In an earlier study, infection of human pancreatic islets with epidemic strains of echovirus (E4, E16, E30), with proven but differently ability to induce islet autoimmunity, resulted either in a severe damage (i.e. E16 and E30) or proceeded without visible changes in infected islets (i.e. E4). In this study, the ability of these strains to replicate in beta cells and the consequence of such an infection for beta cell lysis and beta cell function was studied in the pancreatic beta cell lines INS-1, MIN6 and NIT-1. The strains of E16 and E30 did replicate in INS1, MIN6, and NIT1 cells and resulted in a pronounced cytopathic effect within three days following infection. By contrast, E4 replicated in all examined insulinoma cells and no apparent cell destruction was. The insulin release in response to high glucose stimulation was hampered in all infected cells (P < 0.05) when no evidence of cytolysis was present; however the adverse effect of E16 and E30 on insulin secretion appeared to be higher than that of the E4 strain. The differential effects of echovirus infection on cell lysis, and beta cell function in the rodent insulinoma INS1, MIN6 and NIT 1 cells reflect those previously obtained in primary human islets and support the notion that the insulin - producing beta cells can harbor a non-cytopathic viral infection. This article is protected by copyright. All rights reserved.
Subject classification (UKÄ)
- Immunology in the medical area