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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

Impaired complement-mediated phagocytosis by HIV type-1-infected human monocyte-derived macrophages involves a

Rula Azzam1, Katherine Kedzierska, Edwin Leeansyah

  • 1AIDS Pathogenesis and Clinical Research Program, Macfarlane Burnet Institute for Medical Research and Public Health, Melbourne, Australia.

AIDS Research and Human Retroviruses
|July 13, 2006
PubMed

Insights

Human immunodeficiency virus type 1 (HIV-1) impairs macrophage phagocytosis by increasing intracellular cyclic adenosine monophosphate (cAMP). Inhibiting cAMP production restores this crucial immune function in HIV-1-infected macrophages.

Area of Science:

  • Immunology
  • Virology
  • Cell Biology

Background:

  • Human immunodeficiency virus type 1 (HIV-1) infection compromises macrophage effector functions, notably phagocytosis of opsonized pathogens.
  • Macrophage phagocytosis is critical for host defense against microbial infections.

Purpose of the Study:

  • To investigate the impact of HIV-1 on complement (C')-mediated phagocytosis by human monocyte-derived macrophages (MDM).
  • To elucidate the underlying molecular mechanisms by which HIV-1 inhibits phagocytosis in MDM.

Main Methods:

  • Utilized C'-opsonized sheep red blood cells (sRBC) as targets to assess phagocytosis in HIV-1-infected MDM.
  • Measured intracellular cyclic adenosine monophosphate (cAMP) levels and employed adenylate cyclase inhibitors (2',5'-dideoxyadenosine, MDL-12,330A).
  • Assessed the role of viral entry and replication using the antiretroviral drug lamivudine.

Main Results:

  • HIV-1 infection in vitro significantly inhibited C'-mediated phagocytosis by MDM.
  • Inhibition was post-receptor-mediated, not due to altered receptor expression or target binding.
  • HIV-1 infection elevated intracellular cAMP levels in MDM, and inhibiting cAMP production restored phagocytic capacity.
  • Defective phagocytosis did not correlate with prostaglandin secretion and showed minimal bystander effect.

Conclusions:

  • HIV-1 impairs C'R-mediated phagocytosis in MDM by increasing intracellular cAMP levels.
  • This mechanism is independent of prostaglandin secretion and contributes to HIV-1-induced immune dysfunction.
  • Understanding this pathway offers insights into mitigating HIV-1's impact on cell-mediated immunity.

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