Infectious bursal disease virus replication is inhibited by avain T cell chemoattractant chemokine CCL19.
CCL19
T cell
chemokine
infectious bursal disease virus
virus replication
Journal
Frontiers in microbiology
ISSN: 1664-302X
Titre abrégé: Front Microbiol
Pays: Switzerland
ID NLM: 101548977
Informations de publication
Date de publication:
2022
2022
Historique:
received:
05
04
2022
accepted:
27
06
2022
entrez:
8
8
2022
pubmed:
9
8
2022
medline:
9
8
2022
Statut:
epublish
Résumé
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.
Identifiants
pubmed: 35935208
doi: 10.3389/fmicb.2022.912908
pmc: PMC9355407
doi:
Types de publication
Journal Article
Langues
eng
Pagination
912908Informations de copyright
Copyright © 2022 Wang, Chu, Zhang, Hu, Lu, Wang, Yu, Zhang, Ma, Xu, Eldemery, Ou and Liu.
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