id	author	title	date	pages	extension	mime	words	sentences	flesch	summary	cache	txt
cord-297323-l3f12hg4	Amor, Sandra	Innate immunity during SARS‐CoV‐2: evasion strategies and activation trigger hypoxia and vascular damage	2020-09-26		.txt	text/plain	4982	304	43	Like many viruses, SARS‐CoV‐2 has evolved strategies to circumvent innate immune detection including low CpG levels in the genome, glycosylation to shield essential elements including the receptor binding domain, RNA shielding and generation of viral proteins that actively impede anti‐viral interferon responses. These subsequently induce expression of type I IFNs (IFNα/β) and interferon stimulated genes (ISGs) [figure 2] many of which have potent antiviral activities, as well as other proinflammatory mediators e.g. cytokines, chemokines and antimicrobial peptides that are essential to initiate the host innate and adaptive immune response. Likewise, viral load, obesity, gender, race, blood groups and comorbidities have all been reported to influence the response to SARS-CoV-2 infection, [ Table 4 ; (101) (102) (103) (104) (105) (106) (107) (108) (109) (110) (111) (112) ] although few studies have fully examined the extent to which subversion and activation of innate immune components contribute to susceptibility in these cases. Toll-Like Receptor 3 Signaling via TRIF Contributes to a Protective Innate Immune Response to Severe Acute Respiratory Syndrome Coronavirus Infection	./cache/cord-297323-l3f12hg4.txt	./txt/cord-297323-l3f12hg4.txt