Enterovirus D68 infection upregulates SOCS3 expression to inhibit JAK-STAT3 signaling and antagonize the innate interferon response of the host
作者机构：School of Life SciencesTianjin UniversityTianjin300072China School of Environmental Science and EngineeringTianjin UniversityTianjin300072China Institute of Tianjin Key Laboratory of Function and Application of Biological Macromolecular StructuresTianjin300072China
出 版 物：《Virologica Sinica》 (中国病毒学(英文版))
年 卷 期：2023年第38卷第5期
页 面：755-766页
核心收录：
学科分类：0710[理学-生物学] 1004[医学-公共卫生与预防医学(可授医学、理学学位)] 100401[医学-流行病与卫生统计学] 10[医学]
基 金：This work was supported by the National Natural Science Foundation of China(32170144)
主 题：Enterovirus D68(EV-D68) Interferon ISG SOCS3 STAT3
摘 要：Enterovirus D68(EV-D68)can cause respiratory diseases and acute flaccid paralysis,posing a great threat to public *** are cytokines secreted by host cells that have broad-spectrum antiviral effects,inducing the expression of hundreds of interferon-stimulated genes(ISGs).EV-D68 activates ISG expression early in infection,but at a later stage,the virus suppresses ISG expression,a strategy evolved by EV-D68 to antagonize ***,we explore a host protein,suppressor of cytokine signaling 3(SOCS3),is upregulated during EV-D68 infection and antagonizes the antiviral effects of type I *** subsequently demonstrate that the structural protein of EV-D68 upregulated the expression of RFX7,a transcriptional regulator of SOCS3,leading to the upregulation of SOCS3 *** exploration revealed that SOCS3 plays its role by inhibiting the phosphorylation of signal transducer and activator of transcription 3(STAT3).The expression of SOCS3 inhibited the expression of ISG,thereby inhibiting the antiviral effect of type I interferon and promoting EV-D68 transcription,protein production,and viral ***,a truncated SOCS3,generated by deleting the kinase inhibitory region(KIR)domain,failed to promote replication and translation of *** on the above studies,we designed a short peptide named SOCS3 inhibitor,which can specifically bind and inhibit the KIR structural domain of SOCS3,significantly reducing the RNA and protein levels of *** summary,our results demonstrated a novel mechanism by which EV-D68 inhibits ISG transcription and antagonizes the antiviral responses of host type I interferon.
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