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TRIM22 通过靶向 JAK-STAT1/2 信号通路抑制呼吸道合胞病毒复制。

TRIM22 inhibits respiratory syncytial virus replication by targeting JAK-STAT1/2 signaling.

机构信息

Institute of Pathogenic Organisms, Shenzhen Center for Disease Control and Prevention, Shenzhen, Guangdong, China.

Department of Biology, Southern University of Science and Technology (SUSTech), Shenzhen, China.

出版信息

J Med Virol. 2021 Jun;93(6):3412-3419. doi: 10.1002/jmv.26436. Epub 2020 Sep 28.

DOI:10.1002/jmv.26436
PMID:32803897
Abstract

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.

摘要

呼吸道合胞病毒(RSV)感染是下呼吸道疾病的主要原因。尽管 RSV 每年造成重大的经济损失,但迄今为止尚未找到有效的治疗方法。最近的研究表明,三结构域含(TRIM)家族在免疫反应中起着至关重要的作用。在这项研究中,我们发现 TRIM22 对 RSV 感染具有抑制作用,下调 TRIM22 可适度增强 RSV 复制。我们的数据进一步表明,RSV 感染通过激活 JAK-STAT1/2 信号诱导 TRIM22 的表达。RSV 感染也诱导了 TRIM22 的表达。总之,这些数据表明,TRIM 家族成员 TRIM22 在抵抗 RSV 感染中起着至关重要的作用,这种作用与 JAK-STAT1/2 途径密切相关。我们的研究结果为 RSV 的预防和治疗提供了有前景的新靶点。

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