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

Furuyama, Wakako; Nanbo, Asuka; Maruyama, Junki et al.

PLoS neglected tropical diseases, 2020, 14(9), e0008602

Permalink : https://hdl.handle.net/2115/79681

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アクセス権
open access
URI
https://hdl.handle.net/2115/79681
タイトル
A complement component C1q-mediated mechanism of antibody-dependent enhancement of Ebola virus infection
著者
Furuyama, Wakako ; Nanbo, Asuka ; Maruyama, Junki ; Marzi, Andrea ; Takada, Ayato
著者名
Furuyama, Wakako
e-Rad_Researcher
60359487
著者名
Nanbo, Asuka
著者名
Maruyama, Junki
著者名
Marzi, Andrea
e-Rad_Researcher
10292062
著者名
Takada, Ayato
言語
英語
発行日
2020-09
出版者
PLOS
収録物名
PLoS neglected tropical diseases
巻(号)
14(9)
ページ
e0008602
抄録
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. Author summary Ebola virus (EBOV) utilizes the complement component C1q for antibody-dependent enhancement (ADE) of infection. We found that an ADE antibody increased viral attachment in the presence of C1q and that there was no significant difference in the efficiency of viral 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 for endocytosis. These results suggest that C1q-mediated ADE of EBOV infection is simply caused by increased viral attachment to the cell surface, most likely via cross-linking of virus-antibody-C1q complexes to cellular C1q receptors.
資源タイプ
学術雑誌論文
出版タイプ
Version of Record
権利情報
Creative Commons CC0 1.0 Universal
PISSN
1935-2735
関連情報 (isIdenticalTo)
出版社版DOI
https://doi.org/10.1371/journal.pntd.0008602