Next Article in Journal
Hsv-1 Endocytic Entry into a Human Oligodendrocytic Cell Line Is Mediated by Clathrin and Dynamin but Not Caveolin
Next Article in Special Issue
Innate Immune Sensing of Influenza A Virus
Previous Article in Journal
Phylogenetic and Timescale Analysis of Barmah Forest Virus as Inferred from Genome Sequence Analysis
Previous Article in Special Issue
Persistent Innate Immune Stimulation Results in IRF3-Mediated but Caspase-Independent Cytostasis
Open AccessReview

Of Keeping and Tipping the Balance: Host Regulation and Viral Modulation of IRF3-Dependent IFNB1 Expression

1
Institute of Genetics, Technische Universität Braunschweig, 38106 Braunschweig, Germany
2
Viral Immune Modulation Research Group, Helmholtz Centre for Infection Research, 38124 Braunschweig, Germany
*
Author to whom correspondence should be addressed.
Viruses 2020, 12(7), 733; https://doi.org/10.3390/v12070733
Received: 15 June 2020 / Revised: 3 July 2020 / Accepted: 3 July 2020 / Published: 7 July 2020
(This article belongs to the Special Issue Innate Immune Sensing of Viruses and Viral Evasion)
The type I interferon (IFN) response is a principal component of our immune system that allows to counter a viral attack immediately upon viral entry into host cells. Upon engagement of aberrantly localised nucleic acids, germline-encoded pattern recognition receptors convey their find via a signalling cascade to prompt kinase-mediated activation of a specific set of five transcription factors. Within the nucleus, the coordinated interaction of these dimeric transcription factors with coactivators and the basal RNA transcription machinery is required to access the gene encoding the type I IFN IFNβ (IFNB1). Virus-induced release of IFNβ then induces the antiviral state of the system and mediates further mechanisms for defence. Due to its key role during the induction of the initial IFN response, the activity of the transcription factor interferon regulatory factor 3 (IRF3) is tightly regulated by the host and fiercely targeted by viral proteins at all conceivable levels. In this review, we will revisit the steps enabling the trans-activating potential of IRF3 after its activation and the subsequent assembly of the multi-protein complex at the IFNβ enhancer that controls gene expression. Further, we will inspect the regulatory mechanisms of these steps imposed by the host cell and present the manifold strategies viruses have evolved to intervene with IFNβ transcription downstream of IRF3 activation in order to secure establishment of a productive infection. View Full-Text
Keywords: interferon regulatory factor; IRF3; innate immunity; antiviral response; immune modulation; viral evasion; antagonist; interferon beta; enhanceosome; NF-κB interferon regulatory factor; IRF3; innate immunity; antiviral response; immune modulation; viral evasion; antagonist; interferon beta; enhanceosome; NF-κB
Show Figures

Figure 1

MDPI and ACS Style

Schwanke, H.; Stempel, M.; Brinkmann, M.M. Of Keeping and Tipping the Balance: Host Regulation and Viral Modulation of IRF3-Dependent IFNB1 Expression. Viruses 2020, 12, 733.

Show more citation formats Show less citations formats
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
Search more from Scilit
 
Search
Back to TopTop