Abstract
Mice infected with reovirus develop abnormalities in glucose homeostasis. Reovirus strain type 3 Abney (T3A) was capable of systemic infection of nonobese diabetic (NOD) mice, an experimental model of autoimmune diabetes. Reovirus antigen was detected in pancreatic islets of T3A-infected mice, and primary cultures of pancreatic islets from NOD mice supported T3A growth. Significantly fewer T3A-infected animals compared to uninfected controls developed diabetes. However, despite the alteration in diabetes penetrance, insulitis was evident in T3A-infected mice. These results suggest that viral infection of NOD mice alters autoimmune responses to β-cell antigens and thereby delays development of diabetes.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 3078-3082 |
| Number of pages | 5 |
| Journal | Journal of virology |
| Volume | 80 |
| Issue number | 6 |
| DOIs | |
| State | Published - Mar 2006 |
ASJC Scopus subject areas
- Microbiology
- Immunology
- Insect Science
- Virology
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Wetzel, J. D., Barton, E. S., Chappell, J. D., Baer, G. S., Mochow-Grundy, M., Rodgers, S. E., Shyr, Y., Powers, A. C., Thomas, J. W., & Dermody, T. S. (2006). Reovirus delays diabetes onset but does not prevent insulitis in nonobese diabetic mice. Journal of virology, 80(6), 3078-3082. https://doi.org/10.1128/JVI.80.6.3078-3082.2006