Activated Platelets Harbor SARS-CoV-2 during Severe COVID-19

Clinical SARS-CoV-2 infection (COVID-19) is characterised by a hyperinflammatory and procoagulant state that increases the risk of thrombosis and death. Despite thromboprophylaxis at least at the conventional doses, incidence as high as 31% has been reported for thrombotic complications in Intensive Care Unit (ICU) patients with COVID-19 infections. Still, it remains unclear how SARS-Cov-2 may initiate and or perpetuates the intractable thrombo-inflammatory states in COVID-19; and the need to understand the underlying mechanisms is urgent. In this image report, we utilised a state-of-the-art high-resolution 3D imaging approach to examine the interactions of SARS-CoV-2 with platelets, erythrocytes and leucocytes in blood samples obtained from COVID-19 patients in our ICU; and we visualised platelet procoagulant activity and the spatial localisation of SARS-CoV-2 in platelet-rich-plasma reconstituted to contain erythrocytes and leucocytes. Strikingly, we observed that activated platelets harboured SARS-Cov-2 during severe COVID-19 in our patient that eventually succumbed to the infection. SARS-Cov-2 internalisation into the cytosol was probably via a passive mechanism, as we have previously established that actin cytoskeleton remodelling and increased membrane permeability occurred during platelet transformation to the procoagulant phenotype. More work is needed to understand platelets' role in the recalcitrant thrombotic states of COVID-19.