Edmonston measles virus prevents increased cell surface expression of peptide-loaded major histocompatibility complex

Mamadi Yilla1, Carole Hickman, Marcia McGrew

  • 1Respiratory and Enteric Viruses Branch, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia 30333, USA. mby7@cdc.gov

Journal of Virology
|August 14, 2003
PubMed

Insights

Measles virus (MV) infection increases major histocompatibility complex (MHC) class I expression on monocytes but does not affect class II expression. MV interferes with peptide-loaded class II complexes, potentially altering T-cell responses.

Area of Science:

  • Immunology
  • Virology

Background:

  • Interferon-gamma (IFN-γ) upregulates MHC expression, while Interferon-alpha/beta (IFN-α/β) can suppress MHC class II. Measles virus (MV) is known to induce IFN-α/β and has been reported to upregulate MHC class II.
  • A paradox exists regarding MV's effect on MHC class II expression, as it induces IFN-α/β, which typically suppresses MHC class II.

Purpose of the Study:

  • To investigate the surface expression of MHC class I and class II proteins in MV-infected peripheral monocytes.
  • To resolve the apparent paradox of MV's influence on MHC class II expression in the presence and absence of IFN-α/β.

Main Methods:

  • Purified monocytes were infected with Edmonston B MV.
  • Surface expression of MHC class I (HLA-A, -B, -C) and class II (HLA-DR) proteins was analyzed.
  • IFN-α/β and IFN-γ levels in supernatant fluids were measured.
  • Monocytes were cocultured with peripheral blood mononuclear cell (PBMC) supernatant.

Main Results:

  • MV infection of monocytes increased cell surface expression of MHC class I proteins but had no effect on MHC class II expression.
  • MV-infected monocytes produced IFN-α/β, with no detectable IFN-γ.
  • MV infection of PBMCs also increased MHC class I expression, without affecting MHC class II expression.
  • MV suppressed class II protein expression independently of IFN-α/β presence.

Conclusions:

  • MV interferes with the expression of peptide-loaded MHC class II complexes on monocytes.
  • This interference may alter CD4(+) T-cell proliferation and regulate cell-mediated immune responses.
  • The findings suggest a mechanism by which MV modulates the host immune system beyond the known effects of IFN-α/β.

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