The clinical implications of hepatitis B virus genotype: Recent advances

Authors

  • Chih-Lin Lin,

    1. Department of Gastroenterology, Ren-Ai branch, Taipei City Hospital, Taipei, Taiwan
    2. Department of Psychology, National Chengchi University, Taipei, Taiwan
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  • Jia-Horng Kao

    Corresponding author
    1. Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan
    2. Graduate Institute of Clinical Medicine, Hepatitis Research Center
    3. Department of Medical Research
    4. National Taiwan University College of Medicine and National Taiwan University Hospital, Taipei, Taiwan
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  • Conflict of interest
    The authors have declared that they have no conflict of interest.

Prof Jia-Horng Kao, Director and Distinguished Professor, Graduate Institute of Clinical Medicine, National Taiwan University College of Medicine, 1 Chang-Te St., Taipei 10002, Taiwan. Email: kaojh@ntu.edu.tw

Abstract

Outcomes of chronic hepatitis B virus (HBV) infection are heterogeneous. Estimates of annual incidence of cirrhosis and hepatocellular carcinoma (HCC) are 2–10% and 1–3%, respectively. Several viral factors, including HBV genotype, viral load and specific viral mutations, have been associated with disease progression. Among these, HBV genotype is not only predictive of clinical outcomes but has also been associated with response to interferon treatment. Currently, at least 10 HBV genotypes and several subtypes have been identified; they have distinct geographic distribution. Acute infection with genotypes A and D results in higher rates of chronicity than genotypes B and C. Compared to genotype A and B cases, patients with genotypes C and D have lower rates of spontaneous hepatitis B e antigen (HBeAg) seroconversion; when this occurs, it tends to be delayed. HBV genotype C has a higher frequency of basal core promoter (BCP) A1762T/G1764A mutation, pre-S deletion and is associated with higher viral load than genotype B. Similarly, genotype D has a higher prevalence of BCP A1762T/G1764A mutation than genotype A. These observations suggest important pathogenic differences between HBV genotypes. These may contribute to more severe liver disease, including cirrhosis and HCC with genotypes C and D HBV infection. In addition, genotype A and B patients have better responses to interferon-based therapy than genotypes C and D, but there are few consistent differences for direct HBV antivirals. In conclusion, genotyping of chronic HBV infections can help practicing physicians identify those at risk of disease progression and determine optimal anti-viral therapy.

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