Mx genes: host determinants controlling influenza virus infection and trans-species transmission

Haller, Otto; Kochs, Georg

doi:10.1007/s00439-019-02092-8

Cited by 53 publications

(38 citation statements)

References 104 publications

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“… 156 However, none of these variants have been linked to influenza susceptibility currently. 157 There is increasing evidence that some viral restriction factors can also play additional, multifaceted roles, for example, acting as innate sensors and triggering innate immune responses. 158 One important viral restriction factor is the IFN-induced transmembrane protein 3 (IFITM3), which restricts cell entry of mainly enveloped RNA viruses including SARS-CoV and IAV.…”

Section: Influence Of Genetic Variation On Viral-induced Inflammationmentioning

confidence: 99%

Genetic influences on viral-induced cytokine responses in the lung

Forbester

Humphreys

2021

Mucosal Immunology

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Section: Influence Of Genetic Variation On Viral-induced Inflammationmentioning

confidence: 99%

Genetic influences on viral-induced cytokine responses in the lung

Forbester

Humphreys

2021

Mucosal Immunology

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“…Unfortunately, no data of IAV infection history from homozygous carriers of these mutations are available. This aspect is nicely reviewed in [ 205 ].…”

Section: Iav Restriction Factorsmentioning

confidence: 99%

Mammalian and Avian Host Cell Influenza A Restriction Factors

McKellar

Rebendenne

Wencker

et al. 2021

Viruses

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The threat of a new influenza pandemic is real. With past pandemics claiming millions of lives, finding new ways to combat this virus is essential. Host cells have developed a multi-modular system to detect incoming pathogens, a phenomenon called sensing. The signaling cascade triggered by sensing subsequently induces protection for themselves and their surrounding neighbors, termed interferon (IFN) response. This response induces the upregulation of hundreds of interferon-stimulated genes (ISGs), including antiviral effectors, establishing an antiviral state. As well as the antiviral proteins induced through the IFN system, cells also possess a so-called intrinsic immunity, constituted of antiviral proteins that are constitutively expressed, creating a first barrier preceding the induction of the interferon system. All these combined antiviral effectors inhibit the virus at various stages of the viral lifecycle, using a wide array of mechanisms. Here, we provide a review of mammalian and avian influenza A restriction factors, detailing their mechanism of action and in vivo relevance, when known. Understanding their mode of action might help pave the way for the development of new influenza treatments, which are absolutely required if we want to be prepared to face a new pandemic.

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“…Finally, we have invited colleagues outside the field of the human genetics of infectious diseases to contribute to this issue with reviews about the genetic basis of infections in other species. In particular, Otto Haller reviews the Mx saga (Haller and Kochs 2019), concerning the first animal/human gene conferring predisposition to a specific infection to be identified (Staeheli et al 1986), and Philippe Gros, who had discovered the molecular basis of the Bcg locus by performing the first positional cloning in mice (Vidal et al 1993), reviews the complex role of IRF8 in mice and humans (Salem et al 2020).…”

Section: Topics Covered In This Special Issuementioning

confidence: 99%

The human genetic determinism of life-threatening infectious diseases: genetic heterogeneity and physiological homogeneity?

Casanova

Abel

2020

Hum Genet

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Multicellular eukaryotes emerged late in evolution from an ocean of viruses, bacteria, archaea, and unicellular eukaryotes. These macroorganisms are exposed to and infected by a tremendous diversity of microorganisms. Those that are large enough can even be infected by multicellular fungi and parasites. Each interaction is unique, if only because it operates between two unique living organisms, in an infinite diversity of circumstances. This is neatly illustrated by the extraordinarily high level of interindividual clinical variability in human infections, even for a given pathogen, ranging from a total absence of clinical manifestations to death. We discuss here the idea that the determinism of human life-threatening infectious diseases can be governed by single-gene inborn errors of immunity, which are rarely Mendelian and frequently display incomplete penetrance. We briefly review the evidence in support of this notion obtained over the last two decades, referring to a number of focused and thorough reviews published by eminent colleagues in this issue of Human Genetics. It seems that almost any life-threatening infectious disease can be driven by at least one, and, perhaps, a great many diverse monogenic inborn errors, which may nonetheless be immunologically related. While the proportions of monogenic cases remain unknown, a picture in which genetic heterogeneity is combined with physiological homogeneity is emerging from these studies. A preliminary sketch of the human genetic architecture of severe infectious diseases is perhaps in sight.

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Mx genes: host determinants controlling influenza virus infection and trans-species transmission

Cited by 53 publications

References 104 publications

Genetic influences on viral-induced cytokine responses in the lung

Genetic influences on viral-induced cytokine responses in the lung

Mammalian and Avian Host Cell Influenza A Restriction Factors

The human genetic determinism of life-threatening infectious diseases: genetic heterogeneity and physiological homogeneity?

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