Modification of encephalomyocarditis virus-induced diabetes in mice by antiviral agents

Powers, Robert D.; Dotson, William M.; Hayden, Frederick G.

doi:10.1016/0166-3542(83)90022-0

Cited by 1 publication

(1 citation statement)

References 27 publications

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“…The availability of drugs targeting different steps of the viral cycle enables combined treatment to avoid viral resistance to the antiviral therapy. Some compounds have shown efficacy to reduce coxsackievirus amplification and to protect pancreatic islets from coxsackievirus-induced cytopathogenic effects 138–141 ; to eradicate the virus in infected pancreatic β cell lines 142 ; and to prevent and/or reduce the incidence of virally-induced diabetes mellitus in mice 140,141 . Adapted antiviral treatment at the pre-diabetic stage could eliminate persistent infection, thus reducing inflammation and the risk of autoimmunity and T1DM.…”

Section: Prevention Of T1dmmentioning

confidence: 99%

Viral infections in type 1 diabetes mellitus — why the β cells?

2016

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Type 1 diabetes mellitus (T1DM) is caused by progressive autoimmune-mediated loss of pancreatic β-cell mass via apoptosis. The onset of T1DM depends on environmental factors that interact with predisposing genes to induce an autoimmune assault against β cells. Epidemiological, clinical and pathology studies in humans support viral infection -particularly by enteroviruses (for example, coxsackievirus) -as an environmental trigger for the development of T1DM. Many candidate genes for T1DM, such as MDA5, PTPN2 and TYK2, regulate antiviral responses in both β cells and the immune system. Cellular permissiveness to viral infection is modulated by innate antiviral responses that vary among different tissues or cell types. Some data indicate that pancreatic islet α cells trigger a more efficient antiviral response to infection with diabetogenic viruses than do β cells, and so are able to eradicate viral infections without undergoing apoptosis. This difference could account for the varying ability of islet-cell subtypes to clear viral infections and explain why chronically infected pancreatic β cells, but not α cells, are targeted by an autoimmune response and killed during the development of T1DM. These issues and attempts to target viral infection as a preventive therapy for T1DM are discussed in the present Review.Type 1 diabetes mellitus (T1DM) arises when the pancreatic β cells undergo long-term autoimmune attack, killing the majority of the β-cell population while the neighbouring α cells and δ cells are spared 1 . Destruction of the β cells manifests as a failure to produce insulin; consequently, patients with T1DM remain insulin-dependent for their lifespan.In most cases, T1DM is characterized by pancreatic islet inflammation (insulitis) and progressive β-cell loss by apoptosis 1,2 . Histological analysis has demonstrated the presence of increased β-cell apoptosis among both patients with new-onset T1DM and those with

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