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Speaker: Professor Edward Conway, Centre for Blood Research, University of British Columbia, Vancouver, Canada
Host: Julien Bergeron
Just over one year ago, the world was visited by a new betacoronavirus, SARS-CoV-2, named for its propensity to cause severe lung damage. But SARS-CoV-2 does more than that: It causes a multisystem disease (COVID-19) that involves multiple organs, and has a high risk of thrombosis, associated with striking elevations in pro-inflammatory cytokines, D-dimers and fibrinogen. Postmortem studies confirm the high incidence of thromboembolism, and reveal diffuse microvascular thrombi with endothelial swelling and deposition of complement activation fragments, consistent with a thrombotic microangiopathy (TMA). The presentation thus parallels that of other genetic disorders, such as atypical hemolytic uremic syndrome (aHUS), that are caused by heightened activation of complement. This raises the specter that the thrombotic complications arising from SARS-CoV-2 may be triggered and/or exacerbated by excess complement activation. Such a finding is potentially relevant, as currently available anti-complement therapies that are highly effective in protecting against thrombosis in aHUS could be efficacious in COVID-19. In this seminar, I will review the evidence for complement participating in the pathophysiology underlying the thrombotic diathesis associated with pathogenic coronaviruses, provide some mechanistic insights, and propose lines of study to identify novel therapeutic targets.