id	author	title	date	pages	extension	mime	words	sentences	flesch	summary	cache	txt
cord-032811-sdbj26ca	Hosoki, Koa	Reply	2020-09-29		.txt	text/plain	666	50	52	They suggest that suppression of angiotensin-converting enzyme-2 (ACE-2) by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) could impair the hydrolysis of des-Arg 9 -bradykinin and stimulate the bradykinin receptor type 1 (BKB1) pathway to induce leakage of fluid into the lungs. 4 However, other studies suggest that SARS-CoV-2 may upregulate the expression of ACE-2 in patients with coronavirus disease 2019 (COVID-19) or influenza pneumonia in alveolar epithelial cells, endothelial cells, and lymphocytes in perivascular tissue than in uninfected control autopsy lung. 7 We favor a third hypothesis, where excessive and prolonged secretion of type I and type III IFNs in the airways contributes to loss of lung epithelial barrier function during COVID-19 and other RNA virus infections (Fig 1, A) . Because IFN-l contributes to loss of lung epithelial barrier function, 8 we hypothesize that entry of SARS-CoV-2 via ACE-2 can stimulate secretion of IFN-l and induce leakage of fluid into the lungs (Fig 1, A) .	./cache/cord-032811-sdbj26ca.txt	./txt/cord-032811-sdbj26ca.txt