Tumor cell lysis via selective viral replication in IFN-deficient tumor cells

This entry does not specify a unique molecular target or receptor. Instead, it refers to the therapeutic principle whereby oncolytic viruses exploit the **deficiency in interferon (IFN)-mediated antiviral responses within tumor cells** to preferentially replicate and cause tumor cell lysis, while sparing normal cells that have intact IFN signaling[1][4][6]. This selective vulnerability serves as the basis for several viral therapies targeting a broad class of tumors rather than a single, well-defined molecule or receptor. References to this mechanism are found in foundational reviews on oncolytic virotherapy, which describe how **viruses such as reovirus, HSV, NDV, and VSV preferentially infect and kill tumor cells that are IFN-deficient, often due to mutations in signal transduction components or pathways like RAS**[1][3][4][6]. Precision targeting is thus achieved by exploiting the intrinsic weakness of tumor antiviral defense mechanisms, rather than by engaging a single proteinaceous target.

Selective viral replication within IFN-deficient tumor cells leads to direct lysis (oncolysis)[1][4][6]. Amplification of anti-tumor immunity through release of tumor antigens and immune activation[4][1].