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MicroRNA-based Regulation of Picornavirus Tropism
Published on: February 6, 2017
Persistent coxsackievirus B4 infection induces microRNA dysregulation in human pancreatic cells
Ilka Engelmann1, Enagnon K Alidjinou1, Antoine Bertin1
1Univ Lille Faculté de Médecine, CHU Lille, Laboratoire de Virologie EA3610, Lille, F-59000, France.
Abstract:
Enterovirus infections are implicated in the development of type 1 diabetes (T1D). MicroRNAs as regulators of gene expression are involved in many physiological and pathological processes. Given that viral infections dysregulate cellular microRNAs, we investigated the impact of persistent coxsackievirus B4 infection on microRNA expression of human pancreatic cells. Next-generation sequencing was used to determine microRNA expression in PANC-1 cells persistently infected (for several weeks) with coxsackievirus B4 and uninfected control cells. Target prediction restricted to T1D risk genes was performed with miRWalk2.0. Functional annotation analysis was performed with DAVID6.7. Expression of selected microRNAs and T1D risk genes was measured by quantitative reverse-transcription polymerase chain reaction. Eighty-one microRNAs were dysregulated in persistently infected PANC-1 cells. Forty-nine of the known fifty-five T1D risk genes were predicted as putative targets of at least one of the dysregulated microRNAs. Most functional annotation terms that were enriched in these 49 putative target genes were related to the immune response or autoimmunity. mRNA levels of AFF3, BACH2, and IL7R differed significantly between persistently infected cells and uninfected cells. This is the first characterization of the microRNA expression profile changes induced by persistent coxsackievirus B4 infection in pancreatic cells. The predicted targeting of genes involved in the immune response and autoimmunity by the dysregulated microRNAs as well as the dysregulated expression of diabetes risk genes shows that persistent coxsackievirus B4 infection profoundly impacts the host cell. These data support the hypothesis of a possible link between persistent coxsackievirus B4 infection and the development of T1D.
Insights
Persistent coxsackievirus B4 infection alters microRNA expression in human pancreatic cells, potentially linking viral infections to type 1 diabetes (T1D) development. This study reveals dysregulated microRNAs targeting T1D risk genes involved in immune responses.
Area of Science:
- Virology
- Molecular Biology
- Immunology
Background:
- Enterovirus infections, specifically coxsackievirus B4, are suspected contributors to type 1 diabetes (T1D) pathogenesis.
- MicroRNAs are key regulators of gene expression implicated in various cellular processes and diseases.
- Viral infections are known to disrupt cellular microRNA homeostasis.
Purpose of the Study:
- To investigate the impact of persistent coxsackievirus B4 infection on microRNA expression in human pancreatic cells.
- To identify potential microRNA targets among known type 1 diabetes risk genes.
- To explore the functional consequences of these microRNA alterations in the context of T1D.
Main Methods:
- Persistent coxsackievirus B4 infection model established in PANC-1 human pancreatic cells.
- Next-generation sequencing utilized for comprehensive microRNA expression profiling.
- Bioinformatic analyses including target prediction (miRWalk2.0) and functional annotation (DAVID6.7).
- Quantitative reverse-transcription polymerase chain reaction (qRT-PCR) for validating microRNA and gene expression.
Main Results:
- Eighty-one microRNAs exhibited dysregulated expression in persistently infected pancreatic cells compared to controls.
- Forty-nine of fifty-five known T1D risk genes were predicted as targets of these dysregulated microRNAs.
- Enriched functional annotations for target genes were predominantly related to immune response and autoimmunity.
- Significant differences in mRNA levels of key genes (AFF3, BACH2, IL7R) were observed between infected and uninfected cells.
Conclusions:
- Persistent coxsackievirus B4 infection significantly alters the microRNA expression profile of human pancreatic cells.
- Dysregulated microRNAs in infected cells target genes crucial for immune function and autoimmunity, suggesting a role in T1D.
- These findings provide novel insights into the molecular mechanisms linking persistent enterovirus infections to type 1 diabetes development.
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