AI Article Synopsis
- Salmon alphavirus (SAV) causes serious pancreas disease in fish like Atlantic salmon and rainbow trout, leading to inflammation.
- A protein from the virus called Nsp2 helps reduce inflammation by activating a signaling pathway called NF-κB, but how it does this was not well understood before this study.
- Researchers found that a host protein named DDX3 interacts with Nsp2, and when DDX3 is more active, it stops Nsp2 from working on NF-κB, but Nsp2 can relieve this inhibition and trigger an immune response.
Article Abstract
Salmon alphavirus (SAV) infection leads to severe pancreas disease (PD) with typical inflammatory responses in Atlantic salmon (Salmo salar) and rainbow trout (Oncorhynchus mykiss). Nsp2, an important nonstructural protein of SAV, can activate NF-κB signaling pathway to reduce inflammatory responses. However, the molecular mechanism remains unclear. In this study, the ML (279-421aa) of Nsp2 was revealed to be the key domain for activating NF-κB. We focused on a host protein, DEAD-box RNA helicase 3 (DDX3), that may interact with Nsp2 to regulate NF-κB-induced inflammatory. The interaction between DDX3 and Nsp2 was confirmed in vitro. Overexpression of DDX3 inhibited the activation of NF-κB by Nsp2. SAV Nsp2 relieves the inhibitory effect of DDX3 on NF-κB, thereby initiating the innate immune response. This study revealed the molecular mechanism of Nsp2-induced inflammatory response by targeting DDX3 to activate NF-κB, providing a theoretical basis for revealing the underlying infection mechanism and pathogenesis of SAV.
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| http://dx.doi.org/10.1016/j.dci.2022.104612 | DOI Listing |
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