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EMC virus and cultured human fetal pancreatic cells. Ultrastructural observations
Abstract:
Tissue cultures of pancreatic acinar cells of seven human fetuses were infected with either the M or the E variant of the encephalomyocarditis (EMC) virus. Between the third and fifth days after infection, severe ultrastructural damage was noted. Margination, condensation, and fragmentation of the nuclear chromatin and the appearance of numerous cytoplasmic vesicles filled with finely granular material were the major changes observed. Viral particles were not identified. One hundred plaque-forming units (PFU) were sufficient to induce these alterations with the M variant while 10,000 PFU were needed to obtain the same results with the EMC-E virus. The described lesions are qualitatively similar to those induced in vivo in experimental CD-1 mice infected with the virus.
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.