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Tumor cell entry receptors and replication machinery refers to a collective set of cellular components exploited by oncolytic viruses to achieve tumor-selective infection and destruction. Entry receptors are surface proteins, such as Nectin-4, CD46, or the Coxsackievirus and adenovirus receptor (CAR), which are frequently upregulated in various malignancies and serve as docking sites for viral attachment (Bergelson et al., 1997, Science; Mühlebach et al., 2011, Nature Medicine). Once the virus enters the cell, it hijacks the host's replication machinery—including DNA/RNA polymerases and ribosomes—to produce viral progeny, a process often facilitated by the dysregulated cell cycle and suppressed antiviral pathways (e.g., IFN signaling) characteristic of cancer cells. This selective propagation leads to direct cell lysis, known as oncolysis, and the subsequent release of tumor-associated antigens that can trigger a systemic anti-tumor immune response (Reid et al., 2016, JITC). While this approach offers high specificity, therapeutic challenges include the presence of pre-existing neutralizing antibodies and the physical barriers of the tumor microenvironment that limit viral spread. This term is considered a functional category rather than a single molecular target.
Selective infection of tumor cells via specific surface receptors followed by hijacking of the host's replication machinery to induce oncolysis and stimulate an anti-tumor immune response.
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