Related Experiment Videos

EMC virus and cultured human fetal pancreatic cells. Ultrastructural observations

Archives of Pathology
|August 1, 1975
PubMed

Insights

Encephalomyocarditis (EMC) virus infection caused severe damage to human fetal pancreatic acinar cells. The M variant was more potent, requiring fewer viral particles to induce cell alterations compared to the E variant.

Area of Science:

  • Virology
  • Cell Biology
  • Pathology

Background:

  • Encephalomyocarditis (EMC) virus is a known pathogen.
  • Human fetal pancreatic acinar cells are a model for studying viral effects on pancreatic tissue.

Purpose of the Study:

  • To investigate the ultrastructural effects of EMC virus variants (M and E) on human fetal pancreatic acinar cell cultures.
  • To compare the pathogenicity of EMC virus M and E variants in vitro.

Main Methods:

  • Human fetal pancreatic acinar cells were cultured and infected with EMC virus M or E variants.
  • Ultrastructural changes were assessed between days 3 and 5 post-infection.
  • Viral infectivity was quantified by plaque-forming units (PFU).

Main Results:

  • Severe ultrastructural damage, including nuclear chromatin changes and cytoplasmic vesicles, was observed in infected cells.
  • The M variant induced significant damage with 100 PFU, whereas the E variant required 10,000 PFU.
  • Viral particles were not identified within the damaged cells.

Conclusions:

  • EMC virus infection induces significant ultrastructural damage in human fetal pancreatic acinar cells.
  • The M variant of EMC virus is more virulent in this in vitro model than the E variant.
  • The observed lesions share similarities with in vivo findings in mice.

Related Concept Videos