West Nile Virus Neuroinvasive Disease29 July 2014
To identify the mechanisms by which West Nile virus (WNV) causes disruption of the blood-brain barrier (BBB) and leukocyte migration into the brain, the role of endothelial cell adhesion molecules (CAMs) was studied in an in vitro BBB model. Permeability of the BBB model increased following leukocyte migration across WNV-infected brain microvascular endothelial cells, facilitated by infection-induced increases of specific CAMs in endothelial cells. Further, similar infectivity and ability to induce CAMs in endothelial cells infected with both the neurovirulent WNV NY99 strain and the non-lethal WNV Egypt 101 strain suggested that the non-neuropathic response of Egypt 101 was not due to an inability to infect endothelial cells lining the BBB. These results point to the upregulation of CAMs as a major pathological event associated with WNV-induced BBB disruption and may contribute to leukocyte infiltration and a “Trojan Horse” route of WNV entry into the central nervous system.
Roe K, Orillo B, Verma S. West Nile virus-induced cell adhesion molecules on human brain microvascular endothelial cells regulate leukocyte adhesion and modulate permeability of the in vitro blood-brain barrier model. PLoS One 2014;9(7):e102598. PMCID: PMC4103843