Tumor cells permissive for oncolytic Herpes Simplex Virus-1 replication

Tumor cells permissive for oncolytic Herpes Simplex Virus-1 (oHSV-1) replication are malignant cells that possess the necessary molecular machinery to support the entry, genome replication, and assembly of engineered HSV-1. Permissiveness is primarily determined by the high expression of viral entry receptors, such as Nectin-1 (CD111) and Herpesvirus Entry Mediator (HVEM), which are frequently upregulated in various solid tumors (Source: PubMed, PMID: 15501979). Furthermore, these cells often exhibit defects in innate antiviral defense pathways, specifically the Type I Interferon (IFN) response and the Protein Kinase R (PKR) pathway, which normally function to inhibit viral protein synthesis (Source: Nature Reviews Cancer, 2009). Oncolytic HSV-1 therapies, such as Talimogene laherparepvec (T-VEC), are designed to exploit these deficiencies, often through the deletion of the ICP34.5 gene to ensure selective replication within the tumor microenvironment while sparing healthy tissues. The interaction between the virus and permissive cells leads to direct oncolysis, releasing tumor-associated antigens and progeny virions that can infect neighboring cancer cells. This process not only destroys the primary tumor mass but also acts as an in situ vaccine, stimulating a systemic immune response against the cancer (Source: FDA, Imlygic Prescribing Information). Consequently, the degree of cellular permissiveness is a critical factor in determining the efficacy of oHSV-1-based virotherapies.

Other names

HSV-1 permissive cancer cellsoHSV-1 target cellsPermissive malignant cellsOncolytic HSV-1 permissive phenotype

Selective viral replication within cells with impaired antiviral signaling and high entry-receptor expression, leading to oncolysis and immune activation.