Mechanisms of coxsackievirus B5 mediated β-cell death depend on the multiplicity of infection

Coxsackievirus infections may trigger and accelerate pancreatic β‐cell death, leading to type I diabetes. Unrestricted coxsackievirus B5 replication in cultured β‐cells inoculated with high multiplicity leads to rapid lytic cell death. Evidence from other virus‐host cell systems indicates that host cell responses to infection may depend on the multiplicity of infection (MOI). Thus, the aim of this study was to compare the mechanisms of β‐cell death during high versus low multiplicity of coxsackievirus B5 infection. Cultures of highly differentiated mouse insulinoma cells and primary adult human islets were infected with coxsackievirus B5 at multiplicities of >1,000 or