FusOn-H2

FusOn-H2 is an **oncolytic virus** engineered from type II herpes simplex virus (HSV-2) by deleting the N-terminal region of the ICP10 gene. This modification confers selective replication in, and lysis of, tumor cells while sparing normal tissue[1][2]. The drug acts by two main mechanisms: direct oncolysis (lysis of tumor cells via viral replication) and induction of a substantial antitumor immune response (including neutrophil and T cell infiltration) against tumor cells. Notably, it is effective against both permissive tumors (via direct viral lysis) and some non-permissive tumors (via immune cell recruitment and inflammation)[1][2]. In clinical models, FusOn-H2 also enhances the homing and persistence of adoptive cellular therapies such as engineered T cells to tumor sites. It is under development primarily as a cancer therapy, with demonstrated activity against a range of solid tumors; efficacy is variable and depends in part on tumor-specific permissiveness to HSV-2 replication[1][2][5].