Next Article in Journal
The Effect of Antimicrobial Resistance Plasmids Carrying blaCMY-2 on Biofilm Formation by Escherichia coli from the Broiler Production Chain
Next Article in Special Issue
Effect of Coxsackievirus B4 Infection on the Thymus: Elucidating Its Role in the Pathogenesis of Type 1 Diabetes
Previous Article in Journal
Pectobacterium brasiliense: Genomics, Host Range and Disease Management
Article

Inhibition of Type III Interferon Expression in Intestinal Epithelial Cells—A Strategy Used by Coxsackie B Virus to Evade the Host’s Innate Immune Response at the Primary Site of Infection?

1
Center for Infectious Medicine, Department of Medicine, Karolinska Institutet, 141 52 Stockholm, Sweden
2
Department of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, 106 91 Stockholm, Sweden
3
Department of Research, Education and Innovation, Karolinska University Hospital, 171 64 Stockholm, Sweden
*
Author to whom correspondence should be addressed.
Microorganisms 2021, 9(1), 105; https://doi.org/10.3390/microorganisms9010105
Received: 29 October 2020 / Revised: 21 December 2020 / Accepted: 30 December 2020 / Published: 5 January 2021
(This article belongs to the Special Issue Coxsackievirus Infection and Associated Diseases)
Increasing evidence highlights the importance of the antiviral activities of the type III interferons (IFNλs; IL-28A, IL-28B, IL29, and IFNλ4) in the intestine. However, many viruses have developed strategies to counteract these defense mechanisms by preventing the production of IFNs. Here we use infection models, a clinical virus isolate, and several molecular biology techniques to demonstrate that both type I and III IFNs induce an antiviral state and attenuate Coxsackievirus group B (CVB) replication in human intestinal epithelial cells (IECs). While treatment of IECs with a viral mimic (poly (I:C)) induced a robust expression of both type I and III IFNs, no such up-regulation was observed after CVB infection. The blunted IFN response was paralleled by a reduction in the abundance of proteins involved in the induction of interferon gene transcription, including TIR-domain-containing adapter-inducing interferon-β (TRIF), mitochondrial antiviral-signaling protein (MAVS), and the global protein translation initiator eukaryotic translation initiation factor 4G (eIF4G). Taken together, this study highlights a potent anti-Coxsackieviral effect of both type I and III IFNs in cells located at the primary site of infection. Furthermore, we show for the first time that the production of type I and III IFNs in IECs is blocked by CVBs. These findings suggest that CVBs evade the host immune response in order to successfully infect the intestine. View Full-Text
Keywords: Coxsackievirus (CVB); enterovirus; IFIH1; immune evasion; innate immunity; interferon; intestine; intestinal epithelial cells; poly I:C; type 1 diabetes Coxsackievirus (CVB); enterovirus; IFIH1; immune evasion; innate immunity; interferon; intestine; intestinal epithelial cells; poly I:C; type 1 diabetes
Show Figures

Figure 1

MDPI and ACS Style

Stone, V.M.; Ringqvist, E.E.; Larsson, P.G.; Domsgen, E.; Holmlund, U.; Sverremark-Ekström, E.; Flodström-Tullberg, M. Inhibition of Type III Interferon Expression in Intestinal Epithelial Cells—A Strategy Used by Coxsackie B Virus to Evade the Host’s Innate Immune Response at the Primary Site of Infection? Microorganisms 2021, 9, 105. https://doi.org/10.3390/microorganisms9010105

AMA Style

Stone VM, Ringqvist EE, Larsson PG, Domsgen E, Holmlund U, Sverremark-Ekström E, Flodström-Tullberg M. Inhibition of Type III Interferon Expression in Intestinal Epithelial Cells—A Strategy Used by Coxsackie B Virus to Evade the Host’s Innate Immune Response at the Primary Site of Infection? Microorganisms. 2021; 9(1):105. https://doi.org/10.3390/microorganisms9010105

Chicago/Turabian Style

Stone, Virginia M., Emma E. Ringqvist, Pär G. Larsson, Erna Domsgen, Ulrika Holmlund, Eva Sverremark-Ekström, and Malin Flodström-Tullberg. 2021. "Inhibition of Type III Interferon Expression in Intestinal Epithelial Cells—A Strategy Used by Coxsackie B Virus to Evade the Host’s Innate Immune Response at the Primary Site of Infection?" Microorganisms 9, no. 1: 105. https://doi.org/10.3390/microorganisms9010105

Find Other Styles
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Access Map by Country/Region

1
Back to TopTop