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Updated: Jul 19, 2026

Genotypic Inference of HIV-1 Tropism Using Population-based Sequencing of V3
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Coreceptor switching in HIV-1 subtype B and subtype C.

T Mugwagwa1, G Witten

  • 1Department of Mathematics and Applied Mathematics, University of Cape Town, Rondebosch 7701, Cape Town, South Africa.

Bulletin of Mathematical Biology
|November 7, 2006
PubMed
Summary

A persistent, efficient lytic immune response prevents coreceptor switching in HIV-1 subtype C. Macrophage availability and viral kinetics also influence R5 strain dominance, impacting HIV disease progression.

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Area of Science:

  • Virology
  • Immunology
  • Mathematical Modeling

Background:

  • HIV-1 exhibits tropism for CCR5 (R5) or CXCR4 (X4) coreceptors.
  • Coreceptor switching from R5 to X4 is common in HIV-1 subtype B but rare in subtype C.
  • Understanding factors influencing coreceptor tropism is crucial for HIV pathogenesis and treatment.

Purpose of the Study:

  • To identify key factors governing the delayed or rare coreceptor switch in HIV-1 subtype C.
  • To elucidate the role of immune responses and host cell availability in HIV-1 tropism.
  • To compare coreceptor switching kinetics between HIV-1 subtypes B and C.

Main Methods:

  • Development and analysis of a mathematical model simulating HIV-1 infection dynamics.
  • Inclusion of target cell populations (macrophages, lymphocytes) for R5 and X4 tropic viruses.

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Last Updated: Jul 19, 2026

Genotypic Inference of HIV-1 Tropism Using Population-based Sequencing of V3
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Published on: December 27, 2010

Prediction of HIV-1 Coreceptor Usage (Tropism) by Sequence Analysis using a Genotypic Approach
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Prediction of HIV-1 Coreceptor Usage (Tropism) by Sequence Analysis using a Genotypic Approach

Published on: December 1, 2011

Conformational Evaluation of HIV-1 Trimeric Envelope Glycoproteins Using a Cell-based ELISA Assay
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  • Incorporation of lytic and non-lytic immune responses.
  • Sensitivity analysis to determine critical model parameters.

    • Main Results:

    • A persistent and efficient lytic immune response suppresses CXCR4-tropic (X4) virus, preventing phenotypic switching.
    • Efficient non-lytic immune responses are less effective in preventing coreceptor switch.
    • Macrophage availability and enhanced viral kinetics favor the dominance of CCR5-tropic (R5) strains.
    • Model simulations predict distinct coreceptor switching patterns between HIV-1 subtypes.

    Conclusions:

    • Persistent, efficient lytic immunity is key to preventing X4 virus emergence in HIV-1 subtype C.
    • Host environment, potentially altered by immune activation, influences differential coreceptor switching kinetics between HIV-1 subtypes.
    • Mathematical modeling provides insights into complex HIV-1 dynamics and tropism determination.