Target intelligence / Profile preview

Vaccinia virus-sensitive tumor cells

Molecular classification
Other
01

Overview

Vaccinia virus-sensitive tumor cells are malignant cells characterized by specific molecular vulnerabilities that allow for selective infection and destruction by oncolytic vaccinia viruses (PMID: 21451545). These cells often exhibit deficiencies in the type I interferon (IFN) signaling pathway, which normally serves as a primary defense against viral infection in healthy cells (Nature Reviews Cancer, 2011). Additionally, the high metabolic rate and elevated levels of thymidine kinase in these tumor cells support rapid viral replication, as the virus relies on the host cell's nucleotide pool (Journal of Virology, 2006). Many sensitive cells also overexpress the epidermal growth factor receptor (EGFR), which can facilitate viral entry and activation of the Ras/MAPK pathway, further promoting viral protein synthesis (Molecular Therapy, 2015). Therapeutic agents like Pexastimogene devacirepvec (Pexa-Vec) are engineered to exploit these characteristics, ensuring that viral replication is restricted to the tumor microenvironment (NIH, ClinicalTrials.gov). Upon infection, the virus induces direct oncolysis, causing the tumor cell to burst and release progeny viruses along with tumor-associated antigens. This process transforms the immunosuppressive tumor microenvironment into an inflamed state, recruiting T-cells and other immune effectors to attack both the infected and uninfected tumor cells (PubMed, PMID: 28934444). Consequently, these cells serve as the primary site for both direct viral therapy and the initiation of a broader systemic anti-cancer immune response.

Other names
Oncolytic vaccinia virus-susceptible cellsVV-sensitive cancer cellsVaccinia-susceptible tumor cellsOncolytic virus-sensitive tumor cells
02

Mechanism of action

Oncolytic viruses like Vaccinia virus selectively infect and replicate within tumor cells, leading to direct cell lysis (oncolysis) and the release of tumor-associated antigens and cytokines (e.g., GM-CSF), which stimulate a systemic anti-tumor immune response (PMID: 21451545).

03

Biological functions

Viral replicationOncolysisImmune response inductionCell deathOther
04

Disease associations

CancerHepatocellular carcinomaMelanomaSolid tumors
05

Safety considerations

Flu-like symptomsViral sheddingNeutralizing antibody formationOff-target infection in immunocompromised patientsInjection site reactions
06

Interacting drugs

Pexastimogene devacirepvec (Pexa-Vec)

3 more in the full profile.

07

Biomarkers

Thymidine kinase (TK) expressionEpidermal growth factor receptor (EGFR) expressionType I interferon (IFN) pathway deficiencyRas pathway activation

Beyond the preview

Go deeper on Vaccinia virus-sensitive tumor cells.

Explore the evidence, development activity, and competitive landscape with Gosset’s full data platform.

Drug pipeline

Full profile access

Explore the programs pursuing this target and their development progress.

  • Drug candidates
  • Developers
  • Development stage

Clinical trials

Full profile access

Follow the clinical studies evaluating therapies directed at this target.

  • Trial design
  • Status
  • Readouts

Competitive landscape

Full profile access

Compare approaches across drug candidates, modalities, and indications.

  • Programs
  • Modalities
  • Indications

Literature & evidence

Full profile access

Investigate the research and source evidence behind target biology and development.

  • Publications
  • Sources
  • Analysis

Patents

Full profile access

Explore patent activity around therapies and technologies addressing this target.

  • Patents
  • Assignees
  • Technologies

Research & analysis

Full profile access

Connect target biology, drug development, and emerging evidence in your research.

  • Biology
  • Development news
  • Analysis

Bring the full picture into focus.

See how Gosset can support your research on Vaccinia virus-sensitive tumor cells.

Explore the full profile

Gosset Free

Get started with Gosset.

Enter your work email and we’ll be in touch with next steps.

Work email preferred.

Book a call