A Theoretical Model of Chronic Hepatitis B Virus with Sub-optimal Adherence and Drug Resistance

In this paper, we formulate and analyze within-host hepatitis B viral theoretical mathematical model for hepatitis B virus infection in the chronic phase of liver cancer with sub-optimal 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 sub-optimal adherence to drugs from both mono-therapies 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 mono-therapies.