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Virus infections in type 1 diabetes

Ken Coppieters UGent, Tobias Boettler and Matthias von Herrath (2012) COLD SPRING HARBOR PERSPECTIVES IN MEDICINE. 2(1).
abstract
The precise etiology of type 1 diabetes (T1D) is still unknown, but viruses have long been suggested as a potential environmental trigger for the disease. However, despite decades of research, the body of evidence supporting a relationship between viral infections and initiation or acceleration of islet autoimmunity remains largely circumstantial. The most robust association with viruses and T1D involves enterovirus species, of which some strains have the ability to induce or accelerate disease in animal models. Several hypotheses have been formulated to mechanistically explain how viruses may affect islet autoimmunity and b-cell decay. The recent observation that certain viral infections, when encountered at the right time and infectious dose, can prevent autoimmune diabetes illustrates that potential relationships may be more complex than previously thought. Here, we provide a concise summary of data obtained in mouse models and humans, and identify future avenues toward a better characterization of the association between viruses and T1D.
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (review)
publication status
published
subject
journal title
COLD SPRING HARBOR PERSPECTIVES IN MEDICINE
Cold Spring Harbor Perspect. Med.
volume
2
issue
1
article_number
a007682
pages
14 pages
JCR category
MEDICINE, RESEARCH & EXPERIMENTAL
JCR impact factor
5.5 (2012)
JCR rank
14/119 (2012)
JCR quartile
1 (2012)
ISSN
2157-1422
DOI
10.1101/cshperspect.a007682
language
English
UGent publication?
no
classification
A2
copyright statement
I have transferred the copyright for this publication to the publisher
id
2120309
handle
http://hdl.handle.net/1854/LU-2120309
date created
2012-05-30 10:01:14
date last changed
2012-06-06 15:01:43
@article{2120309,
  abstract     = {The precise etiology of type 1 diabetes (T1D) is still unknown, but viruses have long been suggested as a potential environmental trigger for the disease. However, despite decades of research, the body of evidence supporting a relationship between viral infections and initiation or acceleration of islet autoimmunity remains largely circumstantial. The most robust association with viruses and T1D involves enterovirus species, of which some strains have the ability to induce or accelerate disease in animal models. Several hypotheses have been formulated to mechanistically explain how viruses may affect islet autoimmunity and b-cell decay. The recent observation that certain viral infections, when encountered at the right time and infectious dose, can prevent autoimmune diabetes illustrates that potential relationships may be more complex than previously thought. Here, we provide a concise summary of data obtained in mouse models and humans, and identify future avenues toward a better characterization of the association between viruses and T1D.},
  articleno    = {a007682},
  author       = {Coppieters, Ken and Boettler, Tobias and von Herrath, Matthias},
  issn         = {2157-1422},
  journal      = {COLD SPRING HARBOR PERSPECTIVES IN MEDICINE},
  language     = {eng},
  number       = {1},
  pages        = {14},
  title        = {Virus infections in type 1 diabetes},
  url          = {http://dx.doi.org/10.1101/cshperspect.a007682},
  volume       = {2},
  year         = {2012},
}

Chicago
Coppieters, Ken, Tobias Boettler, and Matthias von Herrath. 2012. “Virus Infections in Type 1 Diabetes.” Cold Spring Harbor Perspectives in Medicine 2 (1).
APA
Coppieters, K., Boettler, T., & von Herrath, M. (2012). Virus infections in type 1 diabetes. COLD SPRING HARBOR PERSPECTIVES IN MEDICINE, 2(1).
Vancouver
1.
Coppieters K, Boettler T, von Herrath M. Virus infections in type 1 diabetes. COLD SPRING HARBOR PERSPECTIVES IN MEDICINE. 2012;2(1).
MLA
Coppieters, Ken, Tobias Boettler, and Matthias von Herrath. “Virus Infections in Type 1 Diabetes.” COLD SPRING HARBOR PERSPECTIVES IN MEDICINE 2.1 (2012): n. pag. Print.