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Oncolytic virus replication is a therapeutic process in which engineered or naturally occurring viruses selectively infect and multiply within cancer cells, leading to their destruction (NCI, 2023). This selectivity is typically achieved by exploiting defects in cancer cell antiviral defenses, such as impaired interferon signaling or mutations in the p53 and Rb pathways (Lichty et al., 2014). During replication, the virus utilizes the host cell's metabolic and translational machinery to produce viral proteins and genomic material, culminating in cell lysis and the release of progeny virions (Kaufman et al., 2015). This process not only causes direct tumor debulking but also triggers immunogenic cell death, releasing tumor-associated antigens and pathogen-associated molecular patterns that activate the systemic immune system (Marelli et al., 2018). Drugs like Talimogene laherparepvec (T-VEC) utilize this mechanism to treat advanced melanoma by inducing both local and abscopal anti-tumor effects (FDA, 2015). Therapeutic challenges include the presence of neutralizing antibodies that can limit viral spread and the physical barriers of the tumor stroma that impede viral penetration (Lawler et al., 2017).
Selective infection and replication within neoplastic cells leading to direct cytolysis and stimulation of a systemic anti-tumor immune response.
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