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Journal of Virology, June 2006, p. 5637-5643, Vol. 80, No. 11
0022-538X/06/$08.00+0 doi:10.1128/JVI.02361-05
Copyright © 2006, American Society for Microbiology. All Rights Reserved.
Kristen M. Drescher,2
Nora M. Chapman,1 and
Steven Tracy1*
Enterovirus Research Laboratory, Department of Pathology and Microbiology, University of Nebraska Medical Center, 986495 Nebraska Medical Center, Omaha, Nebraska 68198-6495,1 Department of Medical Microbiology and Immunology, Creighton University School of Medicine, Omaha, Nebraska 681782
Received 9 November 2005/ Accepted 14 March 2006
Group B coxsackieviruses can initiate rapid onset type 1 diabetes (T1D) in old nonobese diabetic (NOD) mice. Inoculating high doses of poorly pathogenic CVB3/GA per mouse initiated rapid onset T1D. Viral protein was detectable in islets shortly after inoculation in association with beta cells as well as other primary islet cell types. The virulent strain CVB3/28 replicated to higher titers more rapidly than CVB3/GA in the pancreas and in established beta cell cultures. Exchange of 5'-nontranslated regions between the two CVB3 strains demonstrated a variable impact on replication in beta cell cultures and suppression of in vivo replication for both strains. While any CVB strain may be able to induce T1D in prediabetic NOD mice, T1D onset is linked both to the viral replication rate and infectious dose.
Present address: Department of Internal Medicine and Cardiology, Kitasato University School of Medicine, 1-15-1 Kitasato, Sagamihara 228-8555, Japan.
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