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Ebola Virus Enters Host Cells by Macropinocytosis and Clathrin-Mediated Endocytosis
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Ebola Virus Enters Host Cells by Macropinocytosis and Clathrin-Mediated Endocytosis
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Journal Article
Ebola Virus Enters Host Cells by Macropinocytosis and Clathrin-Mediated Endocytosis
2011
Overview
Virus entry into host cells is the first step of infection and a crucial determinant of pathogenicity. Here we show that Ebola virus-like particles (EBOV-VLPs) composed of the glycoprotein GP₁,₂ and the matrix protein VP40 use macropinocytosis and dathrin-mediated endocytosis to enter cells. EBOV-VLPs applied to host cells induced actin-driven ruffling and enhanced FITC-dextran uptake, which indicated macropinocytosis as the main entry mechanism. This was further supported by inhibition of entry through inhibitors of actin polymerization (latrunculin A), Na⁻/H⁺-exchanger (EIPA), and PI3-kinase (wortmannin). A fraction of EBOV-VLPs, however, colocalized with clathrin heavy chain (CHC), and VLP uptake was reduced by CHC small interfering RNA transfection and expression of the dominant negative dynamin II-K44A mutant. In contrast, we found no evidence that EBOV-VLPs enter cells via caveolae. This work identifies macropinocytosis as the major, and dathrin-dependent endocytosis as an alternative, entry route for EBOV particles. Therefore, EBOV seems to utilize different entry pathways depending on both cell type and virus particle size.
Publisher
Oxford University Press
