Abstract
COVID-19 is associated with an increased risk of thrombotic events. However, the pathogenesis of these complications is unclear and reports on platelet infection and activation by the virus are conflicting. Here, we integrated single-cell transcriptomic data to elucidate whether platelet activation is a specific response to SARS-CoV-2 infection or a consequence of a generalized inflammatory state. Although platelets from patients infected with SARS-CoV-2 over expressed genes involved in activation and aggregation when compared to healthy controls; those differences disappeared when the comparison was made with patients with generalized inflammatory conditions of other etiology than COVID-19. The membrane receptor for the virus, ACE-2, was not expressed by infected or control platelets. Our results suggest that platelet activation in patients with severe COVID-19 is mainly a consequence of a systemic inflammatory state than direct invasion and activation.
【초록키워드】 COVID-19, platelet activation, Pathogenesis, severe COVID-19, SARS-COV-2 infection, Infection, Platelets, virus, ACE-2, Patient, Platelet, Complication, membrane, transcriptomic data, receptor, etiology, Thrombotic events, single-cell, Invasion, inflammatory state, Activation, increased risk, thrombotic, aggregation, healthy controls, expressed genes, inflammatory condition, systemic inflammatory, involved, expressed, expressed gene, healthy controls;, infected with SARS-CoV-2, 【제목키워드】 COVID-19 disease, Platelet, transcriptomic data, Analysis, reveal,