Hepatitis B viral infection and role of alcohol

Muro, Manuel; Collados-Ros, Aurelia; Legáz, Isabel

doi:10.3748/wjg.v28.i35.5233

Cited by 1 publication

(1 citation statement)

References 21 publications

(17 reference statements)

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“…Levels of persistent cccDNA may remain undetectably low in CHB sufferers (Schmeltzer and Sherman, 2010), leading to disease resurgence when the viral-immune balance is disrupted with, for instance, chemotherapy immunosuppression (Hoofnagle, 2009). Tissue damage of fibrotic and cirrhotic pathologies along with carcinomas of the liver can further result (Ikeda et al, 2009), further complicated by, for instance, myriad influences of alcohol on HBV (Muro et al, 2022). Overall, approaches for treatment are aimed at suppression of the virus, such as reverse transcriptase inhibitors, requiring enduring long-term protocols that fail to eradicate cccDNA -leading to the resurgence of HBV once treatment ends.…”

Section: Introductionmentioning

confidence: 99%

Illuminating HBV with multi-scale modeling

Means

Ali²,

Ho³

2023

Front. Syst. Biol.

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Unfortunately for the estimated 250 million sufferers of chronic hepatitis-B viral (HBV) infection worldwide, the liver terrain is typically ignored. An immuno-tolerant environment attractive for pathogens, the essential metabolic roles and structural features of the liver are aligned with distinctive gradients of oxygen and nutrients established along blood flows through fundamental hepatic processing units known as sinusoids. Capillaries surrounded by banks of hepatocytes, sinusoids express spatial configurations and concentrations of not only metabolic roles but also immune cell localisations, blood filtering and transporter specialisations: the liver terrain. HBV targets proteins regulating gluconeogenesis, a crucial liver function of blood glucose management, highly active at blood entry points—the periportal sites of sinusoids. Meanwhile, at these same sites, specialised liver macrophages, Kupffer cells (KC), aggregate and perform critical pathogen capture, detection and signaling for modulating immune responses. In tandem with KC, liver sinusoidal endothelial cells (LSECs) complement KC blood filtration and capture of pathogens as well as determine KC aggregation at the periportal sites. Failure of these systems to establish critical spatial configurations could ironically facilitate HBV invasion and entrenchment. Investigating the impacts of spatial and structural variations on the HBV infection dynamic is experimentally challenging at best. Alternatively, mathematical modeling methods provide exquisite control over said variations, permitting teasing out the subtle and competing dynamics at play within the liver terrain. Coordinating with experimental observations, multi-scale modeling methods hold promise to illuminate HBV reliance on features of the liver terrain, and potentially how it may be defeated.

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