, Jiyuan Luo1,2,3
1National Key Laboratory of Agricultural Microbiology, Hubei Hongshan Laboratory, Huazhong Agricultural University, Wuhan, 430070, P. R. China.
Advanced Science (Weinheim, Baden-Wurttemberg, Germany)
|June 18, 2026
Summary
Japanese encephalitis virus (JEV) infection is promoted by ZNF33B, a host factor that links RNA modification (m6A) to autophagy. This mechanism helps JEV evade antiviral defenses.
Area of Science:
- Virology
- Molecular Biology
- Immunology
Background:
- Japanese encephalitis virus (JEV) poses a significant threat, but its replication mechanisms, particularly epitranscriptomic ones, are unclear.
- Understanding host-pathogen interactions is crucial for developing antiviral strategies.
Purpose of the Study:
- To identify host factors and epitranscriptomic mechanisms that regulate JEV replication.
- To elucidate the role of N6-methyladenosine (m6A) RNA modification in JEV pathogenesis.
Main Methods:
- Investigated the role of ZNF33B in JEV infection using cell culture and in vivo mouse models.
- Employed multi-omics analyses, including m6A profiling and protein-protein interaction studies.
- Utilized adeno-associated virus (AAV) for in vivo gene delivery.
Main Results:
- Identified ZNF33B as a proviral host factor that enhances JEV replication by regulating m6A modification and autophagy.
- ZNF33B stabilizes the METTL3-METTL14 complex, increasing global m6A levels.
- ZNF33B promotes Trim25 decay, counteracting its suppression of autophagy and favoring viral replication.
- In vivo, ZNF33B exacerbates JEV-induced neuropathology and mortality.
Conclusions:
- Discovered a novel ZNF33B-m6A-TRIM25-autophagy pathway exploited by JEV to evade host immunity.
- This axis represents a potential therapeutic target for flaviviral infections.
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