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10.1016/j.trsl.2022.01.007 http://scihub22266oqcxt.onion/10.1016/j.trsl.2022.01.007 35114420!8802623!35114420     free     free     free Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Transl+Res 2022 ; 244 (ä): 47-55 Nephropedia Template TP {{tp|p=35114420|t=2022. Interferon pathway lupus risk alleles modulate risk of death from acute COVID-19 |pdf=|usr=}}{{35114420}} gab.com Text Interferon pathway lupus risk alleles modulate risk of death from acute COVID-19 JO: Transl Res http://www.kidney.de/pget.php?&tw=1&pmid=35114420 #FOAvip Type I interferon (IFN) is critical in our defense against viral infections. Increased type I IFN pathway activation is a genetic risk factor for systemic lupus erythematosus (SLE), and a number of common risk alleles contribute to the high IFN trait. We hypothesized that these common gain-of-function IFN pathway alleles may be associated with protection from mortality in acute COVID-19. We studied patients admitted with acute COVID-19 (756 European-American and 398 African-American ancestry). Ancestral backgrounds were analyzed separately, and mortality after acute COVID-19 was the primary outcome. In European-American ancestry, we found that a haplotype of interferon regulatory factor 5 (IRF5) and alleles of protein kinase cGMP-dependent 1 (PRKG1) were associated with mortality from COVID-19. Interestingly, these were much stronger risk factors in younger patients (OR = 29.2 for PRKG1 in ages 45-54). Variants in the IRF7 and IRF8 genes were associated with mortality from COVID-19 in African-American subjects, and these genetic effects were more pronounced in older subjects. Combining genetic information with blood biomarker data such as C-reactive protein, troponin, and D-dimer resulted in significantly improved predictive capacity, and in both ancestral backgrounds the risk genotypes were most relevant in those with positive biomarkers (OR for death between 14 and 111 in high risk genetic/biomarker groups). This study confirms the critical role of the IFN pathway in defense against COVID-19 and viral infections, and supports the idea that some common SLE risk alleles exert protective effects in antiviral immunity. Twit Text FOAVip Interferon pathway lupus risk alleles modulate risk of death from acute COVID-19 ????Transl Res http://www.kidney.de/pget.php?&tw=1&pmid=35114420 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=35114420 #FOAvip English Wikipedia <ref>{{Cite pmid|35114420}}</ref> Interferon pathway lupus risk alleles modulate risk of death from acute COVID-19 #MMPMID35114420 Nln I; Fernandez-Ruiz R; Muskardin TLW; Paredes JL; Blazer AD; Tuminello S; Attur M; Iturrate E; Petrilli CM; Abramson SB; Chakravarti A; Niewold TB Transl Res 2022[Jun]; 244 (ä): 47-55 PMID35114420show ga Type I interferon (IFN) is critical in our defense against viral infections. Increased type I IFN pathway activation is a genetic risk factor for systemic lupus erythematosus (SLE), and a number of common risk alleles contribute to the high IFN trait. We hypothesized that these common gain-of-function IFN pathway alleles may be associated with protection from mortality in acute COVID-19. We studied patients admitted with acute COVID-19 (756 European-American and 398 African-American ancestry). Ancestral backgrounds were analyzed separately, and mortality after acute COVID-19 was the primary outcome. In European-American ancestry, we found that a haplotype of interferon regulatory factor 5 (IRF5) and alleles of protein kinase cGMP-dependent 1 (PRKG1) were associated with mortality from COVID-19. Interestingly, these were much stronger risk factors in younger patients (OR = 29.2 for PRKG1 in ages 45-54). Variants in the IRF7 and IRF8 genes were associated with mortality from COVID-19 in African-American subjects, and these genetic effects were more pronounced in older subjects. Combining genetic information with blood biomarker data such as C-reactive protein, troponin, and D-dimer resulted in significantly improved predictive capacity, and in both ancestral backgrounds the risk genotypes were most relevant in those with positive biomarkers (OR for death between 14 and 111 in high risk genetic/biomarker groups). This study confirms the critical role of the IFN pathway in defense against COVID-19 and viral infections, and supports the idea that some common SLE risk alleles exert protective effects in antiviral immunity. |*COVID-19/genetics[MESH] |*Lupus Erythematosus, Systemic/genetics[MESH] |Aged[MESH] |Alleles[MESH] |Antiviral Agents[MESH] |Genetic Predisposition to Disease[MESH] |Humans[MESH] |Interferon Regulatory Factors/genetics/metabolism[MESH] |Interferon-alpha/genetics[MESH] |Middle Aged[MESH]Interferon pathway lupus risk alleles modulate risk of death from acut(epmc).pdf DeepDyve Pubget Overpricing