At the initial target recognition level, viral tropism is defined by the molecular complementarity between viral receptor-binding proteins and specific tumor surface markers: Enterovirus A71(EV-A71) selectively infects glioma cells via the Scavenger Receptor Class B Member 2 (SCARB2) scavenger receptor, whereas wild-type HSV relies on NECTIN-1/HVEM receptor-mediated cell entry [97,98]. Here, SCARB2 is linked to neoplasm.