Adaptation of wild-type measles virus to tissue culture

Diane Waku Kouomou1, T Fabian Wild

  • 1INSERM U 404, CERVI, 69365 Lyon Cedex 07, France.

Journal of Virology
|January 5, 2002
PubMed

Insights

Measles virus (MV) adapted to Vero cells expressed viral glycoproteins but failed to bind CD46. Introducing human SLAM restored fusion, indicating SLAM

Area of Science:

  • Virology
  • Immunology
  • Cell Biology

Background:

  • Measles virus (MV) primarily infects humans and captive monkeys.
  • Cellular receptors CD46 and CD150 (SLAM) are known entry points for MV.
  • MV isolates require adaptation for efficient replication in non-B-cell lines.

Purpose of the Study:

  • To investigate the properties of a wild-type MV strain adapted to Vero epithelial cells.
  • To determine the interaction of the adapted MV with cellular receptors CD46 and SLAM.
  • To understand the role of viral glycoproteins in MV infection and cell fusion.

Main Methods:

  • Adaptation of a wild-type MV strain to Vero cells.
  • Analysis of viral glycoprotein expression (hemagglutinin and fusion protein) post-adaptation.
  • Assessment of MV-induced cell fusion (syncytia formation).
  • Investigation of MV interaction with CD46 and SLAM using various experimental approaches.

Main Results:

  • Vero-adapted MV expressed high levels of hemagglutinin and fusion proteins but did not induce syncytia.
  • No amino acid sequence changes were detected in the viral glycoproteins of the adapted strain.
  • The Vero-adapted MV showed no interaction with CD46 during infection.
  • Expression of human SLAM in Vero cells led to rapid syncytia formation and reduced infectious virus yield.

Conclusions:

  • MV adaptation to Vero cells alters its interaction with cellular receptors.
  • CD46 is not essential for the entry or infection of this Vero-adapted MV strain.
  • SLAM plays a critical role in mediating MV-induced cell fusion and infectivity, even in the presence of viral glycoproteins.

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