{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,5]],"date-time":"2026-11-05T12:17:05Z","timestamp":1793881025068,"version":"4.7.0"},"reference-count":43,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2022,7,24]],"date-time":"2022-07-24T00:00:00Z","timestamp":1658620800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Aliment Pharmacol Ther"],"published-print":{"date-parts":[[2022,9]]},"abstract":"<jats:title>Summary<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>Hepatitis B virus (HBV) infection is a serious global health burden. TRIM26 has been reported to affect hepatitis C virus replication.<\/jats:p><\/jats:sec><jats:sec><jats:title>Aims<\/jats:title><jats:p>To manifest the role of TRIM26 on HBV replication and explore if there are single\u2010nucleotide polymorphisms (SNPs) in <jats:italic>TRIM26<\/jats:italic> associated with response to pegylated interferon\u2010alpha (PegIFN\u03b1) treatment in patients with chronic hepatitis B (CHB).<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>We investigated the effect and mechanism of TRIM26 on HBV replication in vitro. The association between SNPs in <jats:italic>TRIM26<\/jats:italic> and PegIFN\u03b1 treatment response was evaluated in two independent cohorts including 238 and 707 patients with HBeAg\u2010positive CHB.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Knockdown of TRIM26 increased, while overexpression of TRIM26 inhibited, HBV replication. Co\u2010immunoprecipitation assays and immunofluorescence showed that TRIM26 interacted and co\u2010localised with HBx. Co\u2010transfection of HBx\u2010HIS and TRIM26\u2010FLAG plasmids in Huh7 cells showed that TRIM26 inhibited the expression of HBx. Furthermore, TRIM26 inhibited HBV replication by mediating HBx ubiquitination degradation, and TRIM26 SPRY domain was responsible for the interaction and degradation of HBx. Besides, IFN increased TRIM26 expression. <jats:italic>TRIM26<\/jats:italic> rs116806878 was associated with response to PegIFN\u03b1 in two CHB cohorts. Moreover, a polygenic score integrating <jats:italic>TRIM26<\/jats:italic> rs116806878, <jats:italic>STAT4<\/jats:italic> rs7574865 and <jats:italic>CFB<\/jats:italic> rs12614 (previously reported to be associated with response to PegIFN\u03b1) was related to response to PegIFN\u03b1 in CHB.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>TRIM26 inhibits HBV replication; IFN promotes TRIM26 expression. TRIM26 exerts an inhibitory effect on HBx by promoting ubiquitin\u2010mediated degradation of HBx. Furthermore, <jats:italic>TRIM26<\/jats:italic> rs116806878 is a potential predictive biomarker of response to PegIFN\u03b1 in patients with CHB.<\/jats:p><\/jats:sec>","DOI":"10.1111\/apt.17124","type":"journal-article","created":{"date-parts":[[2022,7,25]],"date-time":"2022-07-25T05:34:11Z","timestamp":1658727251000},"page":"878-889","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":22,"title":["<scp>TRIM26<\/scp> inhibits hepatitis B virus replication by promoting <scp>HBx<\/scp> degradation and <i>TRIM26<\/i> genetic polymorphism predicts <scp>PegIFN\u03b1<\/scp> treatment response of <scp>HBeAg\u2010positive<\/scp> chronic hepatitis B Patients"],"prefix":"10.1111","volume":"56","author":[{"given":"Mengqi","family":"Luo","sequence":"first","affiliation":[{"name":"State Key Laboratory of Organ Failure Research, Guangdong Key Laboratory of Viral Hepatitis Research, Department of Infectious Diseases and Hepatology Unit 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