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Estimating HIV-1 Fitness Characteristics from Cross-Sectional Genotype Data
Figure 7
Two stage mechanistic model of in vivo HIV-1 infection dynamics [6].
Target cells TU (T-cells) and MU (macrophages) can be infected by infective viruses 
(with effective infection rate constants 
and 
), resulting in early stage infected cells 
and 
, respectively. Infection can also be unsuccessful after fusion of the virus, rendering the cell uninfected and thereby eliminating the virus (
). 
and 
can also possibly return to uninfected states by destruction of essential viral proteins or DNA prior to integration (
). 
cells can enter into a latent state 
(with probability 
) that can get re-activated with a rate constant 
. Integration of viral DNA in the host genome proceeds with reaction rate constant 
in the T-cells and 
in the macrophages, resulting in late stage infected T-cells 
and macrophages 
, respectively. The infected 
cells release new viruses (
) and non-infective (
) viruses (with rate constants 
and 
, respectively) while the infected 
cells release new infective and non-infective viruses (with rate constants 
and 
, respectively). Target cells TU and MU are produced by the immune system at constant rate with rate constants 
and 
, respectively. 
, 
, 
, 
, 
and 
can be cleared by the immune system with reaction rate constants 
, 
, 
, 
, 
and 
, respectively. Viruses are cleared by the immune system with a rate constant 
. Mutations are modelled to occur at the stage of integration of the viral DNA. The incorporation of the various drug classes is indicated by the inhibition of corresponding processes: EI/FI - entry/fusion inhibitors, NRTI/NNRTI - nucleoside/non-nucleoside reverse transcriptase inhibitors, InI - integrase inhibitors, PI/MI - protease/maturation inhibitors.
doi: https://doi.org/10.1371/journal.pcbi.1003886.g007