文献类型： 外文期刊
作者： Nan, Fu Long 1 ; Zhang, He 2 ; Nan, Wen Long 3 ; Xie, Chang Zhan 2 ; Ha, Zhuo 2 ; Chen, Xing 4 ; Xu, Xiao Hong 1 ; Qian, 1 ;
作者机构： 1.Jilin Univ, Coll Vet Med, Coll Anim Sci, Changchun 130062, Peoples R China
2.Acad Mil Med Sci, Inst Mil Vet Med, Changchun 130122, Peoples R China
3.China Anim Hlth & Epidemiol Ctr, Qingdao 266032, Peoples R China
4.Changchun Inst Biol Prod Co Ltd, Changchun 130012, Peoples R China
5.Jiangsu Acad Agr Sci, Inst Vet Med, Nanjing 210014, Peoples R China
6.Chinese Acad Agr Sci, Shanghai Vet Res Inst, Shanghai 200241, Peoples R China
7.Chinese Acad Agr Sci, Harbin Vet Res Inst, State Key Lab Vet Biotechnol, Harbin 150001, Peoples R China
关键词： NDV; V Protein; Virulence; IFN antagonist; Apoptosis
期刊名称：VETERINARY MICROBIOLOGY （ 影响因子：3.293； 五年影响因子：3.599 ）
ISSN： 0378-1135
年卷期： 2021 年 261 卷
页码：
收录情况： SCI
摘要： 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.
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