Mittler, Sulzer, Neumann, Perelson, 1998

Model Status

This is the original unchecked version of the model imported from the previous CellML model repository, 24-Jan-2006.

Model Structure

The time course of HIV-1 infection and immunodeficiency that characterises AIDS typically displays three phases:

One of the challenges of AIDS research is to understand the events that occur during the long latency period. Disturbing this quasi-steady state with antiretroviral drugs has lead to an increased knowledge about the underlying mechanical processes. Mathematical models have been developed which consider free virus, cells susceptible to infection (target cells), and infected cells (see the figure and below). Model simulations have produced parameter values for the decline in HIV-1 plasma levels in patients which have been treated with retroviral drugs. For example, the model by Perelson et al. (1996) suggested that the half-life of the free virus is 6 hours or less. This study, together with others has influenced strategies for treating HIV-1 with antiretroviral drugs.

In this current study by Mittler et al., Perelson et al.'s 6 hour estimate for the viral half-life is tested. The authors extend the Perelson et al. model to account for intracellular delays (the period between the infection of a cell and the production of new virus particles). They concluded that, with the information about the length of the intracellular delay, it is possible to estimate viral clearance rate and other viral dynamic parameters from clinical data sets.

The complete original paper reference is cited below:

Influence of Delayed Viral Production on Viral Dynamics in HIV-1 Infected Patients, John E. Mittler, Bernhard Sulzer, Avidan U. Neumann, and Alan S. Perelson, 1998, Mathematical Biosciences , 152, 143-163. (A PDF version of the article is available on the Mathematical Biosciences website.) PubMed ID: 9780612

Schematic summary of the dynamics of HIV-1 infection in vivo captured by the Perelson et al. 1996 model.
Schematic summary of the dynamics of viral infection in vivo captured by the Herz et al. 1996 model.