文献类型：期刊文献

英文题名：Infectious bursal disease virus replication is inhibited by avain T cell chemoattractant chemokine CCL19

作者：Wang, Qiuxia[1];Chu, Fuming[1];Zhang, Xin[1];Hu, Huilong[1];Lu, Lang[1];Wang, Fang[1];Yu, Yan[1];Zhang, Yanhong[1];Ma, Jinyou[1];Xu, Zhiyong[1];Eldemery, Fatma[2];Ou, Changbo[1,3];Liu, Xingyou[1,4]

第一作者：Wang, Qiuxia

通讯作者：Ou, CB[1];Liu, XY[1];Ou, CB[2];Liu, XY[3]

机构：[1]Henan Inst Sci & Technol, Coll Anim Sci & Vet Med, Xinxiang, Peoples R China;[2]Mansoura Univ, Fac Vet Med, Dept Hyg & Zoonoses, Mansoura, Egypt;[3]Guangxi Univ, Coll Anim Sci & Technol, Nanning, Peoples R China;[4]Xinxiang Univ, Coll Life Sci, Xinxiang, Peoples R China

第一机构：Henan Inst Sci & Technol, Coll Anim Sci & Vet Med, Xinxiang, Peoples R China

通讯机构：[1]corresponding author), Henan Inst Sci & Technol, Coll Anim Sci & Vet Med, Xinxiang, Peoples R China;[2]corresponding author), Guangxi Univ, Coll Anim Sci & Technol, Nanning, Peoples R China;[3]corresponding author), Xinxiang Univ, Coll Life Sci, Xinxiang, Peoples R China.|[1107115]新乡学院生命科学技术学院;[11071]新乡学院;

年份：2022

卷号：13

外文期刊名：FRONTIERS IN MICROBIOLOGY

收录：;Scopus(收录号：2-s2.0-85135456488);WOS:【SCI-EXPANDED(收录号:WOS:000837133300001)】；

基金：Funding This study was supported by grant from the key Scientific and Technological Project of Henan Province (212102110009 and 202102110102), the Modern agricultural industrial technology system of Henan Province (S2012-06-G02), the Program for Innovative Research Team (in Science and Technology) in University of Henan Province (20IRTSTHN025), and the Key Scientific Research Project in University of Henan Province (21A230003).

语种：英文

外文关键词：CCL19; infectious bursal disease virus; virus replication; T cell; chemokine

摘要：Chemokine CCL19, together with its receptor CCR7, is one of the most important factors recruiting immune cells into target organ during virus infection. Our previous study has shown that CCL19 played a vital role in the process of T cell trafficking into bursae during bursal disease virus (IBDV) infection. In this study, we hypothesized that CCL19 could exert direct influences on IBDV replication other than recruiting immune cells. A eukaryotic expression vector of pEGFP-N1/CCL19 was successfully constructed and identified by PCR, double enzymes digestion, and sequencing. Different concentrations of pEGFP-N1/CCL19 plasmids were transfected into DF1 cells and CCL19 protein was highly expressed. Then, DF1 cells were infected with IBDV B87 strain post-transfection. Based on PCR and Western blot results, CCL19 could obviously decrease the gene levels of VP1 and VP2 and the protein levels of VP2 and VP3. When CCL19 was knocked down, the gene levels of VP1 and VP2 were significantly upregulated. Moreover, indirect immunostaining revealed that the IBDV content was largely decreased after CCL19 overexpression. Additionally, CCL19 inhibitory effects might rely on activation of the JNK signal pathway. Taken together, chemokine CCL19 directly blocks IBDV replication in DF1 cells, indicating that CCL19 could play crucial functions other than recruiting T cells during the pathogenesis of IBDV.