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The target described as Tumor cells via undefined viral entry receptors and host replication machinery refers to the biological framework exploited by oncolytic virotherapy. In this approach, viruses are engineered or selected to selectively infect and replicate within malignant cells while sparing healthy tissue (Kaufman et al., 2015, CA: A Cancer Journal for Clinicians). These viruses often utilize various cell surface molecules for entry, such as CD46 or nectin-4, which are frequently overexpressed in tumors, though the specific entry receptor may remain undefined for certain viral strains (Fukuhara et al., 2016, Cancer Science). Once inside, the virus hijacks the host's replication machinery, taking advantage of the impaired interferon signaling and high metabolic activity characteristic of cancer cells (Marelli et al., 2018, Frontiers in Immunology). The resulting viral progeny cause direct oncolysis, releasing tumor-associated antigens and pathogen-associated molecular patterns (PAMPs) into the microenvironment. This process triggers a robust systemic anti-tumor immune response, effectively turning immunologically cold tumors hot (Lichty et al., 2014, Nature Reviews Cancer). The most prominent example of a drug hitting this target is Talimogene laherparepvec (T-VEC), which is used for the treatment of advanced melanoma (Reid et al., 2016, JAMA Oncology).
Selective infection and lysis of tumor cells by oncolytic viruses, followed by the induction of a systemic anti-tumor immune response.
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