id	author	title	date	pages	extension	mime	words	sentences	flesch	summary	cache	txt
cord-343569-9th5bcv0	Fu, Yu-Zhi	SARS-CoV-2 membrane glycoprotein M antagonizes the MAVS-mediated innate antiviral response	2020-10-27		.txt	text/plain	3403	239	51	[28] [29] [30] To identify SARS-CoV-2 proteins that may inhibit the RLR-mediated induction of downstream antiviral genes, we constructed 17 SARS-CoV-2 protein expression clones and screened for candidates that inhibit the Sendai virus (SeV, an RNA virus)-induced activation of the IFNβ promoter in HEK293 cells by reporter assays (Fig. 1A) . In reporter assays, ectopic expression of the M protein dose-dependently inhibited the SeV-induced activation of We next performed ELISA experiments and found that the secretion of IFN-β and TNF-α following SeV infection or poly (I:C) transfection was also impaired in HEK293-M cells (Fig. 1G ). These results suggest that the M protein impairs the recruitment of TRAF3, TBK1 and IRF3 to the MAVS complex, leading to the inhibition of the innate antiviral response. In this study, we identified the SARS-CoV-2 M protein as a factor underlying the inhibition of host antiviral innate immunity by directly targeting the central adaptor MAVS in the RLR-mediated induction of type I IFNs. Several lines of evidence suggest that M directly targets MAVS to inhibit the innate immune response.	./cache/cord-343569-9th5bcv0.txt	./txt/cord-343569-9th5bcv0.txt