Evidence map›Paper›PMID 30498026›Full record

ArticleEMBO molecular medicine2019

Identification and characterization of GLDC as host susceptibility gene to severe influenza.

Jie Zhou, Dong Wang, Bosco Ho-Yin Wong, Cun Li, Vincent Kwok-Man Poon, Lei Wen, Xiaoyu Zhao, Man Chun Chiu, Xiaojuan Liu, Ziwei Ye and 6 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in EMBO molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 19 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 2 pooled it
2.1field-weighted citation impact, top 12% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

19 citing papers in PubMed, 2 syntheses or guidelines pooled it, 24 citations in OpenAlex.

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  19. Host susceptibility to severe influenza A virus infection.Critical care (London, England) · 2019
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors at 3 institutions in 2 countries.

Jie ZhouState Key Laboratory of Emerging Infectious Diseases, The University of Hong Kong, Pokfulam, Hong Kong.
Dong WangDepartment of Microbiology, The University of Hong Kong, Pokfulam, Hong Kong.
Bosco Ho-Yin WongDepartment of Microbiology, The University of Hong Kong, Pokfulam, Hong Kong.
Cun LiDepartment of Microbiology, The University of Hong Kong, Pokfulam, Hong Kong.
Vincent Kwok-Man PoonDepartment of Microbiology, The University of Hong Kong, Pokfulam, Hong Kong.
Lei WenDepartment of Microbiology, The University of Hong Kong, Pokfulam, Hong Kong.
Xiaoyu ZhaoDepartment of Microbiology, The University of Hong Kong, Pokfulam, Hong Kong.
Man Chun ChiuDepartment of Microbiology, The University of Hong Kong, Pokfulam, Hong Kong.
Xiaojuan LiuDepartment of Microbiology, The University of Hong Kong, Pokfulam, Hong Kong.
Ziwei YeDepartment of Microbiology, The University of Hong Kong, Pokfulam, Hong Kong.
Shuofeng YuanDepartment of Microbiology, The University of Hong Kong, Pokfulam, Hong Kong.
Kong-Hung SzeDepartment of Microbiology, The University of Hong Kong, Pokfulam, Hong Kong.
Jasper Fuk-Woo ChanState Key Laboratory of Emerging Infectious Diseases, The University of Hong Kong, Pokfulam, Hong Kong.
Hin ChuState Key Laboratory of Emerging Infectious Diseases, The University of Hong Kong, Pokfulam, Hong Kong.
Kelvin Kai-Wang ToState Key Laboratory of Emerging Infectious Diseases, The University of Hong Kong, Pokfulam, Hong Kong.
Kwok Yung YuenState Key Laboratory of Emerging Infectious Diseases, The University of Hong Kong, Pokfulam, Hong Kong kyyuen@hku.hk.ORCID 0000-0002-2083-1552
University of Hong Kong · HKUniversity of Hong Kong - Shenzhen Hospital · CNHKU-Pasteur Research Pole · HK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glycine decarboxylase (GLDC) was prioritized as a candidate susceptibility gene to severe influenza in humans. The higher expression of GLDC derived from genetic variations may confer a higher risk to H7N9 and severe H1N1 infection. We sought to characterize GLDC as functional susceptibility gene that GLDC may intrinsically regulate antiviral response, thereby impacting viral replication and disease outcome. We demonstrated that GLDC inhibitor AOAA and siRNA depletion boosted IFNβ- and IFN-stimulated genes (ISGs) in combination with PolyI:C stimulation. GLDC inhibition and depletion significantly amplified antiviral response of type I IFNs and ISGs upon viral infection and suppressed the replication of H1N1 and H7N9 viruses. Consistently, GLDC overexpression significantly promoted viral replication due to the attenuated antiviral responses. Moreover, GLDC inhibition in H1N1-infected BALB/c mice recapitulated the amplified antiviral response and suppressed viral growth. AOAA provided potent protection to the infected mice from lethal infection, comparable to a standard antiviral against influenza viruses. Collectively, GLDC regulates cellular antiviral response and orchestrates viral growth. GLDC is a functional susceptibility gene to severe influenza in humans.

Indexed as

Genetic Predisposition to DiseaseImmunity, InnateAnimalsDisease Models, AnimalEnzyme InhibitorsGlycine Dehydrogenase (Decarboxylating)HumansInfluenza A Virus, H1N1 SubtypeInfluenza A Virus, H7N9 SubtypeInfluenza, HumanMice, Inbred BALB COrthomyxoviridae InfectionsTacrolimusTreatment OutcomeVirus Replication32-ascomycinyloxyacetic acidEnzyme InhibitorsGlycine Dehydrogenase (Decarboxylating)Tacrolimusantiviral responsegenetic susceptibilityGLDCsevere influenzaviral replication

Identifiers

PMID30498026
PMCPMC6328914
OpenAlexW2902547059

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.