Key result
Arteriviruses evade the host innate immune response by utilizing structural and nonstructural proteins to antagonize interferon production and thwart interferon-activated antiviral signaling pathways.
Why the study?
Arteriviruses infect immune cells and establish persistence by antagonizing host IFN production and antiviral signaling pathways to evade innate immunity.
This review outlines the mechanisms by which arteriviruses evade host interferon-mediated immune responses, providing a theoretical basis for vaccine development.
IFN is the most potent antiviral cytokine required for the innate and adaptive immune responses, and its expression can help the host defend against viral infection. Arteriviruses have evolved strategies to antagonize the host cell's innate immune responses, interfering with IFN expression by interfering with RIG, blocking PRR, obstructing IRF-3/7, NF-κB, and degrading STAT1 signaling pathways, thereby assisting viral immune evasion. Arteriviruses infect immune cells and may result in persistence in infected hosts. In this article, we reviewed the strategies used by Arteriviruses to antagonize IFN production and thwart IFN-activated antiviral signaling, mainly including structural and nonstructural proteins of Arteriviruses encoding IFN antagonists directly or indirectly to disrupt innate immunity. This review will certainly provide a better insight into the pathogenesis of the arthritis virus and provide a theoretical basis for developing more efficient vaccines.
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Jian et al. (2022) conducted a review in Arterivirus infection. Arteriviruses was evaluated. Arteriviruses evade the host innate immune response by utilizing structural and nonstructural proteins to antagonize interferon production and thwart interferon-activated antiviral signaling pathways.
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