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Target Concepts:
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Query: UMLS:C0011854 (
type 1 diabetes
)
20,749
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Oral infection
with Herpes Simplex Virus (HSV) is a frequent and well documented complication in immunosuppressed individuals including patients on immunosuppressive medication. We report the development of severe oral infection with HSV type 1 in a 34 year old woman with
type 1 diabetes
mellitus and end stage renal disease (ESRD) following cadaveric renal transplantation at the Western General Hospital, Edinburgh. The role of acyclovir in therapy and chemoprophylaxis is discussed.
...
PMID:Oral herpes simplex virus type 1 infection following cadaveric renal transplantation in a young type 1 diabetic female. The role of acyclovir: a case report. 129 40
Infection modulates
type 1 diabetes
, a common autoimmune disease characterized by the destruction of insulin-producing islet beta cells in the pancreas. Childhood rotavirus infections have been associated with exacerbations in islet autoimmunity. Nonobese diabetic (NOD) mice develop lymphocytic islet infiltration (insulitis) and then clinical diabetes, whereas NOD8.3 TCR mice, transgenic for a T-cell receptor (TCR) specific for an important islet autoantigen, show more rapid diabetes onset.
Oral infection
of infant NOD mice with the monkey rotavirus strain RRV delays diabetes development. Here, the effect of RRV infection on diabetes development once insulitis is established was determined. NOD and NOD8.3 TCR mice were inoculated with RRV aged > or = 12 and 5 weeks, respectively. Diabetes onset was significantly accelerated in both models (P < 0.024), although RRV infection was asymptomatic and confined to the intestine. The degree of diabetes acceleration was related to the serum antibody titer to RRV. RRV-infected NOD mice showed a possible trend toward increased insulitis development. Infected males showed increased CD8(+) T-cell proportions in islets. Levels of beta-cell major histocompatibility complex class I expression and islet tumor necrosis factor alpha mRNA were elevated in at least one model. NOD mouse exposure to mouse rotavirus in a natural experiment also accelerated diabetes. Thus, rotavirus infection after beta-cell autoimmunity is established affects insulitis and exacerbates diabetes. A possible mechanism involves increased exposure of beta cells to immune recognition and activation of autoreactive T cells by proinflammatory cytokines. The timing of infection relative to mouse age and degree of insulitis determines whether diabetes onset is delayed, unaltered, or accelerated.
...
PMID:Rotavirus infection accelerates type 1 diabetes in mice with established insulitis. 1841 62