Journal of Theoretical Medicine
Volume 4 (2002), Issue 2, Pages 147-155
doi:10.1080/1027366021000003289

A New Mathematical Model for Assessing Therapeutic Strategies for HIV Infection

1Department of Mathematics, University of Manitoba, Winnipeg, Manitoba, R3T 2N2, Canada
2The Center for HIV/STDs and Infectious Diseases, The University of North Carolina, Chapel Hill, NC 27599, USA
3Cadham Provincial Laboratory, University of Manitoba, Winnipeg, Manitoba, R3E 0W3, Canada
4Department of Medical Microbiology, University of Manitoba, Winnipeg, Manitoba, R3E 0W3, Canada

Accepted 15 December 2001

Copyright © 2002 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

The requirements for the eradication of HIV in infected individuals are unknown. Intermittent administration of the immune activator interleukin-2 (IL-2) in combination with highly-active antiretroviral therapy (HAART) has been suggested as an effective strategy to realize long-term control of HIV replication in vivo. However, potential latent virus reservoirs are considered to be a major impediment in achieving this goal. In this paper, a new mathematical model is designed and used to monitor the interactions between HIV, CD4+ T-cells, CD8+ T-cells, productively infected and latently infected CD4+ T-cells, and to evaluate therapeutic strategies during the first 3 years of HIV infection. The model shows that current anti-HIV therapies, including intermittent IL-2 and HAART, are insufficient in achieving eradication of HIV. However, it suggests that the HIV eradication may indeed be theoretically feasible if such therapy is administered continuously (without interruption) under some specified conditions. These conditions may realistically be achieved using an agent (such as a putative anti-HIV vaccine) that brings about a concomitant increase in the proliferation of HIVspecific CD4+ T- and CD8+ T-cells and the differentiation of CD8+ T-cells into anti-HIV cytotoxic T lymphocytes (CTLs).