Work performed by ourselves and independent researchers [23, 36, 37] has highlighted that nonocular endothelial cell populations, including endothelial cells from the human umbilical vein and the human dermal microvasculature, are susceptible to infection with DENV, but with a relatively low proportion of cells infected; this has been attributed to both extracellular conditions and cellular phenotype, including the expression of cell surface receptors for the virus. This evidence concerns the gene CD177 and infection.