Integrins modulate the infection efficiency of West Nile virus
West Nile virus (WNV) is a small, enveloped, single-stranded RNA virus in the family Flaviviridae. In the natural transmission cycle WNV circulates between mosquitoes as vectors and birds as reservoir hosts. WNV can infect a wide taxonomical range of vertebrate species but most of them do not sufficiently support virus replication for transmission. Disease symptoms rarely occur, except in humans and horses where WNV infections are frequently accompanied by a mild fever (West Nile fever), which occasionally results in the development of neurological disorders with fatal outcome.
The cellular receptors and determinants that mediate entry of WNV are unclear to date. The notable ability of WNV to infect a broad range of species (mosquitoes, reptiles, birds and mammals), and virtually every in vitro cell line is supposed to be related to cellular proteins, relevant for virus entry and replication, which are highly conserved among divergent host species.
By using integrin knock-out cell lines which lack the particular integrin subunits, this study demonstrate that the presence of αv-, β1- or β3-integrins is not required for the attachment of four different WNV strains to the cell surface.