What is the pathophysiology of West Nile virus infection?

Updated: Apr 02, 2018
  • Author: Jess D Salinas, Jr, MD; Chief Editor: Elizabeth A Moberg-Wolff, MD  more...
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Examining the ways in which the West Nile virus may cross the blood-brain barrier to infect the nervous system, Verma et al infected primary human brain microvascular endothelial (HBMVE) cells with NY99, a neurovirulent strain of the virus. [11] The authors noted that the virus did not have a cytopathic effect on the HBMVE cells. Increased mRNA (messenger ribonucleic acid) and protein expression of the tight-junction protein claudin-1 and of 2 cell adhesion molecules (vascular cell adhesion molecule and E-selectin) were seen 2-3 days after cellular infection, the same time at which West Nile virus replication had peaked.

The study provided evidence that infection of HBMVE cells by the West Nile virus enables the cell-free virus to enter the central nervous system without disturbing the barrier's integrity. In addition, the authors suggested that cell adhesion molecules may help to traffic West Nile virus – infected immune cells into the central nervous system.

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