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Host involvement in vaccinia virus replication.

V Zaslavsky, P H Hofschneider

    Intervirology
    |January 1, 1986
    PubMed
    Summary
    This summary is machine-generated.

    Nutrient deprivation inhibits vaccinia virus replication by altering host cell functions essential for early viral events. Restoring nutrient levels restores viral propagation, suggesting a host factor is involved.

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    Area of Science:

    • Virology
    • Cell Biology
    • Molecular Biology

    Background:

    • Host cell conditions significantly influence viral replication.
    • Nutrient availability is a critical factor in cellular processes.
    • Understanding host-virus interactions is key to controlling viral infections.

    Purpose of the Study:

    • To investigate the impact of nutrient depletion on vaccinia virus permissiveness.
    • To identify specific early vaccinia virus-induced events affected by nutrient status.
    • To explore the role of host factors in supporting vaccinia virus replication.

    Main Methods:

    • Culturing uninfected cell monolayers under nutrient-depleted and normal conditions.
    • Infecting cells with vaccinia virus and mengovirus to assess viral propagation.

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  • Analyzing host cell responses, including DNA synthesis-independent events and viral DNA sensitivity.

    • Main Results:

    • Nutrient-depleted cells became nonpermissive for vaccinia virus but supported mengovirus.
    • Inhibited cells supported DNA synthesis-independent early events (thymidine kinase synthesis) but not others (DNA polymerase induction, DNase sensitivity).
    • Reversal of nutrient depletion restored vaccinia virus propagation.

    Conclusions:

    • Nutrient depletion imposes an inhibited state in host cells, selectively blocking vaccinia virus replication.
    • Specific early events of vaccinia virus infection, dependent on host factors, are impaired under nutrient-depleted conditions.
    • The findings suggest a crucial role for host factors in the induction of early vaccinia virus-induced events.