Multi-point Infection Dynamics of Hepatitis B in the Presence of Sub-Viral Particles

TL;DR

This study introduces a novel mathematical model for hepatitis B infection that incorporates sub-viral particles and capsid recycling, revealing their significant roles in infection persistence and propagation, especially under multi-point infection scenarios.

Contribution

The paper presents the first mathematical model including sub-viral particles and capsid recycling effects in hepatitis B infection dynamics.

Findings

SVPs enhance intracellular viral replication and gene expression.

Capsid recycling increases SVP concentration.

Multi-point infections lead to rapid infection propagation.

Abstract

Hepatitis B virus (HBV) is considered as etiological agent of the lethal liver disease hepatitis B. Globally, hepatitis B is recognized as one of the prevailing infectious diseases with a significant impact on human health. In spite of being non-infectious in nature, sub-viral particles (SVPs) , composed with mainly viral surface proteins, play critical roles in the persistence and progression of the infection. Although the understanding on the functions of these non-infectious SVPs remains limited and incomplete. In this study, a mathematical model is proposed for the first time by incorporating the roles of SVPs and including the effects of capsids recycling. The impacts of spatial mobility of capsids, viruses, SVPs and antibodies are also taken into account in this model. Overall, this model carry unique characteristics in the context of this viral infection. This study investigates the changes in the dynamics of infection considering both single-point as well as multi-point infection initial condition. As a result, it is observed that SVPs can significantly enhance intracellular viral replication and gene expression by reducing the neutralization of virus particles by antibodies. The recycling of capsids substantially increase the concentration of SVPs. The experiments which are carried out on single-point as well as multi-point infection initial conditions show that if the liver is infected at more than one point, infection propagates rapidly. The outcomes of the proposed model strongly recommend that it is imperative to consider the diffusion term while HBV infection dynamics are illustrated.