Coxsackievirus-mediated hyperglycemia is enhanced by reinfection and this occurs independent of T cells

Marc S. Horwitz, Alex Ilic, Cody Fine, Enrique Rodriguez, Nora Sarvetnick

Research output: Contribution to journalArticle

17 Citations (Scopus)

Abstract

The induction of autoimmunity by viruses has been hypothesized to occur by a number of mechanisms. Coxsackievirus B4 (CB4) induces hyperglycemia in SJL mice resembling diabetes in humans. While virus is effectively cleared within 2 weeks, hyperglycemia does not appear until about 8-12 weeks postinfection at a time when replicative virus is no longer detectable. In SJL mice, reinfection with CB4 enhanced the development of hyperglycemia. As predicted, the immune system responded more rapidly to the second infection and virus was cleared more swiftly. However, while infiltrating T cells were found within the pancreas, depletion of the CD4 T cell population prior to secondary infection or use of CD8 knock-out mice had no effect on the development of virus-mediated hyperglycemia. In conclusion, enhanced hyperglycemia induced by CB4 occurs independent of the T cell response.

Original languageEnglish (US)
Pages (from-to)510-520
Number of pages11
JournalVirology
Volume314
Issue number2
DOIs
StatePublished - Sep 30 2003

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Enterovirus
Hyperglycemia
T-Lymphocytes
Viruses
Virus Activation
Virus Diseases
Autoimmunity
Coinfection
Knockout Mice
Pancreas
Immune System
Population

Keywords

  • Coxsackievirus
  • Insulin-dependent diabetes mellitus
  • T lymphocytes

ASJC Scopus subject areas

  • Virology

Cite this

Coxsackievirus-mediated hyperglycemia is enhanced by reinfection and this occurs independent of T cells. / Horwitz, Marc S.; Ilic, Alex; Fine, Cody; Rodriguez, Enrique; Sarvetnick, Nora.

In: Virology, Vol. 314, No. 2, 30.09.2003, p. 510-520.

Research output: Contribution to journalArticle

Horwitz, Marc S. ; Ilic, Alex ; Fine, Cody ; Rodriguez, Enrique ; Sarvetnick, Nora. / Coxsackievirus-mediated hyperglycemia is enhanced by reinfection and this occurs independent of T cells. In: Virology. 2003 ; Vol. 314, No. 2. pp. 510-520.
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