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Experimental measles encephalitis: a genetic analysis.

M V Haspel, R Duff, F Rapp

    Infection and Immunity
    |October 1, 1975
    PubMed
    Summary
    This summary is machine-generated.

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    Researchers studied temperature-sensitive measles virus mutants in hamsters to assess their potential to cause encephalitis. Most mutants were attenuated, but two remained virulent, and one caused hydrocephalus, offering insights into measles virus pathogenesis.

    Area of Science:

    • Virology
    • Neuroscience
    • Immunology

    Background:

    • Measles virus can cause acute encephalitis.
    • Temperature-sensitive (ts) mutants offer a tool to study viral pathogenesis.
    • Understanding measles virus attenuation is crucial for vaccine development.

    Purpose of the Study:

    • To evaluate the encephalitogenic potential of nine temperature-sensitive (ts) measles virus mutants in vivo.
    • To characterize the virulence and genetic properties of these ts mutants.
    • To elucidate the mechanism of measles virus attenuation.

    Main Methods:

    • Newborn golden Syrian hamsters were inoculated with parental measles virus and nine ts mutants.
    • Clinical signs of encephalitis and hydrocephalus were monitored.

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  • Complementation analysis was performed to group the ts mutants based on genetic defects.

    • Main Results:

    • The parental measles virus induced acute encephalitis in hamsters.
    • Six of the nine ts mutants showed attenuation of virulence.
    • Two ts mutants remained virulent, and one induced hydrocephalus; these belonged to distinct complementation groups.

    Conclusions:

    • Temperature-sensitive measles virus mutants exhibit varying degrees of neurovirulence.
    • Attenuation in these mutants is likely due to partial defectiveness under permissive conditions, not solely temperature-induced replication inhibition.
    • Genetic characterization of ts mutants provides insights into measles virus replication and pathogenesis, aiding in the development of safer vaccines.