Modeling and Identification of Regulatory Mechanisms of MicroRNA Action in Hepatitis B Virus

This study proposes a mathematical framework for modeling the regulatory interactions between hepatocyte molecular-genetic systems and hepatitis B viruses, with a focus on the role of viral microRNAs in governing system dynamics. A set of nonlinear differential equations was developed to describe these interactions, and computational experiments were conducted using a custom-built software package. The simulations revealed multiple dynamic regimes depending on the concentration of viral microRNAs, including viral clearance, stable symbiosis, regular oscillations, irregular oscillations, and abrupt destructive transitions. A key finding indicates that the transition from stable physiological function to instability and destructive behavior occurs when the resource supply parameter markedly increases. This parameter reflects the energetic and metabolic capacity of hepatocytes, which under certain conditions promotes viral replication and disrupts regulatory balance. The analysis further demonstrated that low microRNA concentrations sustain stability or clearance, intermediate levels produce oscillatory patterns, and high levels drive the system toward unpredictable pathological outcomes. The results provide critical insights into the regulatory mechanisms underlying virus-host interactions. By identifying thresholds and critical ranges of viral microRNA content, the model distinguishes normal physiological states from pathological fluctuations. These findings highlight the potential of viral microRNAs as diagnostic biomarkers and therapeutic targets. In the future, this modeling approach may inform clinical decision-making by predicting disease progression, guiding treatment optimization, and ultimately improving hepatocyte function and patient outcomes in viral hepatitis management.

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