ArticleInfection and drug resistance2025
Impact of PC/BCP Mutations on Seroconversion and Relapse in HBeAg-Positive Chronic Hepatitis B Patients Treated with Nucleoside Analogues.
Article in Infection and drug resistance, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- qHBsAg Trajectories with Peg-IFNα-2b Add-on Therapy in Nucleos(t)ide Analog-experienced HBeAg-positive Chronic Hepatitis B.Journal of clinical and translational hepatology · 2026Article
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Precore/Basal core promotor (PC/BCP) mutations are critical mechanisms by which hepatitis B virus (HBV) evades host immunity and antiviral therapy. These mutations are prevalent in HBeAg-positive chronic hepatitis B (CHB) patients, potentially leading to suboptimal responses to nucleos(t)ide analogues (NAs) and high relapse risk after treatment discontinuation. Objective: This study aimed to investigate the impact of PC/BCP mutations on seroconversion and relapse rates and analyze their association with drug resistance mechanisms. The study also evaluated the significance of mutation count (one, two, or three mutations) and specific types of mutations (A1762T, G1764A, G1896A) in relation to the seroconversion and relapse processes. Methods: From 2016 to 2019, 48 HBeAg-positive CHB patients were collected and divided into mutation (n=37) and non-mutation (n=11) groups based on PC/BCP status. Seroconversion rates after 144 weeks of NA therapy and relapse rates after 48 weeks of treatment discontinuation were analyzed. Baseline viral load (HBV DNA), liver function (ALT), and Precore/ Basal Core Promoter (PC/BCP) mutation status were analyzed for their correlation with clinical outcomes. Results: Among the 37 patients in the mutation group, 9 exhibited G1896A mutation, 15 exhibited A1762T/G1764A double mutations, 13 exhibited A1762T/G1764A/G1896A triple mutations. The mutation group showed significantly lower seroconversion rates than the non-mutation group (37.8% vs 81.8%, Conclusion: PC/BCP mutations are independent risk factors for poor NA response and high relapse rates in HBeAg-positive CHB patients. Patients with these mutations should be managed as "occult HBeAg-negative CHB" to avoid premature treatment discontinuation. Routine PC/BCP mutation testing is recommended to guide individualized treatment duration in HBeAg-positive CHB patients.
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