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Updated: Aug 9, 2026
11:10
Genotypic Inference of HIV-1 Tropism Using Population-based Sequencing of V3
Published on: December 27, 2010
Viral determinants of cellular tropism
1Division of Infectious Diseases, West Los Angeles VA Medical Center, Calif. 90073.
Summary
Human immunodeficiency virus type 1 (HIV-1) primarily infects mononuclear phagocytes in tissues, contributing to AIDS. A specific gp120 region, separate from the CD4 binding site, dictates macrophage tropism and entry efficiency.
Area of Science:
- Virology
- Immunology
- Cell Biology
Background:
- Mononuclear phagocytes are key producers of HIV-1 in extravascular tissues.
- HIV-1 infection of these cells contributes to disease manifestations and immune deficiency in AIDS.
- Differential replication of HIV-1 strains in mononuclear phagocytes suggests specific tropism determinants.
Purpose of the Study:
- To identify the viral determinants responsible for HIV-1 tropism in mononuclear phagocytes.
- To understand the mechanisms underlying efficient HIV-1 entry into macrophages.
Main Methods:
- Utilized recombinant HIV-1 strains to map viral determinants.
- Analyzed the gp120 envelope protein, focusing on a 157-amino acid region.
- Employed quantitative polymerase chain reaction (PCR) to assess early viral DNA levels.
Main Results:
- A 157-amino acid region of gp120, distinct from the CD4 binding domain, confers macrophage tropism.
- This region encompasses the V3 hypervariable domain, a major neutralizing epitope.
- Macrophage tropism differences are established early, at the viral entry stage.
Conclusions:
- HIV-1 entry into mononuclear phagocytes is regulated by interactions involving gp120, beyond the primary CD4 binding site.
- The V3 domain of gp120 plays a crucial role in determining macrophage tropism.
- Understanding these interactions is vital for targeting HIV-1 infection in macrophages.
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