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Interaction of Ross River virus with the complement system.

J G Aaskov, U Hadding, D Bitter-Suermann

    The Journal of General Virology
    |January 1, 1985
    PubMed
    Summary
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    Ross River virus inhibits complement pathways without antibodies. It interferes with C3 cleavage by both classical and alternative pathways, not by disrupting key enzyme complexes.

    Area of Science:

    • Immunology
    • Virology
    • Biochemistry

    Background:

    • The complement system is crucial for innate immunity.
    • Ross River virus (RRV) is an important human pathogen.
    • Understanding RRV's interaction with the complement system is vital for disease control.

    Purpose of the Study:

    • To investigate the mechanism by which Ross River virus interacts with the complement system in the absence of specific antibodies.
    • To determine whether RRV activates or inhibits the classical and alternative complement pathways.
    • To identify the specific step in complement activation that RRV affects.

    Main Methods:

    • Complement activation assays were performed using purified complement components and RRV.
    • The cleavage of C3, Factor B, and Factor D was monitored.

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  • The integrity of complement convertases (C3bBb and C4b2a) was assessed.

    • Main Results:

    • In the absence of anti-RRV antibodies, RRV did not activate the classical or alternative complement pathways.
    • Instead, RRV significantly inhibited the cleavage of C3 by both pathways.
    • RRV's inhibitory effect was not due to the disruption of C3bBb complexes or inhibition of Factor B cleavage by Factor D.
    • RRV was found to directly interfere with the enzymatic activity of the alternative pathway C3 convertase (C3bBb) and the classical pathway C3 convertase (C4b2a).

    Conclusions:

    • Ross River virus actively inhibits the complement system.
    • The virus interferes with the C3 cleavage step mediated by both classical and alternative pathway C3 convertases.
    • This inhibition likely contributes to viral immune evasion and pathogenesis.