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Coronavirus mouse hepatitis virus (MHV)-A59 causes a persistent, productive infection in primary glial cell cultures

E Lavi1, A Suzumura, M Hirayama

  • 1Department of Microbiology, University of Pennsylvania School of Medicine, Philadelphia 19104.

Microbial Pathogenesis
|August 1, 1987
PubMed

Insights

Murine hepatitis virus (MHV-A59) establishes persistent infections in mouse white matter. Glial cells, including oligodendrocytes and astrocytes, support non-lytic but productive viral replication, contributing to chronic demyelinating disease.

Area of Science:

  • Neurovirology
  • Immunology
  • Cell Biology

Background:

  • Murine hepatitis virus (MHV-A59) induces chronic demyelinating disease in mice.
  • Viral genome persistence in white matter is a hallmark of MHV-A59 infection.
  • Glial cells are potential targets for chronic viral infections.

Purpose of the Study:

  • To investigate the role of glial cells in MHV-A59 viral persistence.
  • To determine if glial cells support productive MHV-A59 infection in vitro.
  • To understand the contribution of glial cells to chronic demyelinating disease.

Main Methods:

  • Infection of mixed glial, enriched oligodendrocyte, and enriched astrocyte cultures with MHV-A59 in vitro.
  • Detection of viral antigens in glial cells via immunofluorescence.
  • Quantification of infectious virus release from cultures.
  • Comparison of in vitro infection with cultures derived from infected mice.

Main Results:

  • Oligodendrocytes (10%) and astrocytes (30%) expressed viral antigens post-MHV-A59 infection without significant cell death.
  • Infectious virus was continuously released from all glial cultures for at least 45 days.
  • Glial cultures from previously infected mice mirrored in vitro infection patterns.
  • Glial cells serve as early sites of MHV-A59 infection in vivo and in vitro.

Conclusions:

  • Glial cells support a non-lytic but productive MHV-A59 infection.
  • Glial cells are likely crucial for the persistence of MHV-A59 in the central nervous system.
  • These findings elucidate mechanisms contributing to MHV-A59-induced chronic demyelinating disease.

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