ZFP36 Facilitates Senecavirus A (SVA) replication by inhibiting the production of type I interferon.

Virus Res

National Key Laboratory of Agricultural Microbiology, Hubei Hongshan Laboratory, Huazhong Agricultural University, Wuhan, Hubei 430070, China; College of Veterinary Medicine, Huazhong Agricultural University, Wuhan, Hubei 430070, China; Key Laboratory of Preventive Veterinary Medicine in Hubei Province, The Cooperative Innovation Center for Sustainable Pig Production, Wuhan, Hubei 430070, China; Key Laboratory of Development of Veterinary Diagnostic Products, Ministry of Agriculture of the People's Republic of China, Wuhan, Hubei 430070, China. Electronic address:

Published: December 2024

Zinc finger proteins (ZFPs) play an important role in the host-virus interplay. Zinc finger protein 36 is a member of the zinc finger protein 36 family, which includes two other paralogs, namely ZFP36L1 and ZFP36L2. Studies have demonstrated that ZFP36L1 acts as a host defender against influenza A virus and flaviviruses. However, the role of ZFP36 in host-virus interactions has not been thoroughly investigated. Here, we demonstrated that human zinc finger protein 36 (hZFP36) exhibited potent pro-viral activity during Senecavirus A infection. Overexpression of ZFP36 facilitated Senecavirus A infection, while hZFP36 knockdown inhibited viral replication. The ZF motifs of hZFP36 are key for promoting viral proliferation. hZFP36 stabilized Senecavirus A VP1 by binding to it. Furthermore, hZFP36 inhibited SeV-mediated IFN-β production through inducing caspase-dependent cleavage for MAVS. These findings provide insights into the mechanism of action of ZFP36 in host-virus interactions.

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Source
http://dx.doi.org/10.1016/j.virusres.2024.199498DOI Listing

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