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2015 ; 212 Suppl 2
(Suppl 2
): S247-57
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Analysis of Ebola Virus Entry Into Macrophages
#MMPMID25877552
Dahlmann F
; Biedenkopf N
; Babler A
; Jahnen-Dechent W
; Karsten CB
; Gnirß K
; Schneider H
; Wrensch F
; O'Callaghan CA
; Bertram S
; Herrler G
; Becker S
; Pöhlmann S
; Hofmann-Winkler H
J Infect Dis
2015[Oct]; 212 Suppl 2
(Suppl 2
): S247-57
PMID25877552
show ga
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
?V, 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 ?V promote
phagocytosis of apoptotic cells, support the concept that EBOV relies on
apoptotic mimicry to invade target cells.
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