Key result
Diabetogenic EMC-D virus attaches ~6 times more to murine primary beta-cells than nondiabetogenic EMC-B.
Population
Primary beta-cells extracted from male ICR Swiss mice
Comparison
Encephalomyocarditis virus D variant (EMC-D) vs Encephalomyocarditis virus B variant (EMC-B)
Design
Preclinical
Authors
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Attachment differences may underlie EMC variant diabetogenicity in mice; leaves open relevance to human viral triggers of beta-cell loss.
Effect estimate: up to six times more
The diabetogenic potential of the EMC-D virus variant in mice may be explained by its higher attachment rate to pancreatic beta-cells compared to the nondiabetogenic EMC-B variant, rather than differences in interferon induction.
Kaptur et al. (1989) studied Insulin-dependent diabetes mellitus (IDDM)-like syndrome. EMC-D virus vs. EMC-B virus was evaluated on Virus attachment to primary beta-cells (up to six times more). Up to six times more diabetogenic EMC-D virus attaches to primary beta-cells extracted from male ICR Swiss mice compared to the nondiabetogenic EMC-B virus.
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