Interferons and viruses: an evolutionary arms race of molecular interactions

Hoffmann, Hans Heinrich; Schneider, William M.; Rice, Charles M.

doi:10.1016/j.it.2015.01.004

Cited by 338 publications

(330 citation statements)

References 191 publications

(200 reference statements)

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“…This is supported by the extensive retention of WGD-generated duplicates of CytoR signaling components compared with the average retention rate of just 3-4% (73) and is consistent with other studies indicating that WGDs played a crucial role in adaptive immunity by providing new genetic materials for a range of essential components (99). Additional evidence for immunity as a key driver can be gleaned from the significant divergence in the IFN-responsive CytoRs between teleosts and tetrapods (51), likely as a result of the powerful selective forces associated with combatting everchanging pathogens, particularly viruses, which develop subversion mechanisms to counter the antiviral effects of IFNs in fish and mammals (53,80,100). This is borne out, for example, by other data showing that the majority of type I IFNs have been subjected to purifying selection (101).…”

Section: Consequences and Driversmentioning

confidence: 85%

“…The diversification also appears to reflect some lineage-specific environmental adaptations. For example, the divergence in IFNRs likely reflects the different pathogen spectrum and dynamics between water-dwelling teleosts and largely land-dwelling tetrapods (80). The role for the somatolactin receptor in body color regulation (81) and PRLR in osmoregulation (70) within teleosts also falls into this category.…”

Section: Diversification Of the Pathwaymentioning

confidence: 99%

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Evolution of Cytokine Receptor Signaling

Liongue

Sertori

Ward

2016

The Journal of Immunology

103

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Cytokines represent essential mediators of cell–cell communication with particularly important roles within the immune system. These secreted factors are produced in response to developmental and/or environmental cues and act via cognate cytokine receptors on target cells, stimulating specific intracellular signaling pathways to facilitate appropriate cellular responses. This review describes the evolution of cytokine receptor signaling, focusing on the class I and class II receptor families and the downstream JAK–STAT pathway along with its key negative regulators. Individual components generated over a long evolutionary time frame coalesced to form an archetypal signaling pathway in bilateria that was expanded extensively during early vertebrate evolution to establish a substantial “core” signaling network, which has subsequently undergone limited diversification within discrete lineages. The evolution of cytokine receptor signaling parallels that of the immune system, particularly the emergence of adaptive immunity, which has likely been a major evolutionary driver.

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Section: Consequences and Driversmentioning

confidence: 85%

Section: Diversification Of the Pathwaymentioning

confidence: 99%

Evolution of Cytokine Receptor Signaling

Liongue

Sertori

Ward

2016

The Journal of Immunology

103

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“…In order to favour their own replication, most viruses have evolved mechanisms to counteract the host's immune response (Feng et al, 2014b;Hoffmann et al, 2015;Taylor & Mossman, 2013). Previous studies have shown that enteroviruses such as the coxsackie B viruses (CVBs) block type I IFN production (Feng et al, 2014a;Mukherjee et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

Coxsackievirus counters the host innate immune response by blocking type III interferon expression

Lind

Svedin

Domsgen

et al. 2016

Journal of General Virology

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Type I IFNs play an important role in the immune response to enterovirus infections. Their importance is underscored by observations showing that many enteroviruses including coxsackie B viruses (CVBs) have developed strategies to block type I IFN production. Recent studies have highlighted a role for the type III IFNs (also called IFNls) in reducing permissiveness to infections with enteric viruses including coxsackievirus. However, whether or not CVBs have measures to evade the effects of type III IFNs remains unknown. By combining virus infection studies and different modes of administrating the dsRNA mimic poly I : C, we discovered that CVBs target both Toll-like receptor 3-and MDA5/RIG-I-mediated type III IFN expression. Consistent with this, the cellular protein expression levels of the signal transduction proteins TRIF and IPS1 were reduced and no hyperphosphorylation of interferon regulatory factor 3 was observed following infection with the virus. Notably, decreased expression of full-length TRIF and IPS1 and the appearance of cleavage products was observed upon both CVB3 infection and in cellular protein extracts incubated with recombinant 2A pro , indicating an important role for the viral protease in subverting the cellular immune system. Collectively, our study reveals that CVBs block the expression of type III IFNs, and that this is achieved by a similar mechanism as the virus uses to block type I IFN production. We also demonstrate that the virus blocks several intracellular viral recognition pathways of importance for both type I and III IFN production. The simultaneous targeting of numerous arms of the host immune response may be required for successful viral replication and dissemination.

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“…Together with IRF9, homodimers or heterodimers of phosphorylated STAT1 and STAT2 form the ISGF3 complex, which translocates into the nucleus, binds to specific IFN-stimulated response elements (ISREs) present in the promoters of IFN-stimulated genes (ISGs) and activates their transcription (Schneider et al, 2014). Viruses have evolved various IFN antagonists to counteract IFN induction and signalling at all steps (Randall & Goodbourn, 2008;Hoffmann et al, 2015).…”

mentioning

confidence: 99%

Suppression of type I and type III IFN signalling by NSs protein of severe fever with thrombocytopenia syndrome virus through inhibition of STAT1 phosphorylation and activation

Chaudhary

Zhang

Yuen

et al. 2015

Journal of General Virology

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Severe fever with thrombocytopenia syndrome virus (SFTSV) is an emerging tick-borne pathogen causing significant morbidity and mortality in Asia. NSs protein of SFTSV is known to perturb type I IFN induction and signalling, but the mechanism remains to be fully understood. Here, we showed the suppression of both type I and type III IFN signalling by SFTSV NSs protein is mediated through inhibition of STAT1 phosphorylation and activation. Infection with live SFTSV or expression of NSs potently suppressed IFN-stimulated genes but not NFkB activation. NSs was capable of counteracting the activity of IFN-a1, IFN-b, IFN-l1 and IFN-l2. Mechanistically, NSs associated with STAT1 and STAT2, mitigated IFN-b-induced phosphorylation of STAT1 at S727, and reduced the expression and activity of STAT1 protein in IFN-b-treated cells, resulting in the inhibition of STAT1 and STAT2 recruitment to IFNstimulated promoters. Taken together, SFTSV NSs protein is an IFN antagonist that suppresses phosphorylation and activation of STAT1.

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Interferons and viruses: an evolutionary arms race of molecular interactions

Cited by 338 publications

References 191 publications

Evolution of Cytokine Receptor Signaling

Evolution of Cytokine Receptor Signaling

Coxsackievirus counters the host innate immune response by blocking type III interferon expression

Suppression of type I and type III IFN signalling by NSs protein of severe fever with thrombocytopenia syndrome virus through inhibition of STAT1 phosphorylation and activation

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