Evidence map›Paper›PMID 28036370›Full record

ArticlePLoS pathogens2016

Fcγ-receptor IIa-mediated Src Signaling Pathway Is Essential for the Antibody-Dependent Enhancement of Ebola Virus Infection.

Wakako Furuyama, Andrea Marzi, Aaron B Carmody, Junki Maruyama, Makoto Kuroda, Hiroko Miyamoto, Asuka Nanbo, Rashid Manzoor, Reiko Yoshida, Manabu Igarashi and 2 more

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

30 citing papers in PubMed, 34 citations in OpenAlex.

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  20. An Ebola,Computational and structural biotechnology journal · 2021
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors at 2 institutions in 3 countries.

Wakako FuruyamaDivision of Global Epidemiology, Research Center for Zoonosis Control, Hokkaido University, Sapporo, Japan.
Andrea MarziLaboratory of Virology, Division of Intramural Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rocky Mountain Laboratories, Hamilton, MT, United States of America.
Aaron B CarmodyResearch Technologies Branch, Division of Intramural Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT, United States of America.ORCID http://orcid.org/0000-0003-4772-763X
Junki MaruyamaDivision of Global Epidemiology, Research Center for Zoonosis Control, Hokkaido University, Sapporo, Japan.
Makoto KurodaDivision of Global Epidemiology, Research Center for Zoonosis Control, Hokkaido University, Sapporo, Japan.
Hiroko MiyamotoDivision of Global Epidemiology, Research Center for Zoonosis Control, Hokkaido University, Sapporo, Japan.
Asuka NanboDepartment of Cell Physiology, Hokkaido University Graduate School of Medicine, Sapporo, Japan.ORCID http://orcid.org/0000-0001-8764-1350
Rashid ManzoorDivision of Global Epidemiology, Research Center for Zoonosis Control, Hokkaido University, Sapporo, Japan.
Reiko YoshidaDivision of Global Epidemiology, Research Center for Zoonosis Control, Hokkaido University, Sapporo, Japan.
Manabu IgarashiDivision of Global Epidemiology, Research Center for Zoonosis Control, Hokkaido University, Sapporo, Japan.
Heinz FeldmannLaboratory of Virology, Division of Intramural Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rocky Mountain Laboratories, Hamilton, MT, United States of America.
Ayato TakadaDivision of Global Epidemiology, Research Center for Zoonosis Control, Hokkaido University, Sapporo, Japan.
Hokkaido University · JPNational Institutes of Health · US

Funding

Viral Hemorrhagic Fevers: Disease Modeling and TransmissionZIAAI001089 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI FELDMANN, HEINRICH · 2009 to 2025
$50.7M
6 · The paper itself

Abstract

Antibody-dependent enhancement (ADE) of Ebola virus (EBOV) infection has been demonstrated in vitro, raising concerns about the detrimental potential of some anti-EBOV antibodies. ADE has been described for many viruses and mostly depends on the cross-linking of virus-antibody complexes to cell surface Fc receptors, leading to enhanced infection. However, little is known about the molecular mechanisms underlying this phenomenon. Here we show that Fcγ-receptor IIa (FcγRIIa)-mediated intracellular signaling through Src family protein tyrosine kinases (PTKs) is required for ADE of EBOV infection. We found that deletion of the FcγRIIa cytoplasmic tail abolished EBOV ADE due to decreased virus uptake into cellular endosomes. Furthermore, EBOV ADE, but not non-ADE infection, was significantly reduced by inhibition of the Src family protein PTK pathway, which was also found to be important to promote phagocytosis/macropinocytosis for viral uptake into endosomes. We further confirmed a significant increase of the Src phosphorylation mediated by ADE. These data suggest that antibody-EBOV complexes bound to the cell surface FcγRIIa activate the Src signaling pathway that leads to enhanced viral entry into cells, providing a novel perspective for the general understanding of ADE of virus infection.

Indexed as

AnimalsAntibodies, ViralAntibody-Dependent EnhancementChlorocebus aethiopsGene Knockdown TechniquesHEK293 CellsHemorrhagic Fever, EbolaHumansJurkat CellsK562 CellsReceptors, IgGSignal Transductionsrc-Family KinasesVero CellsVirus InternalizationAntibodies, ViralFc gamma receptor IIAReceptors, IgGsrc-Family Kinases

Identifiers

PMID28036370
PMCPMC5231391
OpenAlexW2565592980

What OpenQuestion holds

Textmetadata
LicenceCC0
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.