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Mutations of glucocorticoid responsive element of HBV DNA

H Suzuki1, M Sata, M Sasaki

  • 1Second Department of Medicine, Kurume University School of Medicine, Japan.

The Kurume Medical Journal
|August 26, 1998
PubMed

Insights

Mutations in the glucocorticoid responsive element (GRE) of Hepatitis B virus (HBV) DNA were identified in a patient with chronic hepatitis B who experienced a fatal outcome after glucocorticoid treatment.

Area of Science:

  • Hepatology
  • Virology
  • Molecular Biology

Background:

  • Chronic hepatitis B (CHB) is a significant global health concern.
  • Glucocorticoids are sometimes used in CHB treatment, but their efficacy and safety can vary.
  • Understanding HBV DNA mutations is crucial for predicting treatment response.

Observation:

  • HBV DNA was analyzed from a CHB patient with a fatal outcome following glucocorticoid administration (GRE-M).
  • Comparative analysis included HBV DNA from two HBeAg-positive CHB patients with minimal mutations (GRE-W1,2).
  • A 212 bp region (nt.274-485) of the HBV DNA, encompassing the GRE, was amplified and sequenced.

Findings:

  • Specific base mismatched sequences were confirmed within the GRE region (G1-G4) and an AP-1 response element (A1).
  • Nucleotide substitutions in GRE-M created three potential loop formation sites (L1-L3).
  • These mutations, particularly L1 and L2, are located near critical response elements, potentially altering DNA structure.

Implications:

  • The identified mutations and subsequent three-dimensional structural changes in HBV DNA may influence glucocorticoid response.
  • This finding could explain the fatal outcome in the patient and suggests a need for personalized treatment strategies in CHB.
  • Further research into GRE mutations in HBV is warranted to optimize antiviral therapies.

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