Reovirus delays diabetes onset but does not prevent insulitis in nonobese diabetic mice.

Wetzel JD, Barton ES, Chappell JD, Baer GS, Mochow-Grundy M, Rodgers SE, Shyr Y, Powers AC, Thomas JW, Dermody TS
J Virol. 2006 80 (6): 3078-82

PMID: 16501117 · PMCID: PMC1395416 · DOI:10.1128/JVI.80.6.3078-3082.2006

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 beta-cell antigens and thereby delays development of diabetes.

MeSH Terms (11)

Animals Animals, Newborn Autoimmune Diseases Diabetes Mellitus Female Islets of Langerhans Mammalian orthoreovirus 3 Mice Mice, Inbred NOD Pancreatic Diseases Reoviridae Infections

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