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A multi-scale spatial model of hepatitis-B viral dynamics.

Quentin Cangelosi1, Shawn A Means2, Harvey Ho2

  • 1Computational and Mathematical Engineering, Institut National des Sciences Appliquées, Toulouse, France.

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Summary

Chronic hepatitis B virus (HBV) infection may persist by exploiting the liver's spatial structure. Mathematical modeling suggests HBV replication and immune responses aligned in specific liver regions contribute to chronic infection persistence.

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Area of Science:

  • Hepatology
  • Mathematical Biology
  • Virology

Background:

  • Chronic hepatitis B viral infection (HBV) affects 250 million globally, with limited treatment options.
  • HBV establishes persistent infection via covalently-closed circular DNA (cccDNA) in hepatocytes.
  • The liver's complex spatial organization may influence HBV chronicity and immune evasion.

Purpose of the Study:

  • To investigate the impact of hepatic spatial heterogeneity on HBV dynamics.
  • To model the influence of nutrient and transporter distribution on HBV replication.
  • To explore the role of immune response spatial distribution in HBV persistence.

Main Methods:

  • Development of a multi-scaled mathematical model of the liver sinusoid and whole-liver representation.
  • Simulation of HBV replication rates, nutrient levels, and transporter distributions within the hepatic microenvironment.
  • Inclusion of immune system activity and extra-hepatic HBV replication in model parameters.

Main Results:

  • HBV replication rates, nutrient availability, and key transporters (e.g., NTCP) co-aligned in the periportal region may promote viral entrenchment.
  • Spatial distribution and intensity of the immune response significantly influence HBV persistence.
  • Extra-hepatic HBV replication demonstrated a nominal effect on persistent liver infection.

Conclusions:

  • Spatial heterogeneity within the liver microenvironment is a critical factor in HBV persistence.
  • Targeting spatially-dependent viral and host factors may offer new therapeutic strategies for chronic HBV.
  • A single cccDNA molecule is sufficient for complete liver re-infection, highlighting challenges in HBV eradication and post-transplant recurrence.