文献类型： 外文期刊

作者： Lv, Lin ¹ ; Zhang, Tianyun ² ; Jia, Hanying ² ; Zhang, Yanyan ³ ; Ahsan, Asif ² ; Zhao, Xiaoyang ² ; Chen, Teng ³ ; Shen, Zhiqiang ⁴ ; Shen, Ning ² ;

作者机构： 1.Zhejiang Univ, Affiliated Hosp 1, Coll Med, Dept Infect Dis, Hangzhou, Zhejiang, Peoples R China

2.Zhejiang Univ, Med Ctr, Liangzhu Lab, Hangzhou, Zhejiang, Peoples R China

3.Chinese Acad Agr Sci, Changchun Vet Res Inst, Changchun, Jilin, Peoples R China

4.Shandong Acad Agr Sci, Shandong Binzhou Acad Anim Sci & Vet Med, Binzhou, Shandong, Peoples R China

5.Shandong Lvdu Biosci & Technol Co Ltd, Binzhou, Shandong, Peoples R China

6.Zhejiang Univ, Affiliated Hosp 1, Coll Med, Dept Hepatobiliary & Pancreat Surg, Hangzhou, Zhejiang, Peoples R China

关键词： ASFV; transcriptome; host-virus interaction; inflammatory; immune response; pathogenicity

期刊名称：FRONTIERS IN IMMUNOLOGY （ 影响因子：8.786； 五年影响因子：8.876 ）

ISSN： 1664-3224

年卷期： 2022 年 13 卷

页码：

收录情况： SCI

摘要： African swine fever virus (ASFV) causes a lethal swine hemorrhagic disease and is currently responsible for widespread damage to the pig industry. The pathogenesis of ASFV infection and its interaction with host responses remain poorly understood. In this study, we profiled the temporal viral and host transcriptomes in porcine alveolar macrophages (PAMs) with virulent and attenuated ASFV strains. We identified profound differences in the virus expression programs between SY18 and HuB20, which shed light on the pathogenic functions of several ASFV genes. Through integrated computational analysis and experimental validation, we demonstrated that compared to the virulent SY18 strain, the attenuated HuB20 quickly activates expression of receptors, sensors, regulators, as well as downstream effectors, including cGAS, STAT1/2, IRF9, MX1/2, suggesting rapid induction of a strong antiviral immune response in HuB20. Surprisingly, in addition to the pivotal DNA sensing mechanism mediated by cGAS-STING pathway, infection of the DNA virus ASFV activates genes associated with RNA virus response, with stronger induction by HuB20 infection. Taken together, this study reveals novel insights into the host-virus interaction dynamics, and provides reference for future mechanistic studies of ASFV pathogenicity.