GSE184831: Persistent Coxsackievirus B1 infection results in extensive changes in the transcriptome of a pancreatic cell line

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GROUP CONDITION SAMPLES
pancreatic ductal-like cell line PANC-1 cells
GSM5597982 GSM5597983 GSM5597984
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Description

Submission Date: Sep 27, 2021

Summary: 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.

GEO Accession ID: GSE184831

PMID: 35024587

Description

Submission Date: Sep 27, 2021

Summary: 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.

GEO Accession ID: GSE184831

PMID: 35024587

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