論文

査読有り 国際共著 国際誌
2020年9月

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

PLoS neglected tropical diseases
  • Wakako Furuyama
  • ,
  • Asuka Nanbo
  • ,
  • Junki Maruyama
  • ,
  • Andrea Marzi
  • ,
  • Ayato Takada

14
9
開始ページ
e0008602
終了ページ
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1371/journal.pntd.0008602

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.

リンク情報
DOI
https://doi.org/10.1371/journal.pntd.0008602
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/32886656
PubMed Central
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7497997
ID情報
  • DOI : 10.1371/journal.pntd.0008602
  • PubMed ID : 32886656
  • PubMed Central 記事ID : PMC7497997

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