In this paper, mathematical analysis of the global dynamics of a viral infection model in vivo is carried out. Though the model is originally to study hepatitis C virus (HCV) dynamics in patients with high baseline viral loads or advanced liver disease, similar models still hold significance for other viral infection, such as hepatitis B virus (HBV) or human immunodeficiency virus (HIV) infection. By means of Volterra-type Lyapunov functions, we know that the basic reproduction number [Formula: see text] is a sharp threshold para-meter for the outcomes of viral infections. If [Formula: see text], the virus-free equilibrium is globally asymptotically stable. If [Formula: see text], the system is uniformly persistent, the unique endemic equilibrium appears and is globally asymptotically stable under a sufficient condition. Other than that, for the global stability of the unique endemic equilibrium, another sufficient condition is obtained by Li–Muldowney global-stability criterion. Using numerical simulation techniques, we further find that sustained oscillations can exist and different maximum de novo hepatocyte influx rate can induce different global dynamics along with the change of overall drug effectiveness. Finally, some biological implications of our findings are given.
Global Stability for a Viral Infection Model with Saturated Incidence Rate
