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J Infect Dis. 2015 Oct 1;212 Suppl 2:S247-57. doi: 10.1093/infdis/jiv140. Epub 2015 Apr 14.

Analysis of Ebola Virus Entry Into Macrophages.

Author information

1
Infection Biology Unit, German Primate Center, Göttingen.
2
Institute of Virology, Philipps-University Marburg.
3
Helmholtz-Institute for Biomedical Engineering, RWTH Aachen University.
4
Infection Biology Unit, German Primate Center, Göttingen Institutes for Cellular Chemistry.
5
Physiological Chemistry, Hannover Medical School.
6
Henry Wellcome Building for Molecular Physiology, University of Oxford, United Kingdom.
7
Institute of Virology, University of Veterinary Medicine Hannover, Germany.

Abstract

Ebolaviruses constitute a public health threat, particularly in Central and Western Africa. Host cell factors required for spread of ebolaviruses may serve as targets for antiviral intervention. Lectins, TAM receptor tyrosine kinases (Tyro3, Axl, Mer), T cell immunoglobulin and mucin domain (TIM) proteins, integrins, and Niemann-Pick C1 (NPC1) have been reported to promote entry of ebolaviruses into certain cellular systems. However, the factors used by ebolaviruses to invade macrophages, major viral targets, are poorly defined. Here, we show that mannose-specific lectins, TIM-1 and Axl augment entry into certain cell lines but do not contribute to Ebola virus (EBOV)-glycoprotein (GP)-driven transduction of macrophages. In contrast, expression of Mer, integrin αV, and NPC1 was required for efficient GP-mediated transduction and EBOV infection of macrophages. These results define cellular factors hijacked by EBOV for entry into macrophages and, considering that Mer and integrin αV promote phagocytosis of apoptotic cells, support the concept that EBOV relies on apoptotic mimicry to invade target cells.

KEYWORDS:

Ebolavirus; Mer; NPC-1; entry; macrophage

PMID:
25877552
PMCID:
PMC4564540
DOI:
10.1093/infdis/jiv140
[Indexed for MEDLINE]
Free PMC Article

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