id	author	title	date	pages	extension	mime	words	sentences	flesch	summary	cache	txt
cord-287487-qeltdch7	Graepel, Kevin W.	Proofreading-Deficient Coronaviruses Adapt for Increased Fitness over Long-Term Passage without Reversion of Exoribonuclease-Inactivating Mutations	2017-11-07		.txt	text/plain	7470	467	49	Alanine substitution of ExoN catalytic residues [ExoN(-)] in severe acute respiratory syndrome-associated coronavirus (SARS-CoV) and murine hepatitis virus (MHV) disrupts ExoN activity, yielding viable mutant viruses with defective replication, up to 20-fold-decreased fidelity, and increased susceptibility to nucleoside analogues. High-or low-fidelity variants are described for many RNA viruses infecting animals, including the coronaviruses (CoVs) murine hepatitis virus (MHV-A59) and severe acute respiratory syndrome-associated coronavirus (SARS-CoV) (13) (14) (15) (16) (17) , as well as foot-and-mouth disease virus (18) (19) (20) (21) (22) , poliovirus (23) (24) (25) (26) (27) (28) (29) , Chikungunya virus (30, 31) , influenza virus (32) , coxsackievirus B3 (33, 34) , and human enterovirus 71 (35) (36) (37) . The evolved mutations in MHV-ExoN(-) nsp14 and nsp12, which encodes the RdRp, accounted for only part of the increased nucleoside analogue resistance of MHV-ExoN(-) P250, implicating multiple replicase proteins in adaptation for viral fitness.	./cache/cord-287487-qeltdch7.txt	./txt/cord-287487-qeltdch7.txt