Journal of Leukocyte Biology
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A more recent version of this article appeared on November 1, 2003

Published online before print August 21, 2003
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© by The Society for Leukocyte Biology
Journal of Leukocyte Biology, doi:10.1189/jlb.0403186

Received for publication April 25, 2003.
Revised July 15, 2003.
Accepted for publication July 26, 2003.

Article

HIV-1 fitness and macrophages

Maureen M. Goodenow *,{dagger}@, 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

@ To whom correspondence should be addressed. E-mail: goodenow{at}ufl.edu.


  Abstract

HIV-1 comprises a collection of closely related, but not identical, viruses or quasi-species. 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 quasi-species and an unexplained discordance between fitness and pathogenesis.

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




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