Type I diabetes (T1D) is an autoimmune disease resulting in gradual cell-mediated destruction of insulin producing beta cells in the pancreatic islets of Langerhans. The most plausible environmental triggers to launch and/or accelerate this process in a genetically predisposed organism including enterovirus infections and oxidative stress. Among other enteroviruses the group B of coxsackieviruses is associated with potential beta cell toxicity. Beta cells are weak in antioxidative defense, which makes them hypersensitive to oxidative stress. Acknowledging the inhibitory potential of in vivo conditions scientists have developed two models resembling a slowly progressing coxsackievirus infection first, by restricting the production of viral progeny with a selective inhibitor of viral RNA replication and second, by means of lowering the multiplicity of infection. Hydrogen peroxide has been established as the oxidative stressor. Recent studies reflect that a productive CVB-infection results in lytic beta cell death. When pharmacologically restricted by guanidine-HCl, the viability increases dramatically through decreased necrosis and associates with simultaneous stimulation of apoptotic death. In summary, the review introduces potential mechanistic models for enterovirus infections in beta cells.
Key words: Oxidative stress, type 1 diabetes, coxsackievirus infection, beta cells, human leukocyte antigen.
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