Immunosuppression caused by measles virus: role of viral proteins

Yann M Kerdiles1, Caroline I Sellin, Johan Druelle

  • 1INSERM U404, IFR 128, Biosciences Lyon-Gerland, 21 Ave. Tony Garnier, 69365 Lyon, France.

Insights

Measles virus (MV) proteins cause profound immunosuppression, increasing susceptibility to secondary infections and child mortality. This review details how MV proteins interact with cellular targets to induce immune abnormalities.

Area of Science:

  • Immunology
  • Virology
  • Molecular Biology

Background:

  • Measles virus (MV) infection leads to significant immunosuppression, increasing the risk of opportunistic infections.
  • These secondary infections are a primary cause of measles-related child mortality globally.
  • MV-induced immune dysfunction includes impaired cell functions and altered cytokine signaling.

Purpose of the Study:

  • To review novel functions of MV proteins contributing to measles-induced immunosuppression.
  • To highlight recent advances in understanding MV protein interactions with cellular targets.
  • To emphasize the role of specific cell membrane receptors in measles pathogenesis.

Main Methods:

  • Literature review focusing on MV proteins and their immunomodulatory effects.
  • Analysis of interactions between MV proteins and cellular receptors (CD46, CD150, TLR2, FcgammaRII).
  • Synthesis of current knowledge on MV-induced immunological abnormalities.

Main Results:

  • Several MV proteins (hemagglutinin, fusion, nucleoprotein, V, C) are implicated in immune suppression.
  • MV proteins interact with key cellular receptors like CD46, CD150, TLR2, and FcgammaRII.
  • These interactions lead to diverse immunological abnormalities, contributing to disease severity.

Conclusions:

  • MV proteins play a critical role in inducing measles-associated immunosuppression.
  • Understanding these protein-receptor interactions offers insights into measles pathogenesis.
  • Targeting these interactions may present future therapeutic strategies against measles complications.

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