Measles virus infects both polarized epithelial and immune cells by using distinctive receptor-binding sites on its...

Area of Science:

• Virology
• Immunology
• Cell Biology

Background:

• Measles virus (MV) is a highly contagious pathogen causing significant childhood illness and death.
• Signaling lymphocyte activation molecule (SLAM), or CD150, is the known receptor for MV on immune cells, explaining its tropism and immunosuppressive effects.
• The mechanism of MV infection in epithelial cells, observed later in disease, remained unclear.

Purpose of the Study:

• To investigate the mechanism by which wild-type MV infects human polarized epithelial cells.
• To identify the viral and cellular factors involved in epithelial cell infection and viral release.
• To elucidate how MV achieves its dual tropism for both immune and epithelial cells.

Main Methods:

• Infection of human polarized epithelial cell lines with wild-type MV.
• Microscopic analysis to observe syncytia formation and viral particle release.
• Identification of specific amino acid residues on the MV attachment protein involved in epithelial cell interaction.

Main Results:

• Wild-type MV infects polarized epithelial cells independently of SLAM and CD46.
• Progeny viral particles are released exclusively from the apical surface of infected epithelial cells.
• Specific aromatic amino acid residues on the MV attachment protein likely mediate interaction with a putative epithelial cell receptor, distinct from SLAM/CD46 binding sites.

Conclusions:

• MV possesses distinct receptor-binding sites on its attachment protein for infecting both epithelial and immune cells.
• The ability to infect epithelial cells and release progeny virus apically likely contributes to MV's efficient aerosol transmission and high contagiousness.
• This study reveals a novel mechanism for MV epithelial cell entry and spread, broadening our understanding of measles pathogenesis.