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The process refers to tumor cell destruction mediated by oncolytic viral replication, wherein specialized viruses (natural or genetically engineered) infect and replicate preferentially within cancer cells. This leads to the bursting (lysis) of tumor cells, the release of new viral particles, and exposure of tumor antigens, which stimulates a local and systemic immune response against the remaining tumor cells[1][2][3][7]. This therapeutic mechanism is utilized in cancer treatment by deploying viruses that exploit cancer-specific defects (e.g., antiviral pathway deficiencies), and is increasingly enhanced by genetic engineering to deliver additional immune-activating proteins or drug payloads directly to the tumor[4][5][8]. The first FDA-approved oncolytic virotherapy, T-VEC, is an engineered herpes simplex virus for melanoma[2][8]. It is important to note that "Tumor cell lysis via oncolytic viral replication" should not be treated as a canonical drug target, molecule, or receptor; instead, individual oncolytic viruses or specific cellular receptors involved in virus entry could be listed as drug targets. This entry is a therapeutic mechanism, not a discrete molecular target.
Selective infection and replication in tumor cells Direct lysis of tumor cells Release of tumor antigens and danger signals, promoting immune recognition Delivery of therapeutic payloads (cytokines, enzymes) via engineered viruses
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