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Updated: Aug 10, 2026
A Murine Model of Dengue Virus-induced Acute Viral Encephalitis-like Disease
Published on: April 28, 2019
A genetically determined host factor controlling susceptibility to encephalomyocarditis virus-induced diabetes in
1Department of Microbiology and Infectious Diseases, Faculty of Medicine, University of Calgary, Alberta, Canada.
Abstract:
Levels of insulin mRNA in pancreata from SJL/J male mice susceptible to encephalomyocarditis (EMC)-D virus-induced diabetes started to decrease rapidly 24 h after injection with EMC-D virus and only a trace remained 72 h after injection. In contrast, insulin mRNA in pancreata from C57BL/6J male mice resistant to EMC-D virus-induced diabetes did not show any significant changes 0 to 96 h after injection. EMC-D viral RNA in pancreata from SJL/J mice started to increase rapidly 24 h after injection, reached its peak at 48 h and then decreased gradually. In contrast, EMC-D viral RNA in pancreata from C57BL/6J mice was undetectable except for the 24 and 48 h points after injection. EMC-D virus could bind readily to freshly isolated beta cells from SJL/J mice but scarcely bound to beta cells from C57BL/6J mice. In contrast, there was no significant difference between SJL/J and C57BL/6J mice in binding of EMC-D virus to their cultured beta cells. The rate of EMC-D viral attachment to beta cells from C57BL/6J mice increased significantly during the first 24 h culture period and reached the same rate of attachment as that seen for beta cells from SJL/J mice. This suggests that viral receptors on the beta cells derived from strains of mice resistant to EMC virus-induced diabetes are not expressed in vivo, but are expressed during cell culture, rendering the beta cells susceptible to EMC viral infection. On the basis of our previous and present observations, we conclude that a genetic factor controlling susceptibility to EMC-D virus-induced diabetes may operate by modulating the expression of viral receptors on the beta cells.
Insights
Susceptible mice show decreased insulin mRNA after encephalomyocarditis (EMC)-D virus infection, while resistant mice do not. A genetic factor likely controls diabetes susceptibility by modulating viral receptor expression on beta cells.
Area of Science:
- Virology
- Immunology
- Genetics
Background:
- Encephalomyocarditis (EMC)-D virus can induce diabetes in susceptible mouse strains.
- Understanding the genetic basis of EMC-D virus-induced diabetes is crucial for developing preventative strategies.
Purpose of the Study:
- To investigate the role of genetic factors in EMC-D virus-induced diabetes susceptibility.
- To explore the mechanism of viral receptor expression on beta cells in different mouse strains.
Main Methods:
- Comparing insulin mRNA and viral RNA levels in susceptible (SJL/J) and resistant (C57BL/6J) mice post-EMC-D virus injection.
- Assessing EMC-D virus binding to freshly isolated and cultured beta cells from both mouse strains.
Main Results:
- SJL/J mice exhibited decreased insulin mRNA and increased viral RNA, unlike C57BL/6J mice.
- EMC-D virus readily bound to beta cells from SJL/J mice in vivo but not C57BL/6J mice.
- In vitro culture led to increased viral binding in C57BL/6J mouse beta cells, suggesting inducible receptor expression.
Conclusions:
- A genetic factor influences EMC-D virus-induced diabetes susceptibility.
- This genetic factor likely modulates the expression of viral receptors on beta cells, with expression being inducible in resistant strains.
