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Coxsackievirus B persistence modifies the secretome of pancreatic ductal cells in a virus-strain-specific manner, part 2

ABSTRACT: The group B Coxsackieviruses can establish persistent infections in human cells, and these infections have been linked to chronic diseases including type 1 diabetes. Still, only little is known about persistent Coxsackievirus B infection induced changes in human pancreas. We have established persistent Coxsackievirus B1 infections in human pancreatic duct cell line using two different virus strains, and studied infection-induced changes in protein secretion using mass spectrometry-based proteomics. Persistent Coxsackievirus B1 infections caused broad changes in protein secretion, for example changes regulated secretory pathway. Strikingly, many changes differed between the virus strains, including extensive shut down of antiviral immune responses by one of the viruses. Our results provide novel information about persistent Coxsackievirus B infection induced changes in human pancreas and about the potential heterogeneity in the outcomes of the infections.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Cell Culture

SUBMITTER: Niina Lietzen

LAB HEAD: Riitta Lahesmaa

PROVIDER: PXD012154 | Pride | 2019-08-06

REPOSITORIES: Pride

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			Action	DRS
	260617_DDA_110min_top12_PANC_S1_1.raw	Raw
	260617_DDA_110min_top12_PANC_S2_1.raw	Raw
	260617_DDA_110min_top12_PANC_S3_1.raw	Raw
	260617_DDA_110min_top12_PANC_S4_1.raw	Raw
	260617_DDA_110min_top12_PANC_S5_1.raw	Raw

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Coxsackievirus B persistence modifies the proteome of pancreatic ductal cells in a virus-strain-specific manner

Project description:In human cells, the group B Coxsackieviruses can establish persistent infections that have been linked to chronic diseases including type 1 diabetes. Still, only little is known about the changes induced by persistent Coxsackievirus B infection in human pancreas. We have established persistent Coxsackievirus B1 infections in human pancreatic duct cell line using two different virus strains, and studied the consequences of these infections on intracellular protein expression using mass spectrometry-based proteomics. Persistent Coxsackievirus B1 infections caused broad changes in protein expression, for example changes in mitochondrial morphology and energy metabolism and in proteins associated with differentiation and survival of pancreatic beta-cells. Strikingly, many of these changes differed between the virus strains, including extensive shut down of antiviral immune responses by one of the viruses. Our results provide novel information about the changes induced by persistent Coxsackievirus B infection in human pancreas and about the potential heterogeneity in the outcomes of the infections.

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