Cancer cells permissive to oncolytic Herpes Simplex Virus-1 replication (oHSV-1 permissive cancer cells)

Cancer cells permissive to oncolytic Herpes Simplex Virus-1 (oHSV-1) replication represent a specific physiological state of malignant cells that allows for the selective entry, replication, and spread of engineered HSV-1 vectors. This permissiveness is primarily driven by the overexpression of viral entry receptors such as Nectin-1 (CD111) or Herpesvirus entry mediator (HVEM), alongside defects in innate antiviral defense mechanisms common in neoplastic cells (Campadelli-Fiume et al., 2007; PMID: 17327401). In healthy cells, the Type I Interferon (IFN) pathway and Protein Kinase R (PKR) typically halt protein synthesis upon viral detection; however, many cancers suppress these pathways to facilitate rapid growth, inadvertently creating a niche for oHSV-1 replication (Mohl et al., 2019; PMID: 31137711). Therapeutic agents like Talimogene laherparepvec (T-VEC) exploit this environment to induce direct oncolysis and stimulate a systemic immune response against the tumor (Reid et al., 2016; PMID: 26787185). While the cell population itself is the therapeutic target in virotherapy, the term refers to a biological state rather than a single molecular entity. Understanding the factors that define permissiveness is crucial for patient selection and the development of next-generation oncolytic therapies.

Other names

HSV-1 permissive tumor cellsOncolytic HSV-1 targetsPermissive cancer cellsoHSV-1 susceptible neoplastic cells

Selective replication within neoplastic cells leading to direct cell lysis (oncolysis) and the release of tumor-derived antigens and cytokines (e.g., GM-CSF), which stimulates a systemic anti-tumor immune response.