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Interaction between vaccinia virus and human blood platelets

T Bik, I Sarov, A Livne

    Blood
    |March 1, 1982
    PubMed
    Summary

    Vaccinia virus binds to human platelets and impairs their function, causing serotonin release and inhibiting aggregation, even without neuraminidase activity. This interaction highlights potential risks associated with viral infections affecting hemostasis.

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    Area of Science:

    • Virology
    • Hematology
    • Immunology

    Background:

    • Human platelets play crucial roles in hemostasis and immune responses.
    • Vaccinia virus is a large DNA virus with implications in infectious disease research.
    • Understanding virus-platelet interactions is vital for assessing disease pathogenesis.

    Purpose of the Study:

    • To characterize the binding of vaccinia virus to human platelets.
    • To investigate the impact of vaccinia virus on platelet functions.
    • To explore the mechanisms underlying vaccinia virus-platelet interactions.

    Main Methods:

    • Incubation of human platelets with 3H-thymidine-labeled vaccinia virus.
    • Analysis of viral binding parameters, including saturation, temperature, and metabolic effects.
    • Measurement of viral adsorption using formaldehyde-fixed platelets and assessment of ionic strength and enzymatic treatments.
    • Evaluation of platelet functions, including serotonin release and aggregation induced by various agonists.

    Main Results:

    • Vaccinia virus binds to platelets with saturation kinetics (approx. 5 particles/platelet).
    • Viral binding is temperature-dependent and sensitive to metabolic inhibitors, suggesting active processes.
    • Adsorption is influenced by ionic strength and reduced by neuraminidase/alkaline phosphatase treatment, indicating electrostatic and sialate/phosphate involvement.
    • Vaccinia virus induces significant serotonin release and inhibits platelet aggregation in response to ADP, collagen, and thrombin.

    Conclusions:

    • Vaccinia virus interacts with human platelets despite lacking neuraminidase activity.
    • The virus significantly impairs platelet functions, including serotonin release and aggregation.
    • Platelet surface sialate and phosphate residues are implicated in vaccinia virus binding.
    • These findings suggest potential hemostatic complications during vaccinia virus infections.

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