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Measles virus and CD46
1Division of Rheumatology, St. Louis, MO 63110, USA.
Abstract:
Measles virus (MV) was isolated in 1954 (Enders and Peeble 1954). It is among the most contagious of viruses and a leading cause of mortality in children in developing countries (Murray and Lopez 1997; Griffin 2001; Bryce et al. 2005). Despite intense research over decades on the biology and pathogenesis of the virus and the successful development in 1963 of an effective MV vaccine (Cutts and Markowitz 1994), cell entry receptor(s) for MV remained unidentified until 1993. Two independent studies showed that transfection of nonsusceptible rodent cells with human CD46 renders these cells permissive to infection with the Edmonston and Halle vaccine strains of measles virus (Dorig et al. 1993; Naniche et al. 1993). A key finding in these investigations was that MV binding and infection was inhibited by monoclonal and polyclonal antibodies to CD46. These reports established CD46 as a MV cell entry receptor. This chapter summarizes the role of CD46 in measles virus infection.
Insights
Measles virus cell entry was identified in 1993, revealing CD46 as the primary receptor. This discovery significantly advanced understanding of measles pathogenesis and vaccine development.
Area of Science:
- Virology
- Immunology
- Cell Biology
Background:
- Measles virus (MV) is highly contagious and a major cause of childhood mortality.
- Despite decades of research and vaccine development, MV cell entry mechanisms remained unclear until the 1990s.
Purpose of the Study:
- To identify the cell entry receptor(s) for measles virus.
- To elucidate the role of identified receptors in MV infection and pathogenesis.
Main Methods:
- Transfection of nonsusceptible rodent cells with human CD46.
- Infection assays using Edmonston and Halle MV vaccine strains.
- Inhibition assays using monoclonal and polyclonal antibodies against CD46.
Main Results:
- Transfection with human CD46 rendered rodent cells susceptible to MV infection.
- Antibodies targeting CD46 effectively inhibited MV binding and infection.
- These findings established CD46 as a functional MV cell entry receptor.
Conclusions:
- CD46 acts as a critical cell entry receptor for measles virus.
- Understanding the CD46-MV interaction is key for measles pathogenesis and therapeutic strategies.
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