Induction of intercellular adhesion molecule 1 gene expression by measles virus in human umbilical vein endothelial

B H Harcourt1, P A Rota, K B Hummel

  • 1Winship Cancer Center, Emory University, Atlanta, Georgia 30322, USA.

Insights

Measles virus (MV) strains differ in their ability to induce intercellular adhesion molecule 1 (ICAM-1) expression. The Moraten strain effectively induces ICAM-1 via NF-kappaB activation, unlike other strains.

Area of Science:

  • Immunology
  • Virology
  • Cell Biology

Background:

  • Endothelial intercellular adhesion molecule 1 (ICAM-1) is crucial for leukocyte adhesion and migration.
  • Measles virus (MV) infection can modulate endothelial cell function.

Purpose of the Study:

  • To investigate strain-specific differences in measles virus-induced ICAM-1 expression in endothelial cells.
  • To elucidate the mechanisms underlying these strain-specific effects.

Main Methods:

  • Comparing ICAM-1 mRNA and protein expression induced by different MV vaccine strains (Moraten, CAM-70) and wild-type (Edmonston).
  • Assessing MV infectivity and de novo protein expression.
  • Analyzing the association between MV proteins and ICAM-1 induction.
  • Evaluating NF-kappaB activation in response to MV strains.

Main Results:

  • The Moraten MV strain rapidly induced high levels of ICAM-1, while CAM-70 and Edmonston strains were less effective.
  • Strain-specific differences were not due to variations in endothelial cell infection rates or de novo protein synthesis.
  • ICAM-1 induction correlated with NF-kappaB activation, suggesting a strain-specific activation mechanism.
  • No direct association was found between MV nucleocapsid or hemagglutinin protein expression and ICAM-1 induction.

Conclusions:

  • Measles virus strains exhibit distinct capabilities in inducing ICAM-1 expression in endothelial cells.
  • The Moraten strain's potent induction of ICAM-1 is linked to its ability to activate NF-kappaB.
  • A preexisting component within MV particles likely mediates strain-specific NF-kappaB activation and subsequent ICAM-1 gene expression.