Early IFN type I response: Learning from microbial evasion strategies

Coccia, Eliana M.; Battistini, Angela

doi:10.1016/j.smim.2015.03.005

Cited by 47 publications

(46 citation statements)

References 260 publications

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“…Secreted interferons bind to cell-surface receptors (IFNAR) in an autocrine and paracrine manner and activate specific kinases (TYK2 and JAK). These enzymes phosphorylate and activate key transcription factors (STATs), thereby inducing signal transduction pathways that establish an antiviral response in target cells via activation of interferon-stimulated genes 90 .…”

Section: Candidate Genesmentioning

confidence: 99%

Viral infections in type 1 diabetes mellitus — why the β cells?

2016

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Type 1 diabetes mellitus (T1DM) is caused by progressive autoimmune-mediated loss of pancreatic β-cell mass via apoptosis. The onset of T1DM depends on environmental factors that interact with predisposing genes to induce an autoimmune assault against β cells. Epidemiological, clinical and pathology studies in humans support viral infection -particularly by enteroviruses (for example, coxsackievirus) -as an environmental trigger for the development of T1DM. Many candidate genes for T1DM, such as MDA5, PTPN2 and TYK2, regulate antiviral responses in both β cells and the immune system. Cellular permissiveness to viral infection is modulated by innate antiviral responses that vary among different tissues or cell types. Some data indicate that pancreatic islet α cells trigger a more efficient antiviral response to infection with diabetogenic viruses than do β cells, and so are able to eradicate viral infections without undergoing apoptosis. This difference could account for the varying ability of islet-cell subtypes to clear viral infections and explain why chronically infected pancreatic β cells, but not α cells, are targeted by an autoimmune response and killed during the development of T1DM. These issues and attempts to target viral infection as a preventive therapy for T1DM are discussed in the present Review.Type 1 diabetes mellitus (T1DM) arises when the pancreatic β cells undergo long-term autoimmune attack, killing the majority of the β-cell population while the neighbouring α cells and δ cells are spared 1 . Destruction of the β cells manifests as a failure to produce insulin; consequently, patients with T1DM remain insulin-dependent for their lifespan.In most cases, T1DM is characterized by pancreatic islet inflammation (insulitis) and progressive β-cell loss by apoptosis 1,2 . Histological analysis has demonstrated the presence of increased β-cell apoptosis among both patients with new-onset T1DM and those with

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Section: Candidate Genesmentioning

confidence: 99%

Viral infections in type 1 diabetes mellitus — why the β cells?

2016

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“…Interferon (IFN) is a cytokine that induces an antiviral state in cells and influences via host cells (Coccia and Battistini, 2015). IFN is divided into type I, II, and III IFN.…”

Section: Introductionmentioning

confidence: 99%

Differential induction of type I interferon by type I and type II feline coronaviruses in vitro

Doki

Yabe

Takano

et al. 2018

Research in Veterinary Science

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A B S T R A C TFeline infectious peritonitis (FIP) is a feline coronavirus (FCoV)-induced fatal disease in wild and domestic cats. There are two FCoV serotypes. Both type I and II FCoV can replicate in Felis catus whole fetus (fcwf)-4 cells, but the replicability of type I FCoV in feline cell lines is lower than that of type II FCoV, the reason for which is unclear. Inhibition of IFNβ production by non-structural and structural proteins, excluding spike protein has been reported in many coronavirus infections. In this study, we investigated whether IFNβ is involved in the difference in replicability in feline cell lines between types I and II FCoV. When fcwf-4 cells were infected with FCoV, the virus titer of type II FCoV in the culture supernatant was higher than that of type I FIPV. When the IFNβ expression level in FCoV-infected fcwf-4 cells was semi-quantitatively analyzed, infection with type I FIPV, excluding type I FIPV UCD-1, highly induced IFNβ expression. In contrast, induction of IFNβ by type II FCoV infection was significantly lower than that by type I FIPV. In addition, when fcwf-4 cells were adsorbed by FIPV and then stimulated with Poly(I:C), type II FCoV infection inhibited Poly(I:C)-induced IFNβ gene expression. Also, the proliferation of type I FIPV was enhanced by a IFN inhibitor. These findings clarified that, unlike type I FIPV, type II FCoV strongly inhibits IFNβ expression in infected cells. It was also suggested that the IFNβ-inducing ability is different among type I FIPV strains.

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“…Certain viral pathogens have co-evolved immune evasion strategies in order to survive the battle within the host, affording a selective advantage [24]. For example, the RNA virus of the orthomyxoviridae family, influenza A encodes the viral protein NS1 specifically as an IFN antagonist, which interacts with the IFN-β signaling pathway, blocking IRF3 and the IFN-β promoter, allowing permissive virus infection in the absence of IFN [25].…”

Section: Viral Evasion Of Ifn Responsesmentioning

confidence: 99%

“…Underlying chronic inflammatory diseases such as HIV and HCV project heavy burdens on the host that may not be easily lifted with existing treatments. It has been reported that collectively these viruses have evolved up to ninety evasion strategies of innate immunity facilitating the establishment of chronic inflammation that fuels virus replication [24]. Thus improved therapies, taking into consideration such immune activation sequelae, are urgently needed.…”

Section: Chronic Virus Infectionsmentioning

confidence: 99%