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Cell surface activation of the alternative complement pathway by the fusion protein of measles virus

Patricia Devaux1, Dale Christiansen1, Sébastien Plumet1

  • 1Immunité & Infections Virales, CNRS-UCBL UMR 5537, IFR 62 Laennec, Rue Paradin, 69372 Lyon Cedex 08, France.

The Journal of General Virology
|May 29, 2004
PubMed

Insights

Measles virus (MV)-infected cells activate the alternative complement pathway, coating cells and the virus with C3b. This enhances immune targeting of measles antigens via complement receptors.

Area of Science:

  • Immunology
  • Virology

Background:

  • Measles virus (MV) infection can trigger immune responses.
  • The alternative complement pathway plays a role in innate immunity.

Purpose of the Study:

  • To investigate how measles virus infection activates the alternative complement pathway.
  • To determine the role of viral proteins and cellular receptors in this activation.

Main Methods:

  • Assessing complement activation on MV-infected cells and MV particles.
  • Analyzing the involvement of viral fusion (F) protein and complement regulators (CD46, CD55).

Main Results:

  • MV-infected cells and the virus itself activate the alternative complement pathway, leading to C3b deposition.
  • MV fusion (F) protein expression on cell surfaces drives complement activation.
  • C3b/C3bi coating of infected cells and virus enhances immune targeting.

Conclusions:

  • Measles virus infection activates the alternative complement pathway independently of CD46.
  • The fusion protein is a key viral component in initiating complement activation.
  • Complement opsonization of measles virus promotes immune system targeting.

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