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Phagosome Migration and Velocity Measured in Live Primary Human Macrophages Infected with HIV-1
07:32

Phagosome Migration and Velocity Measured in Live Primary Human Macrophages Infected with HIV-1

Published on: September 5, 2016

HIV accomplices and adversaries in macrophage infection

Sharon M Wahl1, Teresa Greenwell-Wild, Nancy Vázquez

  • 1Oral Infection and Immunity Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Building 30, Rm. 320, 30 Convent Dr., MSC 4352, Bethesda, MD 20892-4352, USA. smwahl@dir.nidcr.nih.gov

Journal of Leukocyte Biology
|August 16, 2006
PubMed

Insights

Macrophages uniquely support HIV infection through specific cellular pathways, but also possess innate defenses like APOBEC3 enzymes. Enhancing these antiviral mechanisms, such as with IFN-alpha, could bolster macrophage resistance to HIV.

Area of Science:

  • Virology
  • Immunology
  • Cell Biology

Background:

  • Macrophages play a critical role in lentivirus infection, acting as both hosts and potential reservoirs for HIV.
  • Understanding cellular factors influencing HIV lifecycle in macrophages is key to managing viral burden.
  • HIV co-opts macrophage-specific pathways, distinct from those in T cells, for infection and replication.

Purpose of the Study:

  • To characterize cellular proteins and pathways in macrophages that influence HIV infection.
  • To identify unique macrophage constituents usurped by HIV.
  • To explore innate antiviral mechanisms within macrophages against HIV.

Main Methods:

  • Analysis of cellular proteins involved in lentivirus entry and replication in macrophages.
  • Investigation of macrophage-specific signaling pathways and transcriptional profiles induced by viral binding.
  • Assessment of innate antiviral factors, such as APOBEC3 enzymes, and their regulation.

Main Results:

  • Membrane annexin II facilitates early HIV infection in macrophages, unlike in T cells; blocking this reduces infection.
  • HIV binding triggers macrophage-specific signaling and gene expression (e.g., p21) that benefits the virus.
  • Innate antiviral mechanisms, including APOBEC3 enzymes, are present but often neutralized by HIV; higher APOBEC3 levels and IFN-alpha induction enhance macrophage resistance.

Conclusions:

  • Macrophages possess unique cellular vulnerabilities and strengths in the context of HIV infection.
  • Targeting macrophage-specific pathways like annexin II could be a therapeutic strategy.
  • Leveraging innate immunity, particularly APOBEC3 expression modulated by IFN-alpha, offers a potential approach to enhance macrophage antiviral defense against HIV.

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