Systemic and Ophthalmic Manifestations of West Nile Virus Infection

Yos Priestley; Marcia Thiel; Steven B. Koevary

Disclosures

Expert Rev Ophthalmol. 2008;3(3):279-292. 

In This Article

Immune Response to the Virus

Data suggest that antibody, T-cell, dendritic cell and macrophage responses play important roles in anti-WNV immunity.[22] In fact, it is the replication of the virus in dendritic cells at the site of inoculation and its spread from there to regional lymph nodes that is thought to be the mode of establishment of infection in the body.[23] The binding of double-stranded WNV RNA to Toll-like receptor-3, resulting in the upregulation of TNF-α production and a subsequent increase in blood-brain barrier permeability, appears to play a role in viral penetration into the CNS.[24] The importance of antibodies was made clear in B cell-deficient mice that uniformly died after WNV infection but were protected by passive transfer of immune sera.[25] Consistent with an important role for T cells, it was reported that individuals with hematologic malignancies and impaired T-cell function had an increased risk of developing neuroinvasive WNV infection.[22] Fredericksen et al. reported that WNV induced the expression of IFN-ß and several IFN-stimulated genes late in infection of cultured human cells but that despite this host response, it was still able to replicate efficiently.[26] The foregoing notwithstanding, more recent data suggest that WNV induces an antiviral state in retinal pigment epithelium (RPE) cells by a mechanism that seems to employ the IFN signaling pathway.[27] Interestingly, through an unknown mechanism, flavivirus nonstructural proteins were reported to suppress host antiviral immune responses.[28]

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