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SARS-CoV-2 spike protein induces abnormal inflammatory blood clots neutralized by fibrin immunotherapy

Jae Kyu Ryu, Elif G Sozmen, Karuna Dixit

    Biorxiv : the Preprint Server for Biology
    |October 21, 2021
    PubMed

    Insights

    The SARS-CoV-2 Spike protein causes abnormal blood clots and inflammation. A new antibody targeting fibrin effectively neutralized this effect, offering potential COVID-19 treatment.

    Area of Science:

    • Immunology
    • Virology
    • Hematology

    Background:

    • Blood clots are a serious complication of COVID-19, leading to severe outcomes like pulmonary embolism and stroke.
    • The mechanisms behind abnormal clot formation in COVID-19, even in recovered patients, remain unclear.

    Approach:

    • Investigated the interaction between the SARS-CoV-2 Spike protein and fibrinogen, a key blood coagulation factor.
    • Examined the impact of Spike protein and virions on fibrin-mediated inflammation and lung pathology.
    • Analyzed fibrin autoantibodies in COVID-19 patients and tested a fibrin-targeting monoclonal antibody (5B8) for therapeutic potential.

    Key Points:

    • The SARS-CoV-2 Spike protein directly binds to fibrinogen, inducing structurally abnormal blood clots with increased proinflammatory activity.
    • SARS-CoV-2 Spike virions promote fibrin-mediated microglia activation and fibrinogen-dependent lung pathology.
    • COVID-19 patients exhibit persistent fibrin autoantibodies post-infection.
    • Monoclonal antibody 5B8, targeting a specific fibrin epitope, demonstrated inhibition of SARS-CoV-2-induced thromboinflammation.

    Conclusions:

    • The SARS-CoV-2 Spike protein plays a direct procoagulant role in COVID-19 pathogenesis.
    • Fibrin-targeting therapies represent a promising strategy for treating thromboinflammation associated with COVID-19.

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