HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Kruppenbacher, J. P. Articles by Eggers, H. J. Search for Related Content PubMed PubMed Citation Articles by Kruppenbacher, J. P. Articles by Eggers, H. J. Agricola Articles by Kruppenbacher, J. P. Articles by Eggers, H. J.

Encephalomyocarditis Virus and Diabetes Mellitus: Studies on Virus Mutants in Susceptible and Non-susceptible Mice

Institut für Virologie der Universität zu Köln, Fürst-Pückler Strasse 56, D-5000 Köln 41
and¹ Abteilung für Kinderpathologie der Universität Mainz, Langenbeck Strasse 1, D-6500 Mainz, Federal Republic of Germany

The so-called M-variant (especially subtype D) of encephalomyocarditis virus (EMCV) induces a diabetes-like syndrome in certain mouse strains which may serve as a model of insulin-dependent diabetes mellitus (IDDM) in man. The development and course of diabetes was influenced by a number of virus and host factors, among these being virus strain, virus dose, mouse strain, age, sex, and the host's immunological status. In a D-variant stock of EMCV, we found a virus plaque variant (PV 2) diabetogenic for DBA/2 mice, and at least one variant (PV 7) that did not affect carbohydrate metabolism. Although the diabetogenicity of PV 2 proved to be a genetically stable characteristic after further passages in vivo and in vitro, the incidence of diabetes varied somewhat (mean value 65% in 10-week-old DBA/2 mice infected with 10⁵ p.f.u.). Both lower (10¹ or 10³ p.f.u.) and higher (10⁷ or 10⁸ p.f.u.) virus doses led to a diminished incidence and severity of diabetes. In younger animals (5 weeks) transient hyperglycaemia often appeared, whereas in older animals (20 weeks) there was a higher rate of mortality. Histological examination of the islets of Langerhans in diabetes-susceptible (DBA/2) and resistant (C57BL/6) mice revealed that EMCV-induced hyperglycaemia appeared to develop in parallel to islet cell damage. Even in diabetic animals, some unaffected islets were regularly found. This study demonstrates that EMCV mutants may have completely different biological effects and produce diabetes only in special circumstances. Host factors play a significant role in the development of diabetes.

Keywords: EMC virus, diabetes mellitus, islet cell damage

Received 21 August 1984; accepted 27 November 1984.

This article has been cited by other articles:

				M. G. Mujtaba, C. B. Patel, R. A. Patel, L. O. Flowers, M. A. Burkhart, L. W. Waiboci, J. Martin, M. I. Haider, C. M. Ahmed, and H. M. Johnson The Gamma Interferon (IFN-{gamma}) Mimetic Peptide IFN-{gamma}(95-133) Prevents Encephalomyocarditis Virus Infection both in Tissue Culture and in Mice. Clin. Vaccine Immunol., August 1, 2006; 13(8): 944 - 952. [Abstract] [Full Text] [PDF]

				R. LaRue, S. Myers, L. Brewer, D. P. Shaw, C. Brown, B. S. Seal, and M. K. Njenga A Wild-Type Porcine Encephalomyocarditis Virus Containing a Short Poly(C) Tract Is Pathogenic to Mice, Pigs, and Cynomolgus Macaques J. Virol., September 1, 2003; 77(17): 9136 - 9146. [Abstract] [Full Text] [PDF]