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Pathogenesis of the B variant of encephalomyocarditis virus

R Shafi1, D R Cerutis, D J Giron

  • 1Department of Microbiology and Immunology, Wright State University College of Science and Mathematics and School of Medicine, Dayton, Ohio.

Insights

Encephalomyocarditis virus (EMCV)-B is not typically harmful when injected into the abdomen. However, when administered directly into the brain, EMCV-B causes encephalitis and brain damage in mice.

Area of Science:

  • Virology
  • Neuroscience
  • Immunology

Background:

  • Encephalomyocarditis virus (EMCV) variants are immunologically similar but cause distinct disease syndromes.
  • Most EMCV variants infect the central nervous system (CNS) when inoculated intraperitoneally (i.p.) in mice.
  • EMCV variant B is considered benign, showing no overt signs of infection even at high doses via i.p. inoculation.

Purpose of the Study:

  • To investigate the pathogenicity of EMCV-B when administered intracranially (i.c.) in mice.
  • To identify the specific brain regions infected by EMCV-B following i.c. inoculation.
  • To understand the factors contributing to EMCV-B's differential pathogenicity via i.p. versus i.c. routes.

Main Methods:

  • Intracranial inoculation of EMCV-B in a mouse model.
  • Observation and documentation of clinical signs of infection.
  • Histopathological examination of brain tissue to identify areas of infection and damage.
  • Analysis of viral replication within the CNS.

Main Results:

  • Intracranial administration of EMCV-B induced encephalitis and neuronal necrosis in the hippocampus (Ammon's horn) in mice.
  • Clinical signs of infection were observed following i.c. inoculation, similar to other EMCV variants.
  • EMCV-B replicated within the brain, indicating the presence of susceptible neuronal populations.
  • These findings suggest that EMCV-B possesses the capacity to infect brain cells.

Conclusions:

  • EMCV-B is pathogenic to the mouse brain when delivered directly via the intracranial route.
  • The benign nature of EMCV-B following intraperitoneal inoculation is likely due to its inability to breach the blood-brain barrier.
  • The presence of receptor sites for EMCV-B on brain cells facilitates viral entry and replication within the CNS.

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