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Related Experiment Videos

Target cells during early SIV encephalopathy

B Hurtrel1, L Chakrabarti, M Hurtrel

  • 1Unité d'Oncologie virale, Institut Pasteur, Paris, France.

Research in Virology
|January 1, 1993
PubMed
Summary
This summary is machine-generated.

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Early simian immunodeficiency virus (SIV) brain infection in macaques involves perivascular macrophages. Latency results from low-level viral replication, not a transcription block, with microglia showing low susceptibility.

Area of Science:

  • Neuroscience
  • Virology
  • Immunology

Background:

  • Early encephalopathy is a concern in SIV infection.
  • Understanding viral entry and replication in the brain is crucial.

Purpose of the Study:

  • To investigate the early stages of SIV-mac-251 brain infection in rhesus macaques.
  • To identify the cell types involved and the mechanism of viral latency.

Main Methods:

  • Intravenous (i.v.) and intracerebral (i.c.) SIV-mac-251 inoculation in rhesus macaques.
  • Histopathological analysis, immunophenotyping, combined immunochemistry, and in situ hybridization.
  • Analysis of SIV RNA expression using genome probes.

Main Results:

  • Early infection showed gliosis, perivascular infiltrates, microgliosis, and macrophage infiltration.

Related Experiment Videos

  • Infected cells were primarily perivascular macrophages, indicating their role in viral entry.
  • Latent infection resulted from low-level productive replication, not a complete transcription block.
  • Intracerebral SIV inoculation induced mild encephalitis, with resident microglia showing poor susceptibility.

    • Conclusions:

    • Perivascular macrophages are key in early SIV brain dissemination.
    • Low-level viral replication underlies SIV latency in the brain.
    • Resident microglia are relatively resistant to SIV infection.