{"title":"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。","authors":"Zhen-Yu Xu, Jia-Shi Gao, Ying He, Xin-Qiang Xiao, Guo-Zhong Gong, Min Zhang","doi":"10.4254/wjh.v17.i2.99292","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Hepatitis B virus (HBV) evades the innate immunity and leads to persistent chronic infection, but the molecular mechanism is still not well known.</p><p><strong>Aim: </strong>To investigate whether HBV-miR-3 is involved in HBV immune evasion.</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>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.</p><p><strong>Conclusion: </strong>HBV-miR-3 plays an important role in HBV immunity evasion by targeting cGAS 3'-UTR and interfering with cGAS-Sting-IFN pathway.</p>","PeriodicalId":23687,"journal":{"name":"World Journal of Hepatology","volume":"17 2","pages":"99292"},"PeriodicalIF":2.5000,"publicationDate":"2025-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11866139/pdf/","citationCount":"0","resultStr":"{\"title\":\"Hepatitis B virus confers innate immunity evasion through hepatitis B virus-miR-3 down-regulation of cGAS-Sting-IFN signaling.\",\"authors\":\"Zhen-Yu Xu, Jia-Shi Gao, Ying He, Xin-Qiang Xiao, Guo-Zhong Gong, Min Zhang\",\"doi\":\"10.4254/wjh.v17.i2.99292\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>Hepatitis B virus (HBV) evades the innate immunity and leads to persistent chronic infection, but the molecular mechanism is still not well known.</p><p><strong>Aim: </strong>To investigate whether HBV-miR-3 is involved in HBV immune evasion.</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>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.</p><p><strong>Conclusion: </strong>HBV-miR-3 plays an important role in HBV immunity evasion by targeting cGAS 3'-UTR and interfering with cGAS-Sting-IFN pathway.</p>\",\"PeriodicalId\":23687,\"journal\":{\"name\":\"World Journal of Hepatology\",\"volume\":\"17 2\",\"pages\":\"99292\"},\"PeriodicalIF\":2.5000,\"publicationDate\":\"2025-02-27\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11866139/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"World Journal of Hepatology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.4254/wjh.v17.i2.99292\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"GASTROENTEROLOGY & HEPATOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"World Journal of Hepatology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.4254/wjh.v17.i2.99292","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"GASTROENTEROLOGY & HEPATOLOGY","Score":null,"Total":0}
引用次数: 0
摘要
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。
Hepatitis B virus confers innate immunity evasion through hepatitis B virus-miR-3 down-regulation of cGAS-Sting-IFN signaling.
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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