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TRIM22 inhibits respiratory syncytial virus replication by targeting JAK‐STAT1/2 signaling
Author(s) -
Wang Yishu,
Chen Yiling,
Lin Ying,
Quan Yingqin,
Xiao Xiaoping,
Zhang Renli
Publication year - 2021
Publication title -
journal of medical virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.782
H-Index - 121
eISSN - 1096-9071
pISSN - 0146-6615
DOI - 10.1002/jmv.26436
Subject(s) - virology , virus , viral replication , stat1 , downregulation and upregulation , immune system , biology , immunology , interferon , gene , genetics
Respiratory syncytial virus (RSV) infection is a major cause of lower respiratory tract disease. Although RSV causes major economic losses every year, effective treatments have not been found so far. Recent studies have shown that the tripartite motif‐containing (TRIM) superfamily plays an essential role in the immune response. In this study, we found that TRIM22 had an inhibitory effect on RSV infection, and downregulation of TRIM22 moderately enhanced RSV replication. Our data further demonstrated that RSV infection induced TRIM22 expression through the activation of JAK‐STAT1/2 signaling. RSV infection also induced TRIM22 expression. Taken together, these data points showed that the TRIM family member, TRIM22, had an essential role in resisting RSV infection, and this effect was closely related to the JAK‐STAT1/2 pathway. Our results provide promising evidence for a novel target for the prevention and treatment of RSV.