Integrins modulate the infection efficiency of West Nile virus into cells.

Article Details

Citation

Schmidt K, Keller M, Bader BL, Korytar T, Finke S, Ziegler U, Groschup MH

Integrins modulate the infection efficiency of West Nile virus into cells.

J Gen Virol. 2013 Aug;94(Pt 8):1723-33. doi: 10.1099/vir.0.052613-0. Epub 2013 May 8.

PubMed ID
23658209 [ View in PubMed
]
Abstract

The underlying mechanisms allowing West Nile virus (WNV) to replicate in a large variety of different arthropod, bird and mammal species are largely unknown but are believed to rely on highly conserved proteins relevant for viral entry and replication. Consistent with this, the integrin alphavbeta3 has been proposed lately to function as the cellular receptor for WNV. More recently published data, however, are not in line with this concept. Integrins are highly conserved among diverse taxa and are expressed by almost every cell type at high numbers. Our study was designed to clarify the involvement of integrins in WNV infection of cells. A cell culture model, based on wild-type and specific integrin knockout cell lines lacking the integrin subunits alphav, beta1 or beta3, was used to investigate the susceptibility to WNV, and to evaluate binding and replication efficiencies of four distinct strains (New York 1999, Uganda 1937, Sarafend and Dakar). Though all cell lines were permissive, clear differences in replication efficiencies were observed. Rescue of the beta3-integrin subunit resulted in enhanced WNV yields of up to 90 %, regardless of the virus strain used. Similar results were obtained for beta1-expressing and non-expressing cells. Binding, however, was not affected by the expression of the integrins in question, and integrin blocking antibodies failed to have any effect. We conclude that integrins are involved in WNV infection but not at the level of binding to target cells.

DrugBank Data that Cites this Article

Polypeptides
NameUniProt ID
Integrin beta-3P05106Details
Integrin alpha-VP06756Details