The dexd/H-box helicase DHX40 is a novel negative regulator during GCRV infection via targeting the host RLR helicases and viral nonstructural protein NS38.
Autor: | Liu WJ; College of life sciences, Jiangxi Normal university, Nanchang, Jiangxi, China; Key Laboratory of Aquaculture Disease Control, Ministry of Agriculture, Institute of Hydrobiology, Chinese Academy of Sciences, Wuhan 430072, China., Chen Y; Key Laboratory of Aquaculture Disease Control, Ministry of Agriculture, Institute of Hydrobiology, Chinese Academy of Sciences, Wuhan 430072, China; University of Chinese Academy of Sciences, Beijing 100049, China., Liu Y; College of life sciences, Jiangxi Normal university, Nanchang, Jiangxi, China. Electronic address: yiliusan@jxnu.edu.cn., Chang MX; Key Laboratory of Aquaculture Disease Control, Ministry of Agriculture, Institute of Hydrobiology, Chinese Academy of Sciences, Wuhan 430072, China; University of Chinese Academy of Sciences, Beijing 100049, China. Electronic address: mingxianchang@ihb.ac.cn. |
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Jazyk: | angličtina |
Zdroj: | Fish & shellfish immunology [Fish Shellfish Immunol] 2024 Aug; Vol. 151, pp. 109730. Date of Electronic Publication: 2024 Jun 26. |
DOI: | 10.1016/j.fsi.2024.109730 |
Abstrakt: | RLR helicases RIG-I and MDA5, which are known as pattern recognition receptors to sense cytoplasmic viral RNAs and trigger antiviral immune responses, are DExD/H-box helicases. In teleost, whether and how non-RLR helicases regulate RLR helicases to affect viral infection remains unclear. Here, we report that the non-RLR helicase DHX40 from grass carp (namely gcDHX40) is a negative regulator of grass carp reovirus (GCRV) infection and RLR-mediated type I IFN production. GcDHX40 was a cytoplasmic protein. Ectopic expression of gcDHX40 facilitated GCRV replication and suppressed type I IFN production induced by GCRV infection and by those genes involved the RLR antiviral signaling pathway. Mechanistically, gcDHX40 promoted the generation of viral inclusion bodies (VIBs) by interacting with the NS38 protein of GCRV. Additionally, gcDHX40 interacted with RLR helicase, and impaired the formation of RLR-MAVS functional complexes. Taken together, our results indicate that gcDHX40 is a novel important proviral host factor involving in promoting the generation of GCRV VIBs and inhibiting the production of RLR-mediated type I IFNs. (Copyright © 2024 Elsevier Ltd. All rights reserved.) |
Databáze: | MEDLINE |
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