Effects on isolated human pancreatic islet cells after infection with strains of enterovirus isolated at clinical presentation of type 1 diabetes.

Enterovirus (EV) infections have been associated with the pathogenesis of type 1 diabetes (T1D). They may cause beta-cell destruction either by cytolytic infection of the cells or indirectly by triggering the autoimmune response. Evidence for EV involvement have been presented in several studies, EV-IgM antibodies have been reported in T1D patients, EV-RNA has been found in the blood from T1D patients at onset, and EV have been isolated from newly diagnosed T1D.

Simultaneous type 1 diabetes onset in mother and son coincident with an enteroviral infection.

Enterovirus (EV) infections have been implicated in the development of type 1 diabetes. (T1D). They may cause beta-cell destruction either by cytolytic infection of the cells or indirectly by triggering the autoimmune response.

dsRNA formed as an intermediate during Coxsackievirus infection does not induce NO production in a beta-cell line with or without addition of IFN-gamma.

Virus infection is one environmental factor that has been implicated as a precipitating event initiating beta-cell damage during the development of type 1 diabetes. One aim of this study was to investigate how permissive an insulin-producing beta-cell line, RINm5F, is to enterovirus (EV) infections. A second aim was to study if the viral replicative intermediate, double-stranded RNA (dsRNA), together with IFN-gamma results in nitric oxide (NO) production.