As a severe disease characterized by reproductive failure and respiratory distress, porcine reproductive and respiratory syndrome (PRRS) is one of the most leading threats to the swine industry worldwide. Highly evolving porcine reproductive and respiratory syndrome virus (PRRSV) strains with distinct genetic diversity make the current vaccination strategy much less cost-effective and thus urge alternative protective host directed therapeutic approaches. RACK1-PKC-NF-κB signalling axis was suggested as a potential therapeutic target for PRRS control, therefore we tested the inhibitory effect of PKC inhibitor dequalinium chloride (DECA) on the PRRSV infection in vitro. RT-qPCR, western blot, Co-IP and cytopathic effect (CPE) observations revealed that DECA suppressed PRRSV infection and protected Marc-145 cells and porcine alveolar macrophages (PAMs) from severe cytopathic effects, by repressing the PKCα expression, the interaction between RACK1 and PKCα, and subsequently the NF-κB activation. In conclusion, the data presented in this study shed more light on deeper understanding of the molecular pathogenesis upon PRRSV infection and more importantly suggested DECA as a potential promising drug candidate for PRRS control.

作为一种以生殖衰竭和呼吸窘迫为特征的严重疾病，猪生殖与呼吸综合症（PRRS）是全球养猪业最主要的威胁之一。具有高度遗传多样性的高度发展的猪繁殖与呼吸综合症病毒（PRRSV）菌株使当前的疫苗接种策略的成本效益大大降低，因此敦促采用其他保护性宿主指导的治疗方法。RACK1-PKC-NF-κB信号轴被认为是PRRS控制的潜在治疗靶标，因此我们在体外测试了PKC抑制剂去氯奎宁（DECA）对PRRSV感染的抑制作用。RT-qPCR，Western印迹，Co-IP和细胞病变效应（CPE）观察表明，DECA抑制PKCα表达，相互作用和相互作用，从而抑制PRRSV感染并保护Marc-145细胞和猪肺泡巨噬细胞（PAM）免受严重的细胞病变作用。 RACK1和PKCα，然后激活NF-κB。总之，本研究中提供的数据为更深入地了解PRRSV感染后的分子发病机理提供了更多信息，更重要的是表明DECA作为PRRS控制的潜在有希望的候选药物。