Porcine deltacoronavirus (PDCoV) is a novel swine enteropathogenic coronavirus that causes watery diarrhea, vomiting and mortality in nursing piglets. Type III interferons (IFN-λs) are the major antiviral cytokines in intestinal epithelial cells, the target cells in vivo for PDCoV. In this study, we found that PDCoV infection remarkably inhibited Sendai virus-induced IFN-λ1 production by suppressing transcription factors IRF and NF-κB in IPI-2I cells, a line of porcine intestinal mucosal epithelial cells. We also confirmed that PDCoV infection impeded the activation of IFN-λ1 promoter stimulated by RIG-I, MDA5 and MAVS, but not by TBK1 and IRF1. Although the expression levels of IRF1 and MAVS were not changed, PDCoV infection resulted in reduction of the number of peroxisomes, the platform for MAVS to activate IRF1, and subsequent type III IFN production. Taken together, our study demonstrates that PDCoV suppresses type III IFN responses to circumvent the host’s antiviral immunity.

猪三角冠状病毒（PDCoV）是一种新型的猪肠道致病性冠状病毒，可引起哺乳仔猪腹泻，呕吐和死亡。III型干扰素（IFN-λs）是肠道上皮细胞（体内靶细胞）中的主要抗病毒细胞因子用于PDCoV。在这项研究中，我们发现PDCoV感染通过抑制IPI-2I细胞（猪肠粘膜上皮细胞系）中的转录因子IRF和NF-κB来显着抑制仙台病毒诱导的IFN-λ1产生。我们还证实，PDCoV感染阻止了RIG-1，MDA5和MAVS刺激的IFN-λ1启动子的激活，但不阻止TBK1和IRF1的刺激。尽管IRF1和MAVS的表达水平没有改变，但PDCoV感染导致过氧化物酶体的减少，MAVS激活IRF1的平台以及随后的III型IFN产生。两者合计，我们的研究表明PDCoV抑制III型IFN反应，以规避宿主的抗病毒免疫力。