Decoding type I and III interferon signalling during viral infection

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Abstract

Interferon (IFN)-mediated antiviral responses are central to host defence against viral infection. Despite the existence of at least 20 IFNs, there are only three known cell surface receptors. IFN signalling and viral evasion mechanisms form an immensely complex network that differs across species. In this Review, we begin by highlighting some of the advances that have been made towards understanding the complexity of differential IFN signalling inputs and outputs that contribute to antiviral defences. Next, we explore some of the ways viruses can interfere with, or circumvent, these defences. Lastly, we address the largely under-reviewed impact of IFN signalling on host tropism, and we offer perspectives on the future of research into IFN signalling complexity and viral evasion across species.

Abstract

This Review highlights some of the advances that have been made towards understanding the complexity of differential interferon (IFN) signalling inputs and outputs as well as some of the strategies viruses use to interfere with or circumvent IFN-induced antiviral responses.

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Most cited references 116

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Andreas Pichlmair, Oliver Schulz, Choon Ping Tan … (2006)

Double-stranded RNA (dsRNA) produced during viral replication is believed to be the critical trigger for activation of antiviral immunity mediated by the RNA helicase enzymes retinoic acid-inducible gene I (RIG-I) and melanoma differentiation-associated gene 5 (MDA5). We showed that influenza A virus infection does not generate dsRNA and that RIG-I is activated by viral genomic single-stranded RNA (ssRNA) bearing 5'-phosphates. This is blocked by the influenza protein nonstructured protein 1 (NS1), which is found in a complex with RIG-I in infected cells. These results identify RIG-I as a ssRNA sensor and potential target of viral immune evasion and suggest that its ability to sense 5'-phosphorylated RNA evolved in the innate immune system as a means of discriminating between self and nonself.

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IFN-lambdas mediate antiviral protection through a distinct class II cytokine receptor complex.

Sergei V. Kotenko, Grant Gallagher, Vitaliy V Baurin … (2003)

We report here the identification of a ligand-receptor system that, upon engagement, leads to the establishment of an antiviral state. Three closely positioned genes on human chromosome 19 encode distinct but paralogous proteins, which we designate interferon-lambda1 (IFN-lambda1), IFN-lambda2 and IFN-lambda3 (tentatively designated as IL-29, IL-28A and IL-28B, respectively, by HUGO). The expression of IFN-lambda mRNAs was inducible by viral infection in several cell lines. We identified a distinct receptor complex that is utilized by all three IFN-lambda proteins for signaling and is composed of two subunits, a receptor designated CRF2-12 (also designated as IFN-lambdaR1) and a second subunit, CRF2-4 (also known as IL-10R2). Both receptor chains are constitutively expressed on a wide variety of human cell lines and tissues and signal through the Jak-STAT (Janus kinases-signal transducers and activators of transcription) pathway. This receptor-ligand system may contribute to antiviral or other defenses by a mechanism similar to, but independent of, type I IFNs.

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Paul Sheppard, Wayne Kindsvogel, Wenfeng Xu … (2003)

Cytokines play a critical role in modulating the innate and adaptive immune systems. Here, we have identified from the human genomic sequence a family of three cytokines, designated interleukin 28A (IL-28A), IL-28B and IL-29, that are distantly related to type I interferons (IFNs) and the IL-10 family. We found that like type I IFNs, IL-28 and IL-29 were induced by viral infection and showed antiviral activity. However, IL-28 and IL-29 interacted with a heterodimeric class II cytokine receptor that consisted of IL-10 receptor beta (IL-10Rbeta) and an orphan class II receptor chain, designated IL-28Ralpha. This newly described cytokine family may serve as an alternative to type I IFNs in providing immunity to viral infection.

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Author and article information

Contributors

Alexander Ploss:

ORCID: http://orcid.org/0000-0001-9322-7252

aploss@princeton.edu

Journal

Journal ID (nlm-ta): Nat Microbiol

Journal ID (iso-abbrev): Nat Microbiol

Title: Nature Microbiology

Publisher: Nature Publishing Group UK (London )

ISSN (Electronic): 2058-5276

Publication date (Electronic): 1 April 2019

Publication date (Print): 2019

Volume: 4

Issue: 6

Pages: 914-924

Affiliations

ISNI 0000 0001 2097 5006, GRID grid.16750.35, Lewis Thomas Laboratory, Department of Molecular Biology, , Princeton University, ; Princeton, NJ USA

Author information

Alexander Ploss http://orcid.org/0000-0001-9322-7252

Article

Publisher ID: 421

DOI: 10.1038/s41564-019-0421-x

PMC ID: 6554024

PubMed ID: 30936491

SO-VID: 2648fa17-6445-46f3-b2d7-085c231be82f

License:

This article is made available via the PMC Open Access Subset for unrestricted research re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic.