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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

Macrophages archive HIV-1 virions for dissemination in trans

Natalia Sharova1, Catherine Swingler, Mark Sharkey

  • 1Program in Molecular Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA.

The EMBO Journal
|May 28, 2005
PubMed

Insights

Intracellular human immunodeficiency virus type 1 (HIV-1) virions in macrophages remain infectious for weeks, even after replication stops. This discovery reveals a new HIV-1 persistence mechanism in infected individuals.

Area of Science:

  • Virology
  • Immunology
  • Cell Biology

Background:

  • Human immunodeficiency virus type 1 (HIV-1) persistence is a major barrier to curing infected individuals.
  • Most studies on HIV-1 persistence focus on lymphocytes, with limited understanding of mechanisms in macrophages.
  • HIV-1 assembles within cytoplasmic vesicles in macrophages, but the infectious stability of these intracellular virions is unknown.

Purpose of the Study:

  • To evaluate the infectious stability of HIV-1 virions that assemble intracellularly within primary macrophages.
  • To investigate potential mechanisms contributing to HIV-1 persistence in macrophages.

Main Methods:

  • Primary macrophages were infected with HIV-1.
  • Viral replication was blocked using specific inhibitors.
  • Infectious virions were recovered from macrophage cytoplasmic lysates at various time points post-infection.
  • Cell-associated virus decay was measured.
  • Transmission of infectious virus from macrophages to peripheral blood lymphocytes (in trans) was assessed.

Main Results:

  • Intracellularly assembled HIV-1 virions in macrophages retained infectivity for extended periods (at least 6 weeks).
  • Infectious virus was recoverable from macrophage lysates long after viral replication was inhibited.
  • Cell-associated virus showed significant decay between 1-2 weeks but minimal decay thereafter.
  • Virion persistence was independent of viral accessory proteins Vpu and Nef.

Conclusions:

  • Intracellular sequestration of infectious HIV-1 virions within macrophages represents a novel mechanism for viral persistence.
  • This macrophage-based viral reservoir may contribute to long-term HIV-1 persistence in infected individuals.
  • Understanding this mechanism could inform new therapeutic strategies targeting viral reservoirs.

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