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Complement deposition on endothelial cells and high blood C5a serum levels have been reported in COVID\u201019 patients with severe illness, suggesting vigorous complement activation leading to systemic thrombotic microangiopathy (TMA). Complement regulator gene variants prevalent in African\u2010Americans have been associated with a higher risk for severe TMA and multi\u2010organ injury. Strikingly, severe acute respiratory syndrome Coronavirus 2 (SARS\u2010CoV\u20102)\u2010infected African\u2010Americans suffer from high mortality. These findings allow us to apply our knowledge from other complement\u2010mediated diseases to COVID\u201019 infection to better understand severe disease pathogenesis. Here, we discuss the multiple aspects of complement activation, regulation, crosstalk with other parts of the immune system, and the options to target complement in COVID\u201019 patients to halt disease progression and death.<\/jats:p><\/jats:sec><jats:sec><jats:title>Linked Articles<\/jats:title><jats:p>This article is part of a themed issue on Canonical and non\u2010canonical functions of the complement system in health and disease. 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