  Proliferation of uninfected as well as infected hepatocytes and recycling of
DNA-containing
  capsids are two major mechanisms playing significant roles in the clearance
of hepatitis B
  virus (HBV) infection. In this study, the temporal dynamics of this infection
are investigated
  through two in silico bio-mathematical models considering both proliferation
of hepatocytes
  and the recycling of capsids. Both models are formulated on the basis of a
key finding in the existing literature: mitosis of infected yields in two
uninfected progenies. In the first model,
  we examine regular proliferation (occurs continuously), while the second
model deals with the
  irregular proliferation (happens when the total number of liver cells
decreases to less than 70%
  of its initial volume). The models are calibrated with the experimental data
obtained from
  an adult chimpanzee. Results of this study suggest that when both hepatocytes
proliferate
  with equal rate, proliferation aids the individual in a rapid recovery from
the acute infection
  whereas in the case of chronic infection, the severity of the infection
increases if the proliferation
  occurs frequently. On the other hand, if the infected cells proliferate at a
slower rate than uninfected cells, the proliferation of uninfected hepatocytes
contributes to increase the infection,
  but the proliferation of infected hepatocytes acts to reduce the infection
from the long-term
  perspective. Furthermore, it is also observed that the differences between
the outcomes of
  regular and irregular proliferations are substantial and noteworthy.
