Hepatitis B virus confers innate immunity evasion through hepatitis B virus-miR-3 down-regulation of cGAS-Sting-IFN signaling  

作　　者：Zhen-Yu Xu Jia-Shi Gao Ying He Xin-Qiang Xiao Guo-Zhong Gong Min Zhang 

机构地区：[1]Department of Infectious Diseases,The Second Xiangya Hospital,Central South University,Changsha 410011,Hunan Province,China [2]Institute of Hepatology and Department of Infectious Diseases,The Second Xiangya Hospital,Central South University,Changsha 410011,Hunan Province,China

出　　处：《World Journal of Hepatology》2025年第2期159-169,共11页世界肝病学杂志(英文)

基　　金：Supported by National Natural Science Foundation of China,Key Project,No.82430071;The Scientific Research Program of FuRong Laboratory,No.2023SK2108;Clinical Medical Research Center for Viral Hepatitis of Hunan Province,No.2023SK4009;Hunan Provincial Natural Science Foundation,No.2023JJ60440;Hunan Provincial Health Commission Research Program,No.C202303088786.

摘　　要：BACKGROUND Hepatitis B virus(HBV)evades the innate immunity and leads to persistent chronic infection,but the molecular mechanism is still not well known.AIM To investigate whether HBV-miR-3 is involved in HBV immune evasion.METHODS HBV-miR-3 agomir and antagomir were employed to verify the effectiveness of HBV-miR-3 on cGAS-Sting-IFN pathway through the experiments on relative luciferase activity,cGAS protein expression,Sting phosphorylation and interferon(IFN)production.RESULTS HBV-miR-3 down-regulates cGAS protein expression post-transcriptionally by inhibition of cGAS 3’-untranslated region(3’-UTR)activity,which results in lower Sting phosphorylation and IFN production.HBV-miR-3 antagomir rescued cGAS protein expression,Sting phosphorylation and IFN-βproduction.CONCLUSION HBV-miR-3 plays an important role in HBV immunity evasion by targeting cGAS 3’-UTR and interfering with cGAS-Sting-IFN pathway.

关 键 词：Hepatitis B virus HBV-miR-3 cGAS Sting IFN-Β 

分 类 号：R51[医药卫生—内科学]