Hermann Salmhofer

The current severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic has refocused scientific interest on gaining insight into the pathophysiology of systemic viral diseases. Complement activation has been characterized as a driver of endothelial injury and microvascular thrombosis in acute respiratory distress syndrome as well as hantavirus hemorrhagic fever with renal syndrome. On this occasion, we wish to report a case of severe hantavirus disease with coinciding SARS-CoV-2 infection mimicking thrombotic microangiopathy with rapid response of inflammatory markers, hematologic parameters and proteinuria to eculizumab. These findings support a disease model of virus-associated endothelial injury involving alternative pathway complement activation. Future studies are needed to explore whether end organ damage can be mitigated by complement inhibition in life-threatening viral disease.