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Published on: May 6, 2013
Fighting Enteroviral Infections to Prevent Type 1 Diabetes
Magloire Pandoua Nekoua1, Ambroise Mercier1, Abdulaziz Alhazmi1,2
1Laboratoire de Virologie ULR3610, Université de Lille, CHU Lille, 59000 Lille, France.
Abstract:
Enteroviruses (EVs), especially coxsackieviruses B (CVB), are believed to trigger or accelerate islet autoimmunity in genetically susceptible individuals that results in type 1 diabetes (T1D). Therefore, strategies are needed to fight against EV infections. There are no approved antiviral drugs currently available, but various antiviral drugs targeting viral or host cell proteins and vaccines have recently shown potential to combat CVB infections and may be used as new therapeutic strategies to prevent or reduce the risk of T1D and/or preserve β-cell function among patients with islet autoantibodies or T1D.
Insights
Enteroviruses, particularly coxsackieviruses B, may trigger type 1 diabetes (T1D) in susceptible individuals. Antiviral drugs and vaccines show promise for preventing T1D by combating these viral infections.
Area of Science:
- Virology
- Immunology
- Endocrinology
Background:
- Enteroviruses (EVs), especially coxsackieviruses B (CVB), are implicated in triggering or accelerating islet autoimmunity.
- This autoimmune process in genetically susceptible individuals can lead to type 1 diabetes (T1D).
Purpose of the Study:
- To highlight the need for strategies to combat EV infections.
- To review potential antiviral therapies and vaccines for CVB infections.
Main Methods:
- Review of existing research on enteroviruses and type 1 diabetes.
- Analysis of current antiviral drug development and vaccine research targeting CVB.
Main Results:
- No approved antiviral drugs are currently available for EV infections.
- Emerging antiviral drugs and vaccines show potential in combating CVB.
Conclusions:
- Antiviral strategies targeting viral or host cell proteins offer potential therapeutic options.
- These strategies may prevent or reduce the risk of T1D and preserve beta-cell function in at-risk individuals.
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