Cited by 56Diabetes and associated disordersViral Infections and Immunology ResearchPancreatic function and diabetes

The DOI matches its Crossref record; 30 of the 30 references it cites were found in a registry or an index.

Viruses Cause Type 1 Diabetes in Animals

YOON, JI‐WON, JUN, HEE‐SOOK·2006·Annals of the New York Academy of Sciences

Abstract

Abstract: More than 10 viruses have been reported to be associated with the development of type 1 diabetes‐like symptoms in animals, with the best evidence coming from studies on the D variant of encephalomyocarditis (EMC‐D) virus in mice and Kilham rat virus (KRV) in rats. A high titer of EMC‐D viral infection results in the development of diabetes within 3 days, primarily due to the rapid destruction of β cells by viral replication within the cells. A low titer of EMC‐D viral infection results in the recruitment of macrophages to the islets. Soluble mediators produced by activated macrophages play a critical role in the destruction of residual β cells. A single amino acid at position 776 of the EMC viral genome controls the diabetogenicity of the virus. In contrast, KRV causes autoimmune type 1 diabetes in diabetes‐resistant BioBreeding (DR‐BB) rats without direct infection of β cells. Macrophages play an important role in the development of diabetes in KRV‐infected DR‐BB rats. As well, KRV infection preferentially activates effector T cells, such as Th1‐like CD45RC+CD4+ T cells and CD8+ T cells, and downregulates regulatory T cells, such as Th2‐like CD45RC−CD4+ T cells. This results in the breakdown of the immune balance, contributing to the development of diabetes in KRV‐infected DR‐BB rats.

Overview

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Registry

Crossref · 10.1196/annals.1375.021

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30 of 30 references verified0 citation errors · 0 not checkable

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  • Upon low-dose infection of mice the virus initially replicates in pancreatic β cells, leading to the recruitment of macrophages that are activated at the pancreatic islets.

    “It appears that upon low-dose infection of mice the virus initially replicates in pancreatic β cells, leading to the recruitment of macrophages that are activated at the pancreatic islets.”

    From The encephalomyocarditis virus (2012) · cites this paper as [120]

  • Activated macrophages produce soluble mediators like interleukin-1 β (IL-1 β) and produce TNFα and nitric oxide (NO), which induce apoptosis in β cells.

    “These activated macrophages produce soluble mediators like interleukin-1 β (IL-1 β) and produce TNFα and nitric oxide (NO), which induce apoptosis in β cells (for review see ref. 120).”

    From The encephalomyocarditis virus (2012) · cites this paper as [120]

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Metadata

Authors
YOON, J., & JUN, H.
Affiliations
Rosalind Franklin University of Medicine and Science (US)
Corresponding author
JUN, HEE‐SOOK
Venue
Annals of the New York Academy of Sciences
Publisher
Wiley
Published
2006-10
Volume
1079
Issue
1
Pages
138-146
ISSN
  • 0077-8923 (ISSN-L)
  • 1749-6632
OpenAlex
W2062129673
Cited by
56
References
30
Citations by year
2026: 1 · 2025: 1 · 2024: 3 · 2023: 2 · 2022: 3 · 2020: 4 · 2019: 2 · 2018: 1 · 2017: 2 · 2016: 2 · 2015: 2 · 2014: 5 · 2013: 3 · 2012: 7
FWCI
1.70
Type
journal article
Language
en
Open access
closed
Locations
  • Annals of the New York Academy of Sciences (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Diabetes and associated disorders
  • Health Sciences › Medicine › Infectious Diseases › Viral Infections and Immunology Research
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Pancreatic function and diabetes
Keywords
type 1 diabetes, viral etiology of diabetes, Kilham rat virus, beta cell destruction, macrophage recruitment, islets, autoimmune diabetes, BioBreeding rat, regulatory T cells, Th1/Th2 balance
MeSH terms
Animals, Diabetes Mellitus, Type 1, Disease Models, Animal, Encephalomyocarditis virus, Islets of Langerhans, Macrophages, T-Lymphocytes, Parvovirus, Mice, Rats

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