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10.1093/nar/gkac513 http://scihub22266oqcxt.onion/10.1093/nar/gkac513 35713540!9262603!35713540     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Nucleic+Acids+Res 2022 ; 50 (12): 6769-6785 Nephropedia Template TP {{tp|p=35713540|t=2022. Body temperature variation controls pre-mRNA processing and transcription of antiviral genes and SARS-CoV-2 replication |pdf=|usr=}}{{35713540}} gab.com Text Body temperature variation controls pre-mRNA processing and transcription of antiviral genes and SARS-CoV-2 replication JO: Nucleic Acids Res http://www.kidney.de/pget.php?&tw=1&pmid=35713540 #FOAvip Antiviral innate immunity represents the first defense against invading viruses and is key to control viral infections, including SARS-CoV-2. Body temperature is an omnipresent variable but was neglected when addressing host defense mechanisms and susceptibility to SARS-CoV-2 infection. Here, we show that increasing temperature in a 1.5 degrees C window, between 36.5 and 38 degrees C, strongly increases the expression of genes in two branches of antiviral immunity, nitric oxide production and type I interferon response. We show that alternative splicing coupled to nonsense-mediated decay decreases STAT2 expression in colder conditions and suggest that increased STAT2 expression at elevated temperature induces the expression of diverse antiviral genes and SARS-CoV-2 restriction factors. This cascade is activated in a remarkably narrow temperature range below febrile temperature, which reflects individual, circadian and age-dependent variation. We suggest that decreased body temperature with aging contributes to reduced expression of antiviral genes in older individuals. Using cell culture and in vivo models, we show that higher body temperature correlates with reduced SARS-CoV-2 replication, which may affect the different vulnerability of children versus seniors toward severe SARS-CoV-2 infection. Altogether, our data connect body temperature and pre-mRNA processing to provide new mechanistic insight into the regulation of antiviral innate immunity. Twit Text FOAVip Body temperature variation controls pre-mRNA processing and transcription of antiviral genes and SARS-CoV-2 replication ????Nucleic Acids Res http://www.kidney.de/pget.php?&tw=1&pmid=35713540 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=35713540 #FOAvip English Wikipedia <ref>{{Cite pmid|35713540}}</ref> Body temperature variation controls pre-mRNA processing and transcription of antiviral genes and SARS-CoV-2 replication #MMPMID35713540 Los B; Preussner M; Eschke K; Vidal RM; Abdelgawad A; Olofsson D; Keiper S; Paulo-Pedro M; Grindel A; Meinke S; Trimpert J; Heyd F Nucleic Acids Res 2022[Jul]; 50 (12): 6769-6785 PMID35713540show ga Antiviral innate immunity represents the first defense against invading viruses and is key to control viral infections, including SARS-CoV-2. Body temperature is an omnipresent variable but was neglected when addressing host defense mechanisms and susceptibility to SARS-CoV-2 infection. Here, we show that increasing temperature in a 1.5 degrees C window, between 36.5 and 38 degrees C, strongly increases the expression of genes in two branches of antiviral immunity, nitric oxide production and type I interferon response. We show that alternative splicing coupled to nonsense-mediated decay decreases STAT2 expression in colder conditions and suggest that increased STAT2 expression at elevated temperature induces the expression of diverse antiviral genes and SARS-CoV-2 restriction factors. This cascade is activated in a remarkably narrow temperature range below febrile temperature, which reflects individual, circadian and age-dependent variation. We suggest that decreased body temperature with aging contributes to reduced expression of antiviral genes in older individuals. Using cell culture and in vivo models, we show that higher body temperature correlates with reduced SARS-CoV-2 replication, which may affect the different vulnerability of children versus seniors toward severe SARS-CoV-2 infection. Altogether, our data connect body temperature and pre-mRNA processing to provide new mechanistic insight into the regulation of antiviral innate immunity. |*COVID-19/genetics[MESH] |*SARS-CoV-2/genetics[MESH] |Aged[MESH] |Antiviral Agents[MESH] |Body Temperature[MESH] |Child[MESH] |Humans[MESH]Body temperature variation controls pre-mRNA processing and transcript(epmc).pdf DeepDyve Pubget Overpricing