Published by International Electronic Journal of Pure and Applied Mathematics Volume 6 No. 2 2013, 83-103Mathematical models are used to provide insights into the mechanisms
and dynamics of the progression of viral infection in vivo. Untangling the dynamics
between HIV and CD4+ cellular populations and molecular interactions can be
used to investigate the effective points of interventions in the HIV life cycle. With
that in mind, we develop and analyze a stochastic model for In-Host HIV dynamics that includes combined therapeutic treatment and intracellular delay between the infection of a cell and the emission of viral particles. The unique feature is that both therapy and the intracellular delay are incorporated into the model. We show the usefulness of our stochastic approach towards modeling combined HIV treatment by obtaining probability generating function, the moment structures of the healthy CD4+ cell, and the virus particles at any time t and the probability of virus clearance. Our analysis show that, when it is assumed that the drug is not completely effective, as is the case of HIV in vivo, the predicted rate of decline in plasma HIV virus concentration depends on three factors: the initial viral load before therapeutic intervention, the efficacy of therapy and the length of the intracellular delay.Mathematical models are used to provide insights into the mechanisms and dynamics of the progression of viral infection in vivo. Untangling the dynamics between HIV and CD4+ cellular populations and molecular interactions can be used to investigate the effective points of interventions in the HIV life cycle. With that in mind, we develop and analyze a stochastic model for In-Host HIV dynamics that includes combined therapeutic treatment and intracellular delay between the infection of a cell and the emission of viral particles. The unique feature is that both therapy and the intracellular delay are incorporated into the model. We show the usefulness of our stochastic approach towards modeling combined HIV treatment by obtaining probability generating function, the moment structures of the healthy CD4+ cell, and the virus particles at any time t and the probability of virus clearance. Our analysis show that, when it is assumed that the drug is not completely effective, as is the case of HIV in vivo, the predicted rate of decline in plasma HIV virus concentration depends on three factors: the initial viral load before therapeutic intervention, the efficacy of therapy and the length of the intracellular delay
