Discovery and Assessment of New Target Sites for Anti-HIV Therapies

Abstract

Human immunodeficiency virus (HIV) infects cells by endocytosis and takes over parts of the cell’s reaction pathways in order to reproduce itself and spread the infection. One such pathway taken over by HIV becomes the inflammatory pathway which uses Nuclear Factor κB (NF-κB) as the principal transcription factor. Therefore, knocking out the NF-κB pathway would prevent HIV from reproducing itself. In this report, our goal is to produce a simple model for this pathway with which we can identify potential targets for anti-HIV therapies and test out various hypotheses. We present a very simple model with four coupled first-order ODEs and see what happens if we treat IκK concentration as a parameter that can be controlled (by some unspecified means). In Section 3, we augment this model to account for activation and deactivation of IκK, which is controlled (again, by some unspecified means) by TNF.