Pii: S0025-5564(02)00099-8

Models of HIV-1 infection that include intracellular delays are more accurate representations of the biology and change the estimated values of kinetic parameters when compared to models without delays. We develop and analyze a set of models that include intracellular delays, combination antiretroviral therapy, and the dynamics of both infected and uninfected T cells. We show that when the drug efficacy is less than perfect the estimated value of the loss rate of productively infected T cells, d, is increased when data is fit with delay models compared to the values estimated with a non-delay model. We provide a mathematical justification for this increased value of d. We also provide some general results on the stability of non-linear delay differential equation infection models. 2002 Elsevier Science Inc. All rights reserved.