Abstract
Abstract West-Nile virus (WNV) is an arbovirus usually transmitted to humans via a mosquito vector. Less than one percent of cases result in a serious neurological illness such as meningitis or encephalitis Studies have shown that WNV infection efficiency is enhanced by expression of DC-SIGNR on target cells, which normally do not express DC-SIGNR. To investigate WNV tropism, we established 293T kidney epithelial cell lines that stably express vector or DC-SIGNR. We demonstrated uniformly high levels of DC-SIGNR expression in selected cells. Virus replicon particles (VRPs), replication-incompetent viral particles containing necessary structural proteins for infection and a viral plasmid including a GFP reporter are used to safely and conveniently study viral entry. Entry assays using WNV (NY99) VRPs as well as a variant of WNV (NY99) which contains the beta-lactamase enzyme show significant entry into DC-SIGNR expressing cell lines, but not in controls that do not express DC-SIGNR. Future studies will focus on discovering which regions of the DC-SIGNR surface glycoprotein are required for WNV entry.
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