Persistent Coxsackievirus B1 infection results in extensive changes in the transcriptome of a pancreatic cell line

Enteroviruses, particularly the group B Coxsackieviruses have been associated with the development of type 1 diabetes. Several CVB serotypes can establish chronic infection in human cells in vivo and in vitro. However, the mechanisms of leading to enterovirus persistency and, possibly, bell-cell autoimmunity are not fully understood. We established a carrier-state persistent infection model in human pancreatic ductal-like cell line PANC-1 using two distinct CVB1 strains and profiled infection-induced changes in cellular transcriptome. In the current study we observed clear changes in the gene expression of factors associated with the pancreatic microenvironment, the secretory pathway and lysosomal biogenesis during persistent CVB1 infections. Moreover, we gained deeper insights into immune-related genes which differed clearly between the two persistent infections. Overall our study reveals extensive transcriptional responses in persistently CVB1 infected pancreatic cell line with strong opposite but also common changes between the two strains. Carrier-state persistent infection in human pancreatic ductal-like cell line PANC-1 cells using two distinct CVB1 strains (ATCC and 10796, 3 replicates in each) was established and compared to non-infected controls (3 replicates) for infection-induced changes in cellular transcriptome.