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Oncolytic virus-mediated cancer cell lysis via selective viral replication

Molecular classification
Other (Oncolytic viruses are not a single molecule, receptor, or protein but rather a therapeutic strategy using engineered or naturally occurring viruses)
01

Overview

"Cancer cell lysis via selective viral replication" refers to the use of oncolytic viruses—viruses that preferentially infect and replicate within cancer cells—to induce targeted destruction (lysis) of malignant tissue. This approach exploits differences between normal and neoplastic cells; for example, many cancers overexpress certain surface receptors such as CAR, laminin receptors, CD155, and CD46 that facilitate higher uptake by specific viruses. Some oncolytic viruses are further engineered with deletions in genes essential for their survival in normal but not cancerous tissues—such as thymidine kinase—ensuring they replicate only where these factors are abundant. The process results both in direct killing through cellular rupture upon virion release and indirect effects by stimulating an anti-tumor immune response through exposure to tumor antigens. While highly promising as a therapeutic strategy against various cancers—including those resistant to conventional therapies—this is not a single molecular target like an enzyme or receptor but rather describes a class/mechanism involving multiple molecular interactions between virus and host.

Other names
Oncolytic virusOncolytic virotherapySelective viral oncolysisCancer-selective viral replication
02

Mechanism of action

Selective infection and replication within cancer cells leading to direct lysis of tumor cells; Induction of immune response against tumor antigens released during cell lysis.

03

Biological functions

Cell death (cancer cell lysis)Induction of antitumor immunitySelective infection and replication in cancer cells
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Disease associations

Cancer
05

Safety considerations

Off-target infection/lysis of normal cells if selectivity is insufficientImmune-related adverse events due to induction of systemic immune responsesPotential for uncontrolled viral spread or reversion to pathogenicity
06

Biomarkers

Selection for therapy may depend on expression of certain viral entry receptors such as CAR, CD155, CD46, EGFR/RAS pathway activation, or high thymidine kinase activity in tumors

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