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Enterovirus Infections of β-Cells : A Mechanism of Induction of Type 1 Diabetes?

Berg, Anna-Karin, 1976- (författare)
Uppsala universitet,Institutionen för kvinnors och barns hälsa
Frisk, Gun (preses)
Tuvemo, Torsten (preses)
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Andersson, Arne (preses)
Roivainen, Merja, Docent (opponent)
Enterovirus Laboratory, National Public Health Institute, Helsingfors
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 (creator_code:org_t)
ISBN 9155463738
Uppsala : Acta Universitatis Upsaliensis, 2005
Engelska 63s.
Serie: Digital Comprehensive Summaries of Uppsala Dissertations from the Faculty of Medicine, 1651-6206 ; 79
  • Doktorsavhandling (övrigt vetenskapligt)
Abstract Ämnesord
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  • The process of β-cell destruction that leads to type 1 diabetes (T1D) is incompletely understood and it is believed to be a result of both genetic and environmental factors. Enterovirus (EV) infections of the β-cells have been proposed to be involved, however, the effects of EV infections on human β-cells have been little investigated. This thesis summarises studies of three different Coxsackie B4 virus strains that have previously been shown to infect human islets. The effects of infections with these EV were studied in vitro in human islets and in a rat insulin-producing cell line. In addition, a pilot study was performed on isolated human islets to investigate the ability to treat such infections with an antiviral compound.It was found that one of the virus strains replicated in human β-cells without affecting their main function for at least seven days, which in vivo may increase a virus’s ability to persist in islets.Nitric oxide was induced by synthetic dsRNA, poly(IC), but not by viral dsRNA in rat insulinoma cells in the presence of IFN-γ, suggesting that this mediator is not induced by EV infection in β-cells and that poly(IC) does not mimic an EV infection in this respect.All three virus strains were able to induce production of the T-cell chemoattractant interferon-γ-inducible protein 10 (IP-10) during infection of human islets, suggesting that an EV infection of the islets might trigger insulitis in vivo.Antiviral treatment was feasible in human islets, but one strain was resistant to the antiviral compound used in this study.To conclude, a potential mechanism is suggested for the involvement of EV infections in T1D. If EV infections induce IP-10 production in human islet cells in vivo, they might recruit immune cells to the islets. Together with viral persistence and/or virus-induced β-cell damage, this might trigger further immune-mediated β-cell destruction in vivo.

Ämnesord

MEDICAL AND HEALTH SCIENCES  -- Clinical Medicine -- Pediatrics (hsv//eng)
MEDICIN OCH HÄLSOVETENSKAP  -- Klinisk medicin -- Pediatrik (hsv//swe)
MEDICIN OCH HÄLSOVETENSKAP  -- Klinisk medicin (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Clinical Medicine (hsv//eng)

Nyckelord

Pediatrics
enterovirus
type 1 diabetes
β-cells
human pancreatic islets
picornavirus
chemokines
nitric oxide
Pediatrik
Paediatric medicine
Pediatrisk medicin

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Berg, Anna-Karin ...
Frisk, Gun
Tuvemo, Torsten
Andersson, Arne
Roivainen, Merja ...
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MEDICIN OCH HÄLSOVETENSKAP
MEDICIN OCH HÄLS ...
och Klinisk medicin
och Pediatrik
MEDICIN OCH HÄLSOVETENSKAP
MEDICIN OCH HÄLS ...
och Klinisk medicin
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Uppsala universitet

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