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Journal of Virology, March 2006, p. 3078-3082, Vol. 80, No. 6
0022-538X/06/$08.00+0 doi:10.1128/JVI.80.6.3078-3082.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.
James D. Chappell,2,4
Geoffrey S. Baer,2,3,
Michelle Mochow-Grundy,2,3,
Steven E. Rodgers,2,3,¶
Yu Shyr,5
Alvin C. Powers,6,7
James W. Thomas,3,6 and
Terence S. Dermody1,2,3*
Departments of Pediatrics,1 Microbiology and Immunology,3 Pathology,4 Biostatistics,5 Medicine,6 Elizabeth B. Lamb Center for Pediatric Research, Vanderbilt University School of Medicine, Nashville, Tennessee 37232,2 VA Tennessee Valley Healthcare System, Nashville, Tennessee 372127
Received 11 January 2005/ Accepted 19 December 2005
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 ß-cell antigens and thereby delays development of diabetes.
Present address: Department of Pathology, Washington University School of Medicine, Campus Box 8118, 660 S. Euclid Avenue, St. Louis, MO 63110.
Present address: Department of Orthopaedic Surgery, University of Virginia School of Medicine, Charlottesville, VA 22908.
Present address: Department of Medical Administration, Vanderbilt University School of Medicine, Nashville, TN 37232.
¶ Present address: Department of Surgical Oncology, M. D. Anderson Cancer Center, Houston, TX 77030.
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