Abstract :
[en] Beyond acute clinical conditions, the role of enteroviruses (EVs) in chronic human diseases has been described. Although they are considered as highly cytolytic viruses, EVs can persist in various tissues. The persistence is believed to play a major role in the pathogenesis of EV related chronic dis- eases such as type 1 diabetes (T1D). T1D is charac- terized by an autoimmune destruction of pancreatic beta cells, and results from interplay between a genetic predisposition, the immune system, and environmental factors. EVs and especially group B coxsackieviruses (CVB) have been the most incrimi- nated as exogenous agents involved in the develop- ment of T1D. Enteroviral persistence is the result of a virus-host coevolution combining a cell resistance to lysis through mutations or down-regulation of viral receptor, and a decrease of the viral replication by genomic modifications or the production of a sta- ble double-stranded RNA form. CVB can persist in pancreatic cells and therefore could trigger, in genet- ically predisposed individuals, the autoimmune destruction of beta cells mainly through an activa- tion of inflammation. The persistence of the virus in other tissues such as intestine, blood cells, and thy- mus has been described, and could also contribute to some extent to the enteroviral pathogenesis of T1D. The molecular and cellular mechanisms of CVB per- sistence and the link with the development of T1D should be investigated further.
Alidjinou, Enagnon Kazali; Université de Lille II, CHRU de Lille > Laboratoire de Virologie EA3610
Sané, Famara; Université de Lille II, CHRU de Lille > Laboratoire de Virologie EA3610
Engelmann, Ilka; Université de Lille II, CHRU de Lille > Laboratoire de Virologie EA3610
Hober, Didier; Université de Lille II, CHRU de Lille > Laboratoire de Virologie EA3610
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