Journal of Leukocyte Biology
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Originally published online as doi:10.1189/jlb.0403186 on August 21, 2003

Published online before print August 21, 2003
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(Journal of Leukocyte Biology. 2003;74:657-666.)
© 2003 by Society for Leukocyte Biology

HIV-1 fitness and macrophages

Maureen M. Goodenow*,{dagger},1, Stephanie L. Rose*, Daniel L. Tuttle* and John W. Sleasman{ddagger}

* Department of Pathology, Immunology, and Laboratory Medicine and
{dagger} Department of Pediatrics, Division of Immunology and Infectious Diseases, University of Florida College of Medicine; and
{ddagger} Department of Pediatrics, Division of Allergy and Immunology, University of South Florida College of Medicine, and All Children’s Hospital, St. Petersburg, Florida

1 Correspondence: Department of Pathology, Immunology, and Laboratory Medicine, College of Medicine, University of Florida, Box 100275, 1600 SW Archer Road, Gainesville, FL 32610. E-mail: goodenow{at}ufl.edu

HIV-1 comprises a collection of closely related, but not identical, viruses or quasispecies. Fitness represents a selective advantage for propagation among populations of organisms competing in a particular environment and is an important characteristic of viruses because of a link between fitness and pathogenesis. Environmental differences based on the type of cell that is targeted for infection or the cell type that produces virus, impact fitness. CD4-expressing cells of lymphocyte or macrophage lineage are the principal host cells for HIV-1, although the milieu in lymphocytes is distinct from the macrophage environment from the perspective of cell half-life and activation, signal transduction and expression of coreceptors, and bioavailability of antiretroviral drugs. Multiple viral determinants, including entry via envelope glycoproteins, replication by reverse transcriptase, and virion maturation by protease activity, contribute to fitness in different cells and provide targets for current antiretroviral therapies. This review focuses on fitness of HIV-1 in macrophages and examines the impact of protease inhibitors on fitness of quasispecies and an unexplained discordance between fitness and pathogenesis.

Key Words: review • antiretroviral therapy • gag/protease • envelope • tropism • phenotype




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