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HDV Can Constrain HBV Genetic Evolution in HBsAg: Implications for the Identification of Innovative Pharmacological

Luna Colagrossi1, Romina Salpini2, Rossana Scutari3

  • 1Department of Experimental Medicine and Surgery, Tor Vergata University, 00133 Rome, Italy. luna_colagrossi@yahoo.it.

Viruses
|July 11, 2018
PubMed

Insights

Hepatitis D virus (HDV) infection constrains Hepatitis B virus surface antigen (HBsAg) evolution, with conserved regions in both HBsAg and Hepatitis D antigen (HDAg) offering potential therapeutic targets for treating chronic HDV infection.

Area of Science:

  • Virology
  • Hepatology
  • Molecular Biology

Background:

  • Chronic co-infection with Hepatitis B virus (HBV) and Hepatitis D virus (HDV) significantly increases the risk of severe liver disease, including cirrhosis and hepatocellular carcinoma, compared to HBV mono-infection.
  • Currently, no specific antiviral drugs targeting HDV are available in clinical practice, highlighting an unmet medical need for novel therapeutic strategies.

Purpose of the Study:

  • To identify conserved and variable regions within Hepatitis B surface antigen (HBsAg) and Hepatitis D antigen (HDAg) domains in patients with chronic HBV + HDV co-infection.
  • To provide a molecular basis for designing innovative therapeutic agents targeting HDV infection by analyzing genetic variability.

Main Methods:

  • Amino acid variability was quantified using Shannon Entropy (Sn) analysis on HBsAg sequences from HBV + HDV infected and HBV mono-infected patients, and on HDAg sequences.
  • Conserved positions were defined as those with Sn = 0. Statistical comparisons were performed between co-infected and mono-infected groups, with stratification for HBeAg status and patient age.

Main Results:

  • A significantly higher percentage of conserved HBsAg positions was observed in HBV + HDV co-infection compared to HBV mono-infection (p = 0.001).
  • Specific conserved C-terminal HBsAg positions correlated with higher HDV-RNA levels, suggesting a role in maintaining HDV fitness.
  • HDAg exhibited a lower percentage of conserved residues than HBsAg (p < 0.001), indicating greater functional plasticity, although specific HDAg mutations correlated with increased HDV replication.

Conclusions:

  • HDV co-infection imposes evolutionary constraints on HBsAg to maintain HDV fitness, indicating a complex host-pathogen interaction.
  • The identification of conserved regions within HDAg, particularly the virus-assembly signal, provides a foundation for developing novel therapeutic targets against HDV infection.

Keywords:
HBsAgHDAgHDV-RNA

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