AI Article Synopsis
- The study examined how proteins from the influenza virus, specifically hemagglutinin, neuraminidase, nucleoprotein, and membrane protein, affect blood clotting in both lab settings and living organisms.
- Results showed that hemagglutinin and neuraminidase enhance plasma's ability to break down clots and prevent blood clotting, while the membrane protein has the opposite effect, increasing clotting and inhibiting breakdown.
- The combined effects of hemagglutinin and neuraminidase together amplify their individual abilities, while hemagglutinin combined with the membrane protein also increases clot breakdown but not as significantly as hemagglutinin alone.
Article Abstract
We studied the effect of influenza virus proteins--hemagglutinin, neuraminidase, nucleoprotein, and membrane protein--on hemostasis in vitro and in vivo. The obtained data demonstrated that the envelope proteins hemagglutinin and neuraminidase increased the plasma fibrinolytic and anticoagulant activities and the activity of human tissue plasminogen activator. Among the core proteins of influenza virus, membrane protein proved to have the highest activity; in contrast to hemagglutinin and neuraminidase, it inhibited fibrinolysis, increased the coagulation activity of the plasma, and decreased the activity of human tissue plasminogen activator. Combined action of hemagglutinin and neuraminidase increased the plasma fibrinolytic and anticoagulant activities exceeding their individual effects. Combined action of an envelope protein hemagglutinin and membrane protein also increased the plasma fibrinolytic and anticoagulant activities although to a lesser extent as compared to hemagglutinin alone. The obtained data indicate that the viral proteins are physiologically active and can induce hemostatic changes specific for influenza.
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