The V protein of Newcastle disease virus (NDV) has been shown to inhibit the secretion of interferon (IFN) during infection, which is responsible for the promotion of NDV pathogenicity. However, the ability of the V protein to suppress host innate immunity is not well understood. In this study, we explored the function of V protein and its relationship with virulence by generating V protein-inserted recombinant (r) NDVs. Using rNDVs as a model, we examined the efficiency of infection, IFN responses, and apoptosis of host cells during infection. We found that viral propagation occurred smoothly when V protein from lentogenic NDV is inserted instead of the V protein from the velogenic strain. The infection of lentogenic V protein-inserted rNDV induced less expression of IFNs and downstream antiviral proteins via efficient degradation of p-STAT1 and MDA5. Moreover, velogenic V protein triggered a higher apoptosis rate during infection thereby restricting the replication of NDV. Conversely, lentogenic V protein inhibits IFN responses efficiently and induces less apoptosis compared to the velogenic strain. Our findings provide a novel understanding of the role of V protein in NDV pathogenicity.

新城疫病毒 (NDV) 的 V 蛋白已被证明在感染过程中抑制干扰素 (IFN) 的分泌，干扰素 (IFN) 是促进 NDV 致病性的原因。然而，V 蛋白抑制宿主先天免疫的能力尚不清楚。在这项研究中，我们通过产生插入 V 蛋白的重组 (r) NDV 来探索 V 蛋白的功能及其与毒力的关系。使用 rNDV 作为模型，我们检查了感染效率、干扰素反应和感染过程中宿主细胞的凋亡。我们发现，当插入来自慢源 NDV 的 V 蛋白而不是来自 velogenic 毒株的 V 蛋白时，病毒繁殖会顺利进行。慢基因 V 蛋白插入的 rNDV 感染通过 p-STAT1 和 MDA5 的有效降解诱导了 IFN 和下游抗病毒蛋白的较少表达。此外，Velogenic V 蛋白在感染过程中引发更高的细胞凋亡率，从而限制了 NDV 的复制。相反，与 velogenic 菌株相比，lentogenic V 蛋白可有效抑制 IFN 反应并诱导较少的细胞凋亡。我们的发现为 V 蛋白在 NDV 致病性中的作用提供了新的理解。