id	author	title	date	pages	extension	mime	words	sentences	flesch	summary	cache	txt
cord-334624-chnibsa1	Hayn, Manuel	Imperfect innate immune antagonism renders SARS-CoV-2 vulnerable towards IFN-γ and -λ	2020-10-30		.txt	text/plain	5355	432	57	Here, we systematically assessed the impact of 29 SARS-CoV-2 proteins on viral sensing, type I, II and III interferon (IFN) signaling, autophagy and inflammasome formation. Our results identify ineffective type I and II antagonism as weakness of SARS-CoV-2 that may allow to devise safe and effective anti-viral therapies based on targeted innate immune activation. SARS-CoV-1 ORF6 is about 4-fold less potent in antagonizing type I IFN signaling (Fig. 243 4b) but induces higher levels of autophagy (Fig. 4c) . Examination of the functional conservation showed that SARS-CoV-2 Nsp15 was less 319 efficient in blocking innate immune activation, both type I IFN induction and signaling, than SARS-320 Hepatitis C virus viruses to block anti-viral autophagic turnover 50 and thus may represent a common studies will see more mechanistic data to explain the molecular details of the impact of SARS-CoV-2 343 proteins on innate immune activation.	./cache/cord-334624-chnibsa1.txt	./txt/cord-334624-chnibsa1.txt