Afrin, NaziaCiupe, Stanca M.Conway, Jessica M.Gulbudak, Hayriye2026-01-122026-01-122025-05-310025-5564NIHMS2088488PMC12245406S0025-5564(25)00093-8 (PII)https://hdl.handle.net/10919/140749Understanding the mechanisms responsible for different clinical outcomes following hepatitis B infection requires a systems investigation of dynamical interactions between the virus and the immune system. To help elucidate mechanisms of protection and those responsible from transition from acute to chronic disease, we developed a deterministic mathematical model of hepatitis B infection that accounts for cytotoxic immune responses resulting in infected cell death, non-cytotoxic immune responses resulting in infected cell cure and protective immunity from reinfection, and cell proliferation. We analyzed the model and presented outcomes based on three important disease markers: the basic reproduction number R0, the infected cells death rate δ (describing the effect of cytotoxic immune responses), and the liver carrying capacity K (describing the liver susceptibility to infection). Using asymptotic and bifurcation analysis techniques, we determined regions where virus is cleared, virus persists, and where clearance-persistence is determined by the size of viral inoculum. These results can guide the development of personalized intervention.enIn CopyrightAcute infectionBistabilityChronic infectionHepatitis B virusHopf bifurcationMathematical modelingHumansHepatitis B virusModels, BiologicalHepatitis B, ChronicHepatitis BAcute DiseaseBasic Reproduction NumberArticle - Refereedhttps://doi.org/10.1016/j.mbs.2025.109467387Ciupe, Mihaela [0000-0002-5386-6946]1879-3134