Modeling of co-infection dynamics of hepatitis B and alcoholic liver disease: A simulation-based learning

Hepatitis B virus (HBV) and alcoholic liver disease (ALD) are leading causes of liver-related health complications worldwide, with co-infection often resulting in accelerated disease progression and heightened mortality risks. Despite the clinical significance, there is a lack of mathematical modeling studies specifically examining the dynamics of HBV and ALD co-infection. This study constructs a mathematical model to explore the complex interactions between HBV and ALD, factoring in viral load, immune response, and the effects of alcohol on liver function. A comprehensive qualitative analysis is undertaken to validate the model's core properties, including Lipschitzness, uniqueness, positive invariance, and boundedness, ensuring biologically consistent and well-defined dynamics. The model also includes an analysis of the basic reproduction number using the next-generation method, identifying thresholds that indicate the persistence or elimination of HBV and ALD within the population. Latin hypercube sampling and partial rank correlation coefficient, with 1000 iterations, are used to evaluate the sensitivity of R0. Stability analyses, both local and global, are carried out at the disease-free equilibrium to establish conditions for either controlling or maintaining the infection within the population. Using real data from the United States spanning 2013 to 2022 for parameter estimation, we simulate disease progression and evaluate intervention strategies. The parameter estimation results illustrate the model's capacity to capture data dynamics effectively, with a strong fit showcasing its robustness. Co-infection dynamics are modeled through numerical simulations using the Adams–Bashforth method, exploring the impact of vaccination rates, transmission dynamics, and co-infection interactions on stability thresholds and disease persistence. Findings reveal that HBV and ALD co-infection accelerates liver damage significantly more than either condition alone, underscoring the compounded effects of dual pathology. Furthermore, the findings demonstrate that reducing alcohol use and the viral load of HBV can greatly hinder the progression of severe liver disease. This study highlights the necessity of comprehensive interventions and lays the groundwork for future research utilizing patient-specific data to refine treatment strategies.