Retrovirus as trigger, precipitator or marker?

Access through your institution Buy or subscribe Insulin-dependent diabetes mellitus (IDDM) is an autoimmune disease that is characterized by the specific destruction of insulin-producing

β-cells in the pancreatic islets of Langerhans1,2. Despite decades of intensive investigation, the trigger for this self-attack has remained a mystery. But in the 25 July issue of _Cell_,

Conrad _et al_.3 describe new findings which suggest that a virus may be responsible. It has long been thought that human IDDM may be triggered by an infectious agent1,2. The main evidence

is that the concordance rate for monozygotic twins is only about 50 per cent; that incidence varies along a north-south gradient; and that the frequency of diabetes is increasing at a

striking rate in some countries. But there are alternative explanations for these epidemiological phenomena — in fact, most of the variations within and between countries (for example, the

higher incidence in more northern European countries) fit better with the idea that infections nonspecifically protect from, rather than incite, disease. This idea would also be more

consistent with observations on the non-obese diabetic mouse (the most popular animal model of autoimmune diabetes), which has the highest incidence of disease when it is housed under

germ-free conditions. So, because there has never been direct evidence that an infectious agent triggershuman IDDM, support for the hypothesis of an infectious trigger dwindled. This is a

preview of subscription content, access via your institution ACCESS OPTIONS Access through your institution Subscribe to this journal Receive 51 print issues and online access $199.00 per

year only $3.90 per issue Learn more Buy this article * Purchase on SpringerLink * Instant access to full article PDF Buy now Prices may be subject to local taxes which are calculated during

checkout ADDITIONAL ACCESS OPTIONS: * Log in * Learn about institutional subscriptions * Read our FAQs * Contact customer support REFERENCES * Bach, J. F. _Endocr. Revs_ 15, 516–542 (1994).

Google Scholar  * Tisch, R. & McDevitt, H. _Cell_ 85, 291–297 (1996). Google Scholar  * Conrad, B._et al._ _Cell_ 90, 303–313 (1997). Google Scholar  * Conrad, B._et al._ _Nature_ 371,

351–355 (1994). Google Scholar  * MacDonald, H. R. & Acha-Orbea, H. _Nature_ 371, 283– 284 (1994). Article  ADS  CAS  Google Scholar  * Gaskins, H. R., Prochazka, M., Hamaguchi, K.,

Serreze, D. V. & Leiter, E. H. _J. Clin. Invest._ 90, 2220–2227 (1992). Google Scholar  * Suenaga, K. & Yoon, J. -W. _Diabetes_ 37, 1722–1726 (1988). Google Scholar  * André, I._et

al._ _Proc. Natl Acad. Sci. USA_ 93, 2260–2263 (1996). Google Scholar  * Moroni, C. & Schumann, G. _Nature_ 254, 60–61 (1997). Article  Google Scholar  * Leiter, E. H., Fewell, J. W.

& Kuff, E. L. _J. Exp. Med._ 163, 87–100 (1986). Google Scholar  * Perron, H._et al._ _Proc. Natl Acad. Sci. USA_ 94, 7583–7588 (1997). Google Scholar  Download references AUTHOR

INFORMATION AUTHORS AND AFFILIATIONS * Institut de Génétique et de Biologie Moléculaire et Cellulaire (CNRS/INSERM/ULP), 1 rue Laurent Fries, Illkirch, 67404, C.U. de Strasbourg, France

Christophe Benoist & Diane Mathis Authors * Christophe Benoist View author publications You can also search for this author inPubMed Google Scholar * Diane Mathis View author

publications You can also search for this author inPubMed Google Scholar RIGHTS AND PERMISSIONS Reprints and permissions ABOUT THIS ARTICLE CITE THIS ARTICLE Benoist, C., Mathis, D.

Retrovirus as trigger, precipitator or marker?. _Nature_ 388, 833–834 (1997). https://doi.org/10.1038/42145 Download citation * Issue Date: 28 August 1997 * DOI:

https://doi.org/10.1038/42145 SHARE THIS ARTICLE Anyone you share the following link with will be able to read this content: Get shareable link Sorry, a shareable link is not currently

available for this article. Copy to clipboard Provided by the Springer Nature SharedIt content-sharing initiative