Virological and clinical implication of core promoter C1752/V1753 and T1764/G1766 mutations in hepatitis B virus genotype D infection in Mongolia

Authors

  • Abeer Elkady,

    1. Department of Clinical Molecular Informative Medicine, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan; and
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  • Yasuhito Tanaka,

    1. Department of Clinical Molecular Informative Medicine, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan; and
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  • Fuat Kurbanov,

    1. Department of Clinical Molecular Informative Medicine, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan; and
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  • Tsendsuren Oynsuren,

    1. Laboratory of Molecular Biology, The Institute of Biology, Mongolian Academy of Sciences, Ulaanbaatar, Mongolia
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  • Masashi Mizokami

    Corresponding author
    1. Department of Clinical Molecular Informative Medicine, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan; and
      Professor Masashi Mizokami, Department of Clinical Molecular Informative Medicine, Nagoya City University Graduate School of Medical Sciences, Kawasumi 1, Mizhuo, Nagoya 467-8601, Japan. Email: mizokami@med.nagoya-cu.ac.jp
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Professor Masashi Mizokami, Department of Clinical Molecular Informative Medicine, Nagoya City University Graduate School of Medical Sciences, Kawasumi 1, Mizhuo, Nagoya 467-8601, Japan. Email: mizokami@med.nagoya-cu.ac.jp

Abstract

Background and Aim:  The aim of the present study was to reveal virological and clinical features of hepatitis B virus (HBV) genotype D infection.

Methods:  One hundred and twenty-two Mongolian chronic liver disease (CLD) patients infected with HBV were subjected for serological HBV-markers screening and HBV-enzyme immunoassay (EIA) genotyping. Nucleotide sequences were analyzed for 48 HBV/D strains (23 isolated from hepatocellular carcinoma (HCC) and 25 from CLD patients).

Results:  Prevalence of hepatitis B e antigen (HBeAg) positivity was low (25.9%) in young patients (≤30 years old) indicating early HBeAg seroclearance in HBV/D carriers. The T1764/G1766 double mutation was the most common basal core promoter (BCP) mutation (29.2%) and was frequent in HBeAg-negative patients (39.3%). Patients harboring T1764/G1766 mutants exhibited lower HBV-DNA and HBV core antigen (HBcAg) levels than those with wild-type BCP strains (P = 0.024, 0.049, respectively). C1752 and/or V (not T) 1753 mutation was significantly prevalent in HCC patients (HCC vs CLD; 52.2% vs 20%, P = 0.033). T1762/A1764 mutation was detected in 75.0% of HCC patients with high viral load (≥5 log copies/mL). Precore stop codon mutation A1896 was detected in (70.8%) of HBV/D-infected patients.

Conclusions:  In Mongolians infected with HBV/D, C1752 and/or V1753 mutation was associated with HCC.

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