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10.1371/journal.ppat.1008986 http://scihub22266oqcxt.onion/10.1371/journal.ppat.1008986 33064743!7592919!33064743     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       PLoS+Pathog 2020 ; 16 (10): e1008986 Nephropedia Template TP {{tp|p=33064743|t=2020. Qualitative Differences Between the IFNalpha subtypes and IFNbeta Influence Chronic Mucosal HIV-1 Pathogenesis |pdf=|usr=}}{{33064743}} gab.com Text Qualitative Differences Between the IFNalpha subtypes and IFNbeta Influence Chronic Mucosal HIV-1 Pathogenesis JO: PLoS Pathog http://www.kidney.de/pget.php?&tw=1&pmid=33064743 #FOAvip The Type I Interferons (IFN-Is) are innate antiviral cytokines that include 12 different IFNalpha subtypes and IFNbeta that signal through the IFN-I receptor (IFNAR), inducing hundreds of IFN-stimulated genes (ISGs) that comprise the 'interferome'. Quantitative differences in IFNAR binding correlate with antiviral activity, but whether IFN-Is exhibit qualitative differences remains controversial. Moreover, the IFN-I response is protective during acute HIV-1 infection, but likely pathogenic during the chronic stages. To gain a deeper understanding of the IFN-I response, we compared the interferomes of IFNalpha subtypes dominantly-expressed in HIV-1-exposed plasmacytoid dendritic cells (1, 2, 5, 8 and 14) and IFNbeta in the earliest cellular targets of HIV-1 infection. Primary gut CD4 T cells from 3 donors were treated for 18 hours ex vivo with individual IFN-Is normalized for IFNAR signaling strength. Of 1,969 IFN-regulated genes, 246 'core ISGs' were induced by all IFN-Is tested. However, many IFN-regulated genes were not shared between the IFNalpha subtypes despite similar induction of canonical antiviral ISGs such as ISG15, RSAD2 and MX1, formally demonstrating qualitative differences between the IFNalpha subtypes. Notably, IFNbeta induced a broader interferome than the individual IFNalpha subtypes. Since IFNbeta, and not IFNalpha, is upregulated during chronic HIV-1 infection in the gut, we compared core ISGs and IFNbeta-specific ISGs from colon pinch biopsies of HIV-1-uninfected (n = 13) versus age- and gender-matched, antiretroviral-therapy naive persons with HIV-1 (PWH; n = 19). Core ISGs linked to inflammation, T cell activation and immune exhaustion were elevated in PWH, positively correlated with plasma lipopolysaccharide (LPS) levels and gut IFNbeta levels, and negatively correlated with gut CD4 T cell frequencies. In sharp contrast, IFNbeta-specific ISGs linked to protein translation and anti-inflammatory responses were significantly downregulated in PWH, negatively correlated with gut IFNbeta and LPS, and positively correlated with plasma IL6 and gut CD4 T cell frequencies. Our findings reveal qualitative differences in interferome induction by diverse IFN-Is and suggest potential mechanisms for how IFNbeta may drive HIV-1 pathogenesis in the gut. Twit Text FOAVip Qualitative Differences Between the IFNalpha subtypes and IFNbeta Influence Chronic Mucosal HIV-1 Pathogenesis ????PLoS Pathog http://www.kidney.de/pget.php?&tw=1&pmid=33064743 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33064743 #FOAvip English Wikipedia <ref>{{Cite pmid|33064743}}</ref> Qualitative Differences Between the IFNalpha subtypes and IFNbeta Influence Chronic Mucosal HIV-1 Pathogenesis #MMPMID33064743 Guo K; Shen G; Kibbie J; Gonzalez T; Dillon SM; Smith HA; Cooper EH; Lavender K; Hasenkrug KJ; Sutter K; Dittmer U; Kroehl M; Kechris K; Wilson CC; Santiago ML PLoS Pathog 2020[Oct]; 16 (10): e1008986 PMID33064743show ga The Type I Interferons (IFN-Is) are innate antiviral cytokines that include 12 different IFNalpha subtypes and IFNbeta that signal through the IFN-I receptor (IFNAR), inducing hundreds of IFN-stimulated genes (ISGs) that comprise the 'interferome'. Quantitative differences in IFNAR binding correlate with antiviral activity, but whether IFN-Is exhibit qualitative differences remains controversial. Moreover, the IFN-I response is protective during acute HIV-1 infection, but likely pathogenic during the chronic stages. To gain a deeper understanding of the IFN-I response, we compared the interferomes of IFNalpha subtypes dominantly-expressed in HIV-1-exposed plasmacytoid dendritic cells (1, 2, 5, 8 and 14) and IFNbeta in the earliest cellular targets of HIV-1 infection. Primary gut CD4 T cells from 3 donors were treated for 18 hours ex vivo with individual IFN-Is normalized for IFNAR signaling strength. Of 1,969 IFN-regulated genes, 246 'core ISGs' were induced by all IFN-Is tested. However, many IFN-regulated genes were not shared between the IFNalpha subtypes despite similar induction of canonical antiviral ISGs such as ISG15, RSAD2 and MX1, formally demonstrating qualitative differences between the IFNalpha subtypes. Notably, IFNbeta induced a broader interferome than the individual IFNalpha subtypes. Since IFNbeta, and not IFNalpha, is upregulated during chronic HIV-1 infection in the gut, we compared core ISGs and IFNbeta-specific ISGs from colon pinch biopsies of HIV-1-uninfected (n = 13) versus age- and gender-matched, antiretroviral-therapy naive persons with HIV-1 (PWH; n = 19). Core ISGs linked to inflammation, T cell activation and immune exhaustion were elevated in PWH, positively correlated with plasma lipopolysaccharide (LPS) levels and gut IFNbeta levels, and negatively correlated with gut CD4 T cell frequencies. In sharp contrast, IFNbeta-specific ISGs linked to protein translation and anti-inflammatory responses were significantly downregulated in PWH, negatively correlated with gut IFNbeta and LPS, and positively correlated with plasma IL6 and gut CD4 T cell frequencies. Our findings reveal qualitative differences in interferome induction by diverse IFN-Is and suggest potential mechanisms for how IFNbeta may drive HIV-1 pathogenesis in the gut. |Adult[MESH] |Antiviral Agents/*pharmacology[MESH] |Case-Control Studies[MESH] |Dendritic Cells/drug effects/*pathology[MESH] |Female[MESH] |Gastrointestinal Tract/drug effects/*pathology[MESH] |Gene Expression Profiling[MESH] |HIV Infections/drug therapy/*pathology/virology[MESH] |HIV-1/*drug effects[MESH] |Humans[MESH] |Interferon-alpha/classification/*pharmacology[MESH] |Interferon-beta/*pharmacology[MESH] |Male[MESH] |Middle Aged[MESH]Qualitative Differences Between the IFNalpha subtypes and IFNbeta Infl(epmc).pdf DeepDyve Pubget Overpricing