Wodarz2007 - HIV/CD4 T-cell interaction

Wodarz2007 - HIV/CD4 T-cell interaction
A deterministic model illustrating how
CD4 T-cells can influence HIV infection.

This model is described in the article:

Infection dynamics in
HIV-specific CD4 T cells: does a CD4 T cell boost benefit the
host or the virus?

Wodarz D, Hamer DH.
Math Biosci 2007 Sep; 209(1):
14-29
Abstract:

Recent experimental data have shown that HIV-specific CD4 T
cells provide a very important target for HIV replication. We
use mathematical models to explore the effect of specific CD4 T
cell infection on the dynamics of virus spread and immune
responses. Infected CD4 T cells can provide antigen for their
own stimulation. We show that such autocatalytic cell division
can significantly enhance virus spread, and can also provide an
additional reservoir for virus persistence during anti-viral
drug therapy. In addition, the initial number of HIV-specific
CD4 T cells is an important determinant of acute infection
dynamics. A high initial number of HIV-specific CD4 T cells can
lead to a sudden and fast drop of the population of
HIV-specific CD4 T cells which results quickly in their
extinction. On the other hand, a low initial number of
HIV-specific CD4 T cells can lead to a prolonged persistence of
HIV-specific CD4 T cell help at higher levels. The model
suggests that boosting the population of HIV-specific CD4 T
cells can increase the amount of virus-induced immune
impairment, lead to less efficient anti-viral effector
responses, and thus speed up disease progression, especially if
effector responses such as CTL have not been sufficiently
boosted at the same time.

This model is hosted on
BioModels Database
and identified by:
BIOMD0000000663.
To cite BioModels Database, please use:
Chelliah V et al. BioModels: ten-year
anniversary. Nucl. Acids Res. 2015, 43(Database
issue):D542-8.

To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to
the public domain worldwide. Please refer to
CC0
Public Domain Dedication for more information.