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

iScience

Anni Honkimaa¹  M. Karoliina Hirvonen¹  Eeva-Liisa Eskelinen¹  Tommi Välikangas²  Heikki Hyöty²  Laura L. Elo²  Riitta Lahesmaa³  Amir-Babak Sioofy-Khojine⁴  Niina Lietzén⁴  Jutta E. Laiho⁴  Tanja Buchacher⁴ 

[1] InFLAMES Research Flagship Center, University of Turku, Turku, Finland;Faculty of Medicine and Health Technology, Tampere University, Tampere FI-33014, Finland;Institute of Biomedicine, University of Turku, Turku FI-20014, Finland;Turku Bioscience Centre, University of Turku and Åbo Akademi University, FI-20520 Turku, Finland;

关键词: Virology;    Cell biology;    Transcriptomics;   

DOI  :  

来源: DOAJ

【 摘 要 】

Summary: 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 antiviral response pathways were activated differently by the two CVB1 strains. Overall, our study reveals extensive transcriptional responses in persistently CVB1-infected pancreatic cells with strong opposite but also common changes between the two strains.

【 授权许可】

Unknown