Measles vaccine strain entry receptors

The host cell entry receptors for the measles vaccine strain (primarily the Edmonston-derived strains) comprise three distinct cell surface proteins: Membrane cofactor protein (CD46), Signaling lymphocytic activation molecule family member 1 (SLAMF1/CD150), and Nectin-4 (PVRL4) (Nature, 2000; Nature, 2011). While wild-type measles virus (MeV) is restricted to using SLAMF1 on immune cells and Nectin-4 on epithelial cells, the vaccine strain has acquired the ability to utilize CD46, which is ubiquitously expressed on all nucleated human cells (Cell, 1993; PNAS, 1994). This expanded tropism allows the vaccine strain to be propagated in various laboratory cell lines, such as Vero cells, which lack SLAMF1 but express CD46 (Journal of Virology, 2001). These receptors interact with the viral hemagglutinin (H) protein, triggering the fusion (F) protein to mediate membrane fusion and viral entry (Trends in Microbiology, 2012). Beyond their role in infection, these receptors are significant targets in oncolytic virotherapy, where engineered measles viruses exploit the overexpression of CD46 or Nectin-4 in certain cancers to selectively infect and destroy tumor cells (Cancer Research, 2010). Additionally, Nectin-4 is a well-established target for antibody-drug conjugates like enfortumab vedotin in the treatment of urothelial carcinoma (PLOS Pathogens, 2011).

Other names

CD46SLAMF1Nectin-4Membrane cofactor proteinSignaling lymphocytic activation molecule family member 1Poliovirus receptor-related 4CD150PVRL4Measles virus receptors

The primary mechanism of action involves the interaction of the viral hemagglutinin (H) protein with these receptors to facilitate membrane fusion and viral entry. Therapeutic agents targeting these receptors act through various mechanisms, including antibody-drug conjugate (ADC) mediated delivery of cytotoxic agents (e.g., enfortumab vedotin), selective oncolytic viral infection and lysis of tumor cells, and induction of protective immunity via live-attenuated viral entry into immune cells.