For example, when oHSV HSV1716 was used as a combinatory therapy with a monoclonal antibody that blocks program death-1 (PD-1) checkpoint in a mouse model of rhabdomyosarcoma, it resulted to an improved survival and increased tumor infiltration of CD4+ and CD8+ T-cells, but not of regulatory T-cells (Tregs), compared to the PD-1 blockade or HSV1716 treatments alone [32]. Here, CD4 is linked to neoplasm.