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<p>Variants in the hepatitis B virus (HBV) PreS/S gene have been suggested to contribute to the development of progressive liver disease. This study aimed to evaluate the association between HBV PreS/S variations and liver histopathology in patients with chronic hepatitis B. A total of 109 patients under clinical follow-up for chronic hepatitis B were included. The HBV PreS/S gene was amplified by PCR and sequenced using the Sanger method. Amino acid substitutions, nonsense mutations, and deletions were analyzed in relation to liver fibrosis stage. Overall, 58 of 389 amino acid sites (14.9%) in the HBV PreS/S gene showed substitutions, with the highest mutation rate observed in the PreS2 region (27.27%). Mutations L54P (PreS1), F130L/S (PreS2), and S207R/N/I/T and I208T (S gene) were significantly more frequent in patients with advanced fibrosis (F ≥ 3) (<i>p</i> &lt; 0.05). Multivariable analysis identified S207R/N/I/T as an independent risk factor for liver fibrosis. Patients with PreS2 mutations had higher fibrosis scores (<i>p</i> &lt; 0.05). The S207R/N/I/T mutation in the C-terminal region of the HBV S protein is independently associated with liver fibrosis, while PreS2 mutations may contribute to fibrosis progression in chronic hepatitis B.</p>

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HBV PreS/S gene mutations in patients with chronic hepatitis B

  • 期刊论文

  • 发表日期：

    2026年7月25日

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  • Bülent Çakal,
  • Bilger Çavuş,
  • Alp Atasoy,
  • Mesut Bulakçı,
  • Mine Güllüoğlu,
  • Filiz Akyüz

摘要

Variants in the hepatitis B virus (HBV) PreS/S gene have been suggested to contribute to the development of progressive liver disease. This study aimed to evaluate the association between HBV PreS/S variations and liver histopathology in patients with chronic hepatitis B. A total of 109 patients under clinical follow-up for chronic hepatitis B were included. The HBV PreS/S gene was amplified by PCR and sequenced using the Sanger method. Amino acid substitutions, nonsense mutations, and deletions were analyzed in relation to liver fibrosis stage. Overall, 58 of 389 amino acid sites (14.9%) in the HBV PreS/S gene showed substitutions, with the highest mutation rate observed in the PreS2 region (27.27%). Mutations L54P (PreS1), F130L/S (PreS2), and S207R/N/I/T and I208T (S gene) were significantly more frequent in patients with advanced fibrosis (F ≥ 3) (p < 0.05). Multivariable analysis identified S207R/N/I/T as an independent risk factor for liver fibrosis. Patients with PreS2 mutations had higher fibrosis scores (p < 0.05). The S207R/N/I/T mutation in the C-terminal region of the HBV S protein is independently associated with liver fibrosis, while PreS2 mutations may contribute to fibrosis progression in chronic hepatitis B.