Single von Willebrand factor C-domain protein confers host defense against white spot syndrome virus by functioning as a pattern recognition receptor in Macrobrachium nipponense
文献类型： 外文期刊
作者： Qin, Nan 1 ; Li, Muyi 1 ; Zhang, Han 1 ; Li, Feifei 1 ; Guo, Xinrui 1 ; Wu, Mengjia 1 ; Zhang, Qingli 3 ; Tang, Ting 1 ; Liu, Fengsong 1 ;
作者机构： 1.Hebei Univ, Coll Life Sci, Key Lab Zool Systemat & Applicat, Baoding 071002, Peoples R China
2.Changzhi Med Coll, Dept Immunol, Changzhi 046000, Peoples R China
3.Chinese Acad Fishery Sci, Yellow Sea Fisheries Res Inst, Qingdao 266071, Peoples R China
关键词： Macrobrachium nipponense; Single von Willebrand factor C -domain protein; Antiviral immunity; Pattern recognition receptor; Phagocytosis
期刊名称：INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES （ 影响因子：8.2； 五年影响因子：7.8 ）
ISSN： 0141-8130
年卷期： 2023 年 241 卷
页码：
收录情况： SCI
摘要： The single von Willebrand factor C-domain proteins (SVWCs), also known as Vago, are primarily found in ar-thropods. Their expression was induced by nutritional status, bacterial and viral infections. Despite the promi-nence of SVWCs in antiviral immunity, the detailed molecular mechanisms remain poorly explained. SVWC has been proposed to elicit antiviral activities through its function as an interferon analog. In contrast, herein, we illustrate that an SVWC homolog from Macrobrachium nipponense (MnSVWC) confers host defense against white spot syndrome virus (WSSV) and covert mortality nodavirus (CMNV) as a pattern recognition receptor (PRR). qRT-PCR analyses demonstrated that the expression of MnSVWC was enhanced upon WSSV infection in all detected tissues, including gills, nerve cords, and hemocytes. Coating WSSV with recombinant MnSVWC (rMnSVWC) promoted the phagocytic activity of hemocytes and subsequent clearance of invasive WSSV from the prawn. On the other hand, the knockdown of MnSVWC with RNAi improved the proliferation ability of WSSV and CMNV in the prawn. Analysis of ELISA and Co-immunoprecipitation (Co-IP) showed that rMnSVWC could bind WSSV by interacting with the vesicle proteins VP26 and VP28. Co-IP analysis verified the interaction be-tween MnSVWC and calmodulin, which implies a vesicle protein-SVWC-calmodulin-clathrin-dependent mech-anism underlying the hemocyte-mediated phagocytosis against WSSV. Subsequently, MnSVWC was recognized to activate the expression of transcription factor STAT and an interferon-stimulating gene Viperin, illustrating its involvement in modulating humoral immunity via activation of the JAK/STAT pathway after WSSV infection. These findings indicate that MnSVWC could bind to WSSV as a PRR and participate in the promotion of hemocyte-mediated phagocytosis and the activation of the JAK/STAT pathway in prawns.
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