They are detargeted from the natural tropism by the deletion of glycoprotein D (gD) residues critical for the interaction with the natural entry receptors nectin1 and Herpesvirus Entry Mediator (HVEM), and retargeted to selected cancer cells by insertion in gD of a single-chain antibody to the cancer-specific antigen of choice, which becomes the new virus receptor [17,18]. Here, ACKR1 is linked to cancer.