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Junin virus-induced astrocytosis is impaired by iNOS inhibition

Ricardo M Gómez1, Alejandra Yep, Mirta Schattner

  • 1Departamento de Microbiología, Facultad de Medicina, Universidad de Buenos Aires, Argentina.

Journal of Medical Virology
|November 19, 2002
PubMed

Insights

Inhibiting inducible nitric oxide synthase (iNOS) in Junin virus-infected mice increased mortality, suggesting nitric oxide (NO) plays a protective role by enhancing astrocyte responses in the central nervous system (CNS).

Area of Science:

  • Neuroscience
  • Virology
  • Immunology

Background:

  • Junin virus (JV) causes mild encephalitis in mice, with unclear lethality mechanisms.
  • Investigating the role of inducible nitric oxide synthase (iNOS) in JV pathogenesis is crucial.

Purpose of the Study:

  • To evaluate the role of iNOS in Junin virus-induced encephalitis.
  • To determine if iNOS inhibition affects mortality and neuropathology in a murine model.

Main Methods:

  • Mice were intracerebrally infected with Junin virus (JV strain #44).
  • Immunoperoxidase staining assessed iNOS, SODm, and GPX expression.
  • Amino guanidine (AG) was used to inhibit iNOS activity.
  • Mortality rates, viral titers, and glial fibrillary acidic (GFAP) labeling (astrocyte marker) were analyzed.

Main Results:

  • Increased expression of iNOS, SODm, and GPX was observed in infected mouse brains.
  • iNOS inhibition with AG significantly increased mortality (70% vs. 40%) compared to controls.
  • AG treatment led to lower astrocytosis (GFAP labeling) despite similar viral loads.
  • No differences in neuronal SODm or GPX expression were found between groups.

Conclusions:

  • Nitric oxide (NO) synthesized by iNOS appears to have a protective role in JV encephalitis.
  • This protection is mediated by enhanced astrocyte activation, not by reduced viral replication.
  • Astrocyte response is a key beneficial factor in mitigating virus-induced central nervous system (CNS) damage.

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