A model of HIV-1 pathogenesis that includes an intracellular delay.

摘要: Mathematical modeling combined with experimental measurements have yielded important insights into HIV-1 pathogenesis. For example, data from experiments in which HIV-infected patients are given potent antiretroviral drugs that perturb the infection process been used to estimate kinetic parameters underlying HIV infection. Many of models analyze assumed drug treatments be completely efficacious and upon a cell instantly begins producing virus. We consider model allows for less then perfect effects includes delay initiation virus production. present detailed analysis this differential equation compare results without delay. Our shows when efficacy is than 100%, as may case vivo, predicted rate decline plasma concentration depends on three factors: death cells, therapy, length Thus, previous estimates infected loss rates can improved by considering more realistic viral