A theoretical model of chronic hepatitis B virus with suboptimal adherence and drug resistance

In this paper, we formulate and analyze a within-host hepatitis B viral theoretical mathematical model for hepatitis B virus infection in the chronic phase of liver cancer with suboptimal adherence and drug resistance. The model incorporates hepatocytes, hepatitis B virus, immune cells, and cytokine dynamics using a system of ordinary differential equations. Treatment was captured using efficacy functions replicating the realistic pharmacokinetics properties of two drugs, one of which is administered intravenously and the other orally. Our results suggest that natural drug resistance increases the hepatitis B virus burden more than suboptimal adherence to drugs from both monotherapies and combined therapies. The results also suggest that the inclusion of both immune cells and cytokine responses is essential and that combination therapies are more significant in reducing hepatitis B virus infection than monotherapies.

Automated summary

The paper presents a theoretical mathematical model of within-host hepatitis B virus infection in the chronic phase of liver cancer, considering suboptimal adherence and drug resistance. The study highlights that natural drug resistance has a stronger impact on increasing the virus burden compared to suboptimal adherence. Combination therapies are more effective in reducing virus infection than monotherapies.