Immune evasion strategies of Seneca Valley virus: mechanisms of host innate immune suppression

Seneca Valley virus (SVV), an emerging picornavirus, poses a significant threat to the global swine industry. Innate immunity acts as the initial defense mechanism of host cells against viral infection. Upon infection, viruses can be detected by the cellular host's pattern recognition receptors (PRRs), which trigger the activation of signaling cascades and the strong production of type I interferon (IFN-I) to limit viral replication. SVV employs diverse strategies to evade innate immunity, primarily through 3C protease, which targets host antiviral proteins to antagonize IFN-I signaling. Additionally, SVV hijacks autophagy, apoptosis, and pyroptosis to facilitate its own replication. In this review, we summarize recent research on the underlying mechanisms employed by SVV to manipulate host innate immune response and programmed cell death pathways. This review will provide insights for the design of SVV vaccines and contribute to the prevention and control of SVV infection.