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10.1016/j.jgar.2021.06.005 http://scihub22266oqcxt.onion/10.1016/j.jgar.2021.06.005 34273592!8279933!34273592     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Glob+Antimicrob+Resist 2021 ; 26 (ä): 239-240 Nephropedia Template TP {{tp|p=34273592|t=2021. Loss-of-function mutations in IFNAR2 in COVID-19 severe infection susceptibility |pdf=|usr=}}{{34273592}} gab.com Text Loss-of-function mutations in IFNAR2 in COVID-19 severe infection susceptibility JO: J Glob Antimicrob Resist http://www.kidney.de/pget.php?&tw=1&pmid=34273592 #FOAvip Recent COVID-19 (coronavirus disease 2019) host genetics studies suggest enrichment of mutations in genes involved in the regulation of type I and type III interferon (IFN) immunity in patients with severe COVID-19 infection. We performed whole-genome sequencing analysis of samples obtained from patients participating in the ongoing ODYSSEY phase 3 study of hospitalised patients with severe COVID-19 infection receiving supplemental oxygen support. We focused on burden testing of categories of rare and common loss-of-function (LOF) variants in all of the IFN pathway genes, specifically with MAF < 0.1% and MAF < 1%. In a model including LOF and missense variants (MAF < 1%), we report a significant signal in both INFAR1 and IFNAR2. We report carriers of rare variants in our COVID-19 cohort, including a stop-gain IFNAR2 (NM_000874:exon9:c.C966A:p.Y322X) amongst carriers of several other IFNAR rare nonsynonymous variants. Furthermore, we report an increased allelic frequency of common IFNAR2 variants in our data, reported also by the COVID-19 Host Genetics Initiative. Twit Text FOAVip Loss-of-function mutations in IFNAR2 in COVID-19 severe infection susceptibility ????J Glob Antimicrob Resist http://www.kidney.de/pget.php?&tw=1&pmid=34273592 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34273592 #FOAvip English Wikipedia <ref>{{Cite pmid|34273592}}</ref> Loss-of-function mutations in IFNAR2 in COVID-19 severe infection susceptibility #MMPMID34273592 Smieszek SP; Polymeropoulos VM; Xiao C; Polymeropoulos CM; Polymeropoulos MH J Glob Antimicrob Resist 2021[Sep]; 26 (ä): 239-240 PMID34273592show ga Recent COVID-19 (coronavirus disease 2019) host genetics studies suggest enrichment of mutations in genes involved in the regulation of type I and type III interferon (IFN) immunity in patients with severe COVID-19 infection. We performed whole-genome sequencing analysis of samples obtained from patients participating in the ongoing ODYSSEY phase 3 study of hospitalised patients with severe COVID-19 infection receiving supplemental oxygen support. We focused on burden testing of categories of rare and common loss-of-function (LOF) variants in all of the IFN pathway genes, specifically with MAF < 0.1% and MAF < 1%. In a model including LOF and missense variants (MAF < 1%), we report a significant signal in both INFAR1 and IFNAR2. We report carriers of rare variants in our COVID-19 cohort, including a stop-gain IFNAR2 (NM_000874:exon9:c.C966A:p.Y322X) amongst carriers of several other IFNAR rare nonsynonymous variants. Furthermore, we report an increased allelic frequency of common IFNAR2 variants in our data, reported also by the COVID-19 Host Genetics Initiative. |*COVID-19[MESH] |Gene Frequency[MESH] |Genetic Predisposition to Disease[MESH] |Humans[MESH] |Mutation[MESH] |Receptor, Interferon alpha-beta/genetics[MESH]Loss-of-function mutations in IFNAR2 in COVID-19 severe infection susc(epmc).pdf DeepDyve Pubget Overpricing