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Enteroviruses and Type 1 Diabetes : Multiple Mechanisms and Factors?

Lloyd, Richard E ; Tamhankar, Manasi and Lernmark, Åke LU orcid (2022) In Annual Review of Medicine 73(1).
Abstract

Type 1 diabetes (T1D) is a chronic autoimmune disease characterized by insulin deficiency and resultant hyperglycemia. Complex interactions of genetic and environmental factors trigger the onset of autoimmune mechanisms responsible for development of autoimmunity to β cell antigens and subsequent development of T1D. A potential role of virus infections has long been hypothesized, and growing evidence continues to implicate enteroviruses as the most probable triggering viruses. Recent studies have strengthened the association between enteroviruses and development of autoimmunity in T1D patients, potentially through persistent infections. Enterovirus infections may contribute to different stages of disease development. We review data from... (More)

Type 1 diabetes (T1D) is a chronic autoimmune disease characterized by insulin deficiency and resultant hyperglycemia. Complex interactions of genetic and environmental factors trigger the onset of autoimmune mechanisms responsible for development of autoimmunity to β cell antigens and subsequent development of T1D. A potential role of virus infections has long been hypothesized, and growing evidence continues to implicate enteroviruses as the most probable triggering viruses. Recent studies have strengthened the association between enteroviruses and development of autoimmunity in T1D patients, potentially through persistent infections. Enterovirus infections may contribute to different stages of disease development. We review data from both human cohort studies and experimental research exploring the potential roles and molecular mechanisms by which enterovirus infections can impact disease outcome. Expected final online publication date for the Annual Review of Medicine, Volume 73 is January 2022. Please see http://www.annualreviews.org/page/journal/pubdates for revised estimates.

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type
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publication status
published
subject
in
Annual Review of Medicine
volume
73
issue
1
publisher
Annual Reviews
external identifiers
  • pmid:34794324
  • scopus:85120822510
ISSN
0066-4219
DOI
10.1146/annurev-med-042320-015952
language
English
LU publication?
yes
id
b401a51b-1a27-495e-8fb7-b6fcf93119ed
date added to LUP
2021-11-24 13:10:28
date last changed
2024-08-08 14:42:39
@article{b401a51b-1a27-495e-8fb7-b6fcf93119ed,
  abstract     = {{<p>Type 1 diabetes (T1D) is a chronic autoimmune disease characterized by insulin deficiency and resultant hyperglycemia. Complex interactions of genetic and environmental factors trigger the onset of autoimmune mechanisms responsible for development of autoimmunity to β cell antigens and subsequent development of T1D. A potential role of virus infections has long been hypothesized, and growing evidence continues to implicate enteroviruses as the most probable triggering viruses. Recent studies have strengthened the association between enteroviruses and development of autoimmunity in T1D patients, potentially through persistent infections. Enterovirus infections may contribute to different stages of disease development. We review data from both human cohort studies and experimental research exploring the potential roles and molecular mechanisms by which enterovirus infections can impact disease outcome. Expected final online publication date for the Annual Review of Medicine, Volume 73 is January 2022. Please see http://www.annualreviews.org/page/journal/pubdates for revised estimates.</p>}},
  author       = {{Lloyd, Richard E and Tamhankar, Manasi and Lernmark, Åke}},
  issn         = {{0066-4219}},
  language     = {{eng}},
  number       = {{1}},
  publisher    = {{Annual Reviews}},
  series       = {{Annual Review of Medicine}},
  title        = {{Enteroviruses and Type 1 Diabetes : Multiple Mechanisms and Factors?}},
  url          = {{http://dx.doi.org/10.1146/annurev-med-042320-015952}},
  doi          = {{10.1146/annurev-med-042320-015952}},
  volume       = {{73}},
  year         = {{2022}},
}