id	author	title	date	pages	extension	mime	words	sentences	flesch	summary	cache	txt
cord-271505-eot38721	Wang, Hongliang	Molecular pathogenesis of severe acute respiratory syndrome	2006-09-28		.txt	text/plain	4959	229	48	demonstrated that the angiotensin-converting enzyme 2 (ACE2) is a functional cellular receptor of SARS-CoV, by using coimmunoprecipitation of the virus glycoprotein (S1) with lysates from cells that are susceptible to virus infection (Vero E6 cells) followed by mass spectrometry analysis [7] . In the case of SARS, apoptosis was observed in patients' lung epithelial cells; thus, SARS-CoV induced apoptosis would certainly have a deleterious pathogenic role, leading to severe tissue damage [26] . This model system allowed us to avoid possible secondary effects resulting from viral replication or infections in vivo and to directly test whether SARS-CoV spike protein might adversely affect acute lung injury through modulation of ACE2. SARS-CoV infection or spike protein treatment can down-regulate the expression of ACE2, and thus aggravate lung injury. Nabel, pH-dependent entry of severe acute respiratory syndrome coronavirus is mediated by the spike glycoprotein and enhanced by dendritic cell transfer through DC-SIGN	./cache/cord-271505-eot38721.txt	./txt/cord-271505-eot38721.txt