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

IF 2.5 Q2 GASTROENTEROLOGY & HEPATOLOGY

World Journal of Hepatology Pub Date : 2025-02-27 DOI:10.4254/wjh.v17.i2.99292

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

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引用次数: 0

Abstract

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-β production.

Conclusion: HBV-miR-3 plays an important role in HBV immunity evasion by targeting cGAS 3'-UTR and interfering with cGAS-Sting-IFN pathway.

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乙型肝炎病毒通过乙型肝炎病毒- mir -3下调cGAS-Sting-IFN信号通路实现先天性免疫逃避。

背景：乙型肝炎病毒（Hepatitis B virus， HBV）可逃避先天免疫，导致持续性慢性感染，但其分子机制尚不清楚。目的：探讨HBV- mir -3是否参与HBV免疫逃避。方法：采用HBV-miR-3 agomir和antagomir，通过荧光素酶相对活性、cGAS蛋白表达、Sting磷酸化和干扰素（IFN）产生实验，验证HBV-miR-3对cGAS-Sting-IFN通路的有效性。结果：HBV-miR-3转录后通过抑制cGAS 3'-非翻译区（3'-UTR）活性下调cGAS蛋白表达，导致Sting磷酸化和IFN产生降低。HBV-miR-3拮抗剂可挽救cGAS蛋白表达、Sting磷酸化和IFN-β的产生。结论：HBV- mir -3通过靶向cGAS 3′-UTR，干扰cGAS- sting - ifn通路，在HBV免疫逃避中发挥重要作用。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

World Journal of Hepatology GASTROENTEROLOGY & HEPATOLOGY-

CiteScore

4.10

自引率

4.20%

发文量

172