Rob Boer, Alan Perelson

Paper #: 96-11-083

We develop various mathematical models of the clinical latency stage of HIV-1 infection assuming that HIV-1 infection is limited either by the availability of cells that HIV can infect or by a specific anti-HIV cellular immune response. The former models we call “target-cell-limited.” Comparing the models by phase plane analysis we find that they all belong to the class of predator-prey models. In the target-cell-limited models the virus is a predator feeding upon target cell prey, while in the immune-control models the virus is a prey that is controlled by an immune response predator. Because both classes of models are of predator-prey type they behave similarly in most circumstances. We find that both types of model can account for the generic picture of disease progression in which the CD4 T-cell count slowly decreases and the viral load slowly increases. Additionally, we find that both types of models can adequately describe the clinically observed changes in the plasma HIV-1 RNA loads in response to retroviral therapies.

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