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Neutralizing antibodies modulate replication of simian immunodeficiency virus SIVmac in primary macaque macrophages

M F McEntee1, M C Zink, M G Anderson

  • 1Division of Comparative Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland.

Journal of Virology
|October 1, 1992
PubMed

Insights

Neutralizing antibodies limit simian immunodeficiency virus (SIV) replication in macaque macrophages if applied early. Early antibody treatment prevents full viral replication, suggesting a threshold is needed for macrophages to become highly infected.

Area of Science:

  • Virology
  • Immunology
  • Cell Biology

Background:

  • Cultured macaque macrophages support simian immunodeficiency virus (SIV) replication.
  • Viral p27 antigen production follows SIVmac251 inoculation in these cells.

Purpose of the Study:

  • To investigate the effect of neutralizing antibodies on SIV replication in macaque macrophages.
  • To determine the impact of antibody timing on viral antigen and nucleic acid levels.

Main Methods:

  • Using cultured macaque macrophages and SIVmac251.
  • Employing neutralizing macaque polyclonal and murine monoclonal antibodies at different time points post-inoculation.
  • Analyzing viral protein expression via Western blot and immunocytochemistry.
  • Quantifying viral RNA and DNA using in situ hybridization and polymerase chain reaction.

Main Results:

  • Pre-incubation of antibodies with SIV prevented infection.
  • Antibodies applied >3 days post-inoculation did not inhibit cytopathic replication.
  • Antibodies applied 24h post-inoculation resulted in sustained, low-level viral antigen production.
  • Western blot, immunocytochemistry, in situ hybridization, and PCR showed reduced viral components in treated cultures compared to controls.

Conclusions:

  • Macrophages may require a minimum viral threshold for maximal replication.
  • Early exposure to neutralizing antibodies before this threshold limits SIV replication in macrophages.
  • Timing of antibody intervention is critical for controlling SIV replication in macrophages.

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