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Measles virus-induced immunosuppression in vitro is associated with deregulation of G1 cell cycle control proteins

O Engelking, L M Fedorov, R Lilischkis

    The Journal of General Virology
    |July 28, 1999
    PubMed

    Insights

    Measles virus (MV) glycoproteins impair T-cell proliferation by causing cell cycle cessation, not apoptosis. This immune suppression involves deregulation of cell cycle genes crucial for the G1/S phase transition in peripheral blood lymphocytes (PBL).

    Area of Science:

    • Immunology
    • Virology
    • Cell Biology

    Background:

    • Virus-induced immunosuppression significantly contributes to measles morbidity and mortality.
    • Measles virus (MV) glycoproteins F and H impair peripheral blood lymphocyte (PBL) proliferation.
    • Previous studies indicated cell cycle arrest in G0/G1 phase, not apoptosis.

    Purpose of the Study:

    • To investigate the mechanism of MV-induced immunosuppression on PBL proliferation.
    • To determine if MV glycoproteins induce cell cycle arrest or cessation.
    • To elucidate the role of cell cycle regulatory proteins in MV-induced unresponsiveness.

    Main Methods:

    • Exposure of human PBL to UV-inactivated MV (UV-MV) or MV glycoproteins.
    • Analysis of PBL cell cycle progression using flow cytometry.
    • Assessment of cell cycle regulatory protein expression and kinase activity (e.g., p27, CDK4/6, cyclin D, CDK2, cyclin E).

    Main Results:

    • MV glycoprotein contact induced cell cycle cessation, not complete arrest, in PBL.
    • The p53 pathway was not significantly involved in this unresponsiveness.
    • Downregulation of p27 was delayed, and CDK4/6-cyclin D and CDK2-cyclin E activities were reduced.
    • Accumulation of CDK4, CDK6, cyclins D3 and E, and CDK2 proteins was impaired after mitogenic stimulation in the presence of UV-MV.

    Conclusions:

    • MV-induced proliferative unresponsiveness in PBL is linked to cell cycle cessation.
    • This unresponsiveness is characterized by deregulation of key cell cycle genes controlling the G1/S phase transition.
    • The findings provide insights into the molecular mechanisms of measles-induced immune evasion.

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