Schematic illustration of the multiscale model.
<p>Left panel: HBV extracellular dynamics, where uninfected hepatocytes (<i>T</i>) are produced at a constant rate and die at per capita rate <i>d</i><sub><i>T</i></sub>. Hepatocytes become infected cells (<i>I</i>), following infecti...
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2025
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| Summary: | <p>Left panel: HBV extracellular dynamics, where uninfected hepatocytes (<i>T</i>) are produced at a constant rate and die at per capita rate <i>d</i><sub><i>T</i></sub>. Hepatocytes become infected cells (<i>I</i>), following infection by HBV DNA (<i>V</i>). Infected cells are lost at per capita rate and secrete HBV RNA (<i>R</i>), HBV DNA, and ALT (<i>A</i>) at constant rates. The HBV RNA and HBV DNA are cleared at rates <i>c</i><sub><i>r</i></sub> and , respectively. Right panel: HBV intracellular life cycle, which begins with a hepatocyte being infected and the release of rcDNA into the cell cytoplasm following the disintegration of its capsid. This rcDNA enters the cell nucleus and is converted to cccDNA. Encapsidated pgRNA (<i>r</i>) is produced by cccDNA at rate . The encapsidated pgRNA is assembled into membrane bound particles and secreted as HBV RNA by the infected cell at rate , decays at rate , or is reverse transcribed into encapsidated rcDNA (<i>v</i>) at rate . The rcDNA is either assembled into viral particles and secreted into the circulation at rate or decays at rate in the cell. Treatment with vebicorvir inhibits the production of encaptidated pgRNA with an effectiveness of (red cross in the right panel).</p> |
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