  Analysis of cell population can reveal the average information about the
viral infection in host whereas single-cell analysis can capture the individual
consideration. Single-cell analysis can also provide new ways to explore viral
diversities and identify the intrinsic extreme phenotype of the cells. In this
study, a single-cell hepatitis B virus (HBV) infection model is proposed by
considering all possible intracellular steps which are observed in the viral
life cycle. To the best of our knowledge, it is the most generalized model to
date. The effects of newly introduced factors or components such as, cccDNA,
HBx proteins, surface proteins, and double-stranded linear DNA-containing
capsids are explained very well by this model. The intracellular delay is also
incorporated into the proposed model, and it is seen that it has no significant
impact on the persistence of infection. The global sensitivity analysis of the
parameters is also performed using partial rank correlation coefficients based
on Latin hypercube sampling method. According to PRCC values, the most positive
and most negative sensitive parameters are identified. Moreover, it is observed
that the availability of viral surface proteins switches the replication
pattern from acute to chronic, whereas there is no considerable contribution of
HBx proteins to the progression of HBV infection. Another striking result is
that the recycling of capsids appears to act as a positive feedback loop
throughout the infection.
