Measles virus entry receptors (CD46, SLAMF1, Nectin-4) (MV receptors)

The target refers to a therapeutic strategy in oncolytic virotherapy where measles virus (MV) strains are used to selectively destroy cancer cells. This selectivity is achieved through two primary mechanisms: the overexpression of MV entry receptors on tumor cells and the presence of innate immunity defects within those cells. The primary receptors involved are CD46 (membrane cofactor protein), which is frequently upregulated in various cancers to evade complement-mediated lysis, and Nectin-4 (PVRL4), an adhesion molecule overexpressed in epithelial tumors such as breast and lung cancer (Source: Mühlebach et al., 2011). Additionally, many tumor cells possess impaired Type I Interferon (IFN) signaling pathways, which normally function to inhibit viral replication (Source: Stojdl et al., 2000). By exploiting these vulnerabilities, oncolytic measles viruses can specifically enter, replicate within, and lyse tumor cells while sparing healthy tissue. This process not only causes direct tumor debulking but also promotes an immunologically hot tumor microenvironment by releasing danger signals and tumor antigens (Source: Russell et al., 2014).

Other names

CD46SLAMF1Nectin-4Membrane cofactor proteinSignaling lymphocytic activation moleculePoliovirus receptor-related 4PVRL4CD150MCP

Oncolytic measles virus strains selectively infect tumor cells by binding to overexpressed receptors such as CD46 or Nectin-4. Once inside, the virus exploits defects in the host cell's innate antiviral signaling, such as impaired Type I Interferon (IFN) responses, to replicate preferentially in malignant cells. This replication leads to direct cell lysis (oncolysis) and the induction of a systemic anti-tumor immune response through the release of tumor antigens and inflammatory cytokines (Source: Russell et al., 2014; Nature Reviews Cancer, 2018).