Tumor cells with defective innate antiviral responses

Tumor cells with defective innate antiviral responses represent a cellular phenotype characterized by the loss of functional Type I Interferon (IFN) signaling or other innate immune sensing pathways. This deficiency often arises as a trade-off during oncogenesis, where the suppression of antiviral pathways helps the tumor evade immune surveillance and resist growth-inhibitory signals (Stojdl et al., 2000, Genes & Dev). However, this lack of defense creates a therapeutic window for oncolytic virotherapy, as these cells cannot effectively restrict viral replication. Drugs such as oncolytic viruses selectively infect, replicate within, and destroy these defective cells while sparing healthy cells that possess intact antiviral machinery (Lichty et al., 2014, Nat Rev Cancer). This process not only causes direct tumor lysis but also releases tumor-associated antigens and danger signals, potentially converting a "cold" tumor into an "immunologically hot" one. Identifying specific defects in pathways like cGAS-STING or JAK-STAT is increasingly used as a biomarker strategy to predict sensitivity to these viral therapies (Xia et al., 2016, Nat Comm).

Other names

Interferon-deficient tumor cellsIFN-pathway defective cancer cellsOncolytic virus-sensitive tumor cellsType I IFN-deficient cancer cells

Selective viral replication and lysis of cells with impaired Type I Interferon (IFN) signaling pathways, leading to immunogenic cell death.