A complement component C1q-mediated mechanism of antibody-dependent enhancement of Ebola virus infection.


Journal

PLoS neglected tropical diseases
ISSN: 1935-2735
Titre abrégé: PLoS Negl Trop Dis
Pays: United States
ID NLM: 101291488

Informations de publication

Date de publication:
09 2020
Historique:
received: 12 11 2019
accepted: 14 07 2020
revised: 17 09 2020
pubmed: 5 9 2020
medline: 29 10 2020
entrez: 4 9 2020
Statut: epublish

Résumé

Besides the common Fc receptor (FcR)-mediated mechanism of antibody-dependent enhancement (ADE), Ebola virus (EBOV) is known to utilize the complement component C1q for ADE of infection. This mechanism is FcR-independent and mediated by cross-linking of virus-antibody-C1q complexes to cell surface C1q receptors, leading to enhanced viral entry into cells. Using confocal microscopy, we found that virus-like particles (VLPs) consisting of EBOV glycoprotein, nucleoprotein, and matrix protein attached to the surface of human kidney 293 cells more efficiently in the presence of an ADE monoclonal antibody and C1q than with the antibody or C1q alone, and that there was no significant difference in the efficiency of VLP uptake into endosomes between the C1q-mediated ADE and non-ADE entry. Accordingly, both ADE and non-ADE infection were similarly decreased by inhibitors of the signaling pathways known to be required for endocytosis. These results suggest that C1q-mediated ADE of EBOV infection is simply caused by increased attachment of virus particles to the cell surface, which is distinct from the mechanism of FcR-mediated ADE requiring intracellular signaling to promote phagocytosis/macropinocytosis.

Identifiants

pubmed: 32886656
doi: 10.1371/journal.pntd.0008602
pii: PNTD-D-19-01921
pmc: PMC7497997
doi:

Substances chimiques

Antibodies, Monoclonal 0
Antibodies, Viral 0
Membrane Glycoproteins 0
Receptors, Complement 0
Viral Proteins 0
complement 1q receptor 0
Complement C1q 80295-33-6

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

e0008602

Déclaration de conflit d'intérêts

The authors have declared that no competing interests exist.

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Auteurs

Wakako Furuyama (W)

Laboratory of Virology, Division of Intramural Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rocky Mountain Laboratories, Hamilton, Montana, United States of America.

Asuka Nanbo (A)

Department of Cell Physiology, Hokkaido University Graduate School of Medicine, Sapporo, Japan.

Junki Maruyama (J)

Division of Global Epidemiology, Research Center for Zoonosis Control, Hokkaido University, Sapporo, Japan.

Andrea Marzi (A)

Laboratory of Virology, Division of Intramural Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rocky Mountain Laboratories, Hamilton, Montana, United States of America.

Ayato Takada (A)

Division of Global Epidemiology, Research Center for Zoonosis Control, Hokkaido University, Sapporo, Japan.
Global Station for Zoonosis Control, Global Institution for Collaborative Research and Education, Hokkaido University, Sapporo, Japan.
School of Veterinary Medicine, the University of Zambia, Lusaka, Zambia.

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Classifications MeSH