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Oncolytic virus-induced tumor lysis

Molecular classification
Other
01

Overview

Oncolytic virus-induced tumor lysis is not a specific molecule or receptor but rather describes a biological process whereby genetically engineered or naturally occurring viruses selectively infect and replicate inside tumor cells, resulting in direct cell destruction (lysis) and the release of antigens and danger signals that provoke systemic antitumor immunity[1][2][3][4][5]. This process is exploited therapeutically in oncolytic virotherapy, where the virus may also deliver therapeutic genes or modulate immune responses to enhance cancer cell killing. The tumor lysis mechanism is multifaceted, involving direct viral cytotoxicity, induction of apoptosis and pyroptosis, and activation of both innate (NK cells, dendritic cells, macrophages) and adaptive (cytotoxic T lymphocytes) immune pathways[1][2][3][4][5]. While oncolytic viruses (OVs) target cancer via tumor-selective entry and replication, "oncolytic virus-induced tumor lysis" itself is not a canonical drug target, receptor, or protein, but a therapeutic endpoint and mechanistic event, making it incorrect to treat as a discrete molecular target. Note: - This entry is not a proper molecular target under standard therapeutic target definitions (such as receptor, enzyme, etc.), but rather describes a process or outcome of oncolytic virotherapy[1][2][3][4][5]. - For structured annotation, specific oncolytic virus names (e.g., HSV-1, Reovirus) and their molecular targets (e.g., viral receptors on tumor cells) should be considered as canonical entries.

02

Mechanism of action

Direct lysis of tumor cells via viral replication; Induction of immunogenic cell death (ICD); Activation of innate and adaptive immune responses; Delivery of therapeutic transgenes (gene therapy effect); Engagement of cell death pathways (apoptosis, pyroptosis)

03

Biological functions

Cell deathApoptosisPyroptosisImmune response
04

Disease associations

Cancer
05

Safety considerations

Pre-existing antiviral immunity may reduce efficacyOff-target infection and toxicitySystemic inflammationImmune clearance and neutralizationTherapeutic resistanceTumor heterogeneity affecting response
06

Interacting drugs

Talimogene laherparepvec (T-VEC)

5 more in the full profile.

07

Biomarkers

Interferon signaling deficiencyTumor-selective viral receptor expressionTumor mutational statusCytokine levels (e.g., IL-1β, TNF-α)DAMPs (damage-associated molecular patterns)

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