TY - JOUR T1 - Plasma ACE2 activity is persistently elevated following SARS-CoV-2 infection: implications for COVID-19 pathogenesis and consequences JF - European Respiratory Journal JO - Eur Respir J DO - 10.1183/13993003.03730-2020 VL - 57 IS - 5 SP - 2003730 AU - Sheila K. Patel AU - Jennifer A. Juno AU - Wen Shi Lee AU - Kathleen M. Wragg AU - P. Mark Hogarth AU - Stephen J. Kent AU - Louise M. Burrell Y1 - 2021/05/01 UR - http://erj.ersjournals.com/content/57/5/2003730.abstract N2 - Coronavirus disease 2019 (COVID-19) causes persistent endothelial inflammation, lung, cardiovascular, kidney and neurological complications, and thromboembolic phenomena of unclear pathogenesis [1]. Severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) utilises the catalytic site of full-length membrane-bound angiotensin converting enzyme 2 (ACE2) for host cell entry [2], which is thought to downregulate membrane-bound ACE2, and thus contribute to ongoing inflammation due to loss of a degradative pathway for angiotensin II. In healthy individuals, ACE2 exists primarily in its membrane-bound form with very low levels of the catalytically active ectodomain of ACE2 present in the circulation [3]. However, in patients with cardiovascular disease, there is increased “shedding” of ACE2, and higher circulating levels are associated with downregulation of membrane-bound ACE2 [4].Plasma ACE2 activity is persistently elevated in patients after COVID-19 infection. Larger studies are needed to determine if this identifies people at risk of prolonged illness following COVID-19. https://bit.ly/2XQlrYFWe thank the generous participation of the study subjects for providing samples. We thank Adam Wheatley, Jane Batten and Helen Kent for help with the COVID-19 cohort, and Ping Huang and Thomas McConville for assistance with the ACE2 activity assays. ER -