Persistent coxsackievirus B1 infection triggers extensive changes in the transcriptome of human pancreatic ductal cells.

ABSTRACT: Enteroviruses, particularly the group B coxsackieviruses (CVBs), have been associated with the development of type 1 diabetes. Several CVB serotypes establish chronic infections in human cells in vivo and in vitro. However, the mechanisms leading to enterovirus persistency and, possibly, beta cell autoimmunity are not fully understood. We established a carrier-state-type persistent infection model in human pancreatic cell line PANC-1 using two distinct CVB1 strains and profiled the 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 found that the anti

SUBMITTER: Buchacher T 

PROVIDER: S-EPMC8728469 | biostudies-literature | 2022 Jan

REPOSITORIES: biostudies-literature