Differing attachment of diabetogenic and nondiabetogenic variants of encephalomyocarditis virus to beta-cells
| Autor: | Donald C. Thomas, David J. Giron, Paulina E. Kaptur |
|---|---|
| Rok vydání: | 1989 |
| Předmět: |
Male
Pancreatic disease Virus Cultivation Ratón Endocrinology Diabetes and Metabolism Enzyme-Linked Immunosorbent Assay Virus Diabetes Mellitus Experimental Pathogenesis Islets of Langerhans Mice Interferon Internal Medicine medicine Animals Inducer Encephalomyocarditis virus Antigens Viral B cell Cell Line Transformed Mice Inbred ICR biology Genetic Variation medicine.disease biology.organism_classification Virology Cardiovirus medicine.anatomical_structure Adsorption Interferons medicine.drug |
| Zdroj: | Diabetes. 38(9) |
| ISSN: | 0012-1797 |
| Popis: | The D variant of encephalomyocarditis (EMC-D) virus does not induce the production of interferon (IFN) and produces an insulin-dependent diabetes mellitus (IDDM)-like syndrome in certain mouse strains. In contrast, the B variant (EMC-B) virus, which is serologically identical to EMC-D virus, is a good inducer of IFN and is nondiabetogenic. It has been postulated that IFN may play a major role in determining the ability of these two viruses to infect pancreatic β-cells. However, recent studies have shown that ICR Swiss and BALB/cByJ male mice are not protected by IFN against EMC-D virus-induced IDDM. Furthermore, treatment of these two strains of mice with anti-IFN γ-globulin before infection with EMC-B virus does not result in diabetes. These observations suggest that mechanisms other than the IFN system are involved in determining the ability of the viruses to infect and destroy β-cells. Studies were initiated to identify other mechanisms of action. In this communication, we show that up to six times more EMC-D than EMC-B virus attaches to primary β-cells extracted from male ICR Swiss mice. This difference in ability to attach to β-cells may account for the difference in the diabetic potential of this mouse strain. |
| Databáze: | OpenAIRE |
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