Author Affiliation: Aaron Diamond AIDS Research Center, Rockefeller University, New York, NY.
A near-uniformly fatal clinical syndrome, acquired immunodeficiency
syndrome (AIDS), has been transformed during the past 5 years into a treatable
infectious disease. The availability of potent antiretroviral agents coincided
with the ability to measure levels of circulating virus in vivo. When used
in tandem, an understanding of human immunodeficiency virus (HIV) replication
dynamics in vivo was made possible, forming the scientific basis for the use
of combination antiretroviral therapy.1 However,
the treatment of HIV infection remains far from perfect, and new issues arise
with regularity. Critical to achieving optimal therapeutic outcomes is an
understanding of treatment failure. Early clinical trials of protease inhibitor
monotherapy suggested that the pathway to treatment failure was exclusively
via drug resistance.2,3 Viral
rebound was thought to reflect failure of all components of a regimen. Furthermore,
it was assumed that the absence of resistance-conferring genotypic changes
reflected patient nonadherence.
Markowitz M. Resistance, Fitness, Adherence, and Potency: Mapping the Paths to Virologic Failure. JAMA. 2000;283(2):250–251. doi:10.1001/jama.283.2.250
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