EPHA2 and infection: The gH-ASAELAAN mutant was generated by combining gH mutations that we had previously found to individually decrease either EphA2 binding (E52A, F53A) or gH/gL complexation (L47A, I49A) [27], which together caused drastically reduced or abrogated gL incorporation into the gH/gL complex (Figure 4A) in addition to loss of binding to EphA2 as evidenced by the inability of soluble EphA2 or ephrin ligands to block infection of KSHV bearing the gH-ASAELAAN mutations (Figure 4B).