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?
| Autor: | Malin Flodström-Tullberg, Pär G. Larsson, Virginia M. Stone, Erna Domsgen, Emma Ringqvist, Eva Sverremark-Ekström, Ulrika Holmlund |
|---|---|
| Rok vydání: | 2021 |
| Předmět: |
0301 basic medicine
Microbiology (medical) type 1 diabetes 030106 microbiology poly I:C Biology Coxsackievirus medicine.disease_cause Microbiology Article Virus 03 medical and health sciences chemistry.chemical_compound Immune system Interferon Virology medicine Coxsackie B virus Coxsackievirus (CVB) lcsh:QH301-705.5 innate immunity intestine IFIH1 immune evasion Innate immune system enterovirus EIF4G interferon biology.organism_classification 030104 developmental biology lcsh:Biology (General) chemistry TRIF intestinal epithelial cells medicine.drug |
| Zdroj: | Microorganisms Volume 9 Issue 1 Microorganisms, Vol 9, Iss 105, p 105 (2021) |
| ISSN: | 2076-2607 |
| Popis: | Increasing evidence highlights the importance of the antiviral activities of the type III interferons (IFN&lambda s IL-28A, IL-28B, IL29, and IFN&lambda 4) 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-&beta (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. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|