Recombinant virus lacking gH is unable to enter epithelial cells, endothelial cells, and fibroblasts, confirming that it is essential for infection [47], while recombinant virus harboring mutations in gH that abrogate EphA2 binding remain infectious [42], suggesting that other receptors and/or functional sites exist on gH/gL. This evidence concerns the gene EPHA2 and infection.