Some viruses encode proteins that promote cell proliferation while others, such as the human immunodeficiency virus (HIV), encode proteins that prevent cell division. It has been hypothesized that the selective advantage determining which strategy evolves depends on the ability of the virus to induce a cellular environment which maximizes both virus production and cell lifespan. In HIV, the protein that causes cell cycle arrest is Vpr.

Recently we developed a mathematical model based on discrete difference equations (Holte S, Emerman M. to appear, Mathematical Biosciences) to study the competition between two genotypes of HIV---one that encodes this protein (Vpr+) and one that does not (Vpr-). Recently, a team of students participating in the 2000 Industrial Mathematics Modeling Workshop for Graduate Students at North Carolina State University extended this model to account for the delay between cellular infection and the production of new viral particles. In particular, we assessed the robustness to perturbations of a number of parameters in the model. The model will also be used to estimate a variety of parameters from data produced in laboratory experiments.

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Connecting Women in Mathematical Sciences to Industry

2000-2001 Program: Mathematics in Multimedia