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10.3389/fmicb.2020.01180 http://scihub22266oqcxt.onion/10.3389/fmicb.2020.01180 32574254!7256192!32574254     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 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\32574254.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Front+Microbiol 2020 ; 11 (ä): 1180 Nephropedia Template TP {{tp|p=32574254|t=2020. The Coronavirus PEDV Evades Type III Interferon Response Through the miR-30c-5p/SOCS1 Axis |pdf=|usr=}}{{32574254}} gab.com Text The Coronavirus PEDV Evades Type III Interferon Response Through the miR-30c-5p/SOCS1 Axis JO: Front Microbiol http://www.kidney.de/pget.php?&tw=1&pmid=32574254 #FOAvip Porcine epidemic diarrhea virus (PEDV) is an economically important pathogen that has evolved several mechanisms to evade type I IFN responses. Type III interferon (IFN-lambda), an innate cytokine that primarily targets the mucosal epithelia, is critical in fighting mucosal infection in the host and has been reported to potently inhibit PEDV infection in vitro. However, how PEDV escapes IFN-lambda antiviral response remains unclear. In this study, we found that PEDV infection induced significant IFN-lambda expression in type I IFN-defective Vero E6 cells, but virus-induced endogenous IFN-lambda did not reduce PEDV titers. Moreover, we demonstrated that PEDV escaped IFN-lambda responses by substantially upregulating the suppressor of cytokine signaling protein 1 (SOCS1) expression, which impaired the induction of IFN-stimulated genes (ISGs) and dampened the IFN-lambda antiviral response and facilitated PEDV replication in Vero E6 cells. We further showed that PEDV infection increased SOCS1 expression by decreasing host miR-30c-5p expression. MiR-30c-5p suppressed SOCS1 expression through targeting the 3' untranslated region (UTR) of SOCS1. The inhibition of IFN-lambda elicited ISGs expression by SOCS1 was specifically rescued by overexpression of miR-30c-5p. Collectively, our findings identify a new strategy by PEDV to escape IFN-lambda-mediated antiviral immune responses by engaging the SOCS1/miR-30c axis, thus improving our understanding of its pathogenesis. Twit Text FOAVip The Coronavirus PEDV Evades Type III Interferon Response Through the miR-30c-5p/SOCS1 Axis ????Front Microbiol http://www.kidney.de/pget.php?&tw=1&pmid=32574254 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=32574254 #FOAvip English Wikipedia <ref>{{Cite pmid|32574254}}</ref> The Coronavirus PEDV Evades Type III Interferon Response Through the miR-30c-5p/SOCS1 Axis #MMPMID32574254 Wang C; Shan L; Qu S; Xue M; Wang K; Fu F; Wang L; Wang Z; Feng L; Xu W; Liu P Front Microbiol 2020[]; 11 (ä): 1180 PMID32574254show ga Porcine epidemic diarrhea virus (PEDV) is an economically important pathogen that has evolved several mechanisms to evade type I IFN responses. Type III interferon (IFN-lambda), an innate cytokine that primarily targets the mucosal epithelia, is critical in fighting mucosal infection in the host and has been reported to potently inhibit PEDV infection in vitro. However, how PEDV escapes IFN-lambda antiviral response remains unclear. In this study, we found that PEDV infection induced significant IFN-lambda expression in type I IFN-defective Vero E6 cells, but virus-induced endogenous IFN-lambda did not reduce PEDV titers. Moreover, we demonstrated that PEDV escaped IFN-lambda responses by substantially upregulating the suppressor of cytokine signaling protein 1 (SOCS1) expression, which impaired the induction of IFN-stimulated genes (ISGs) and dampened the IFN-lambda antiviral response and facilitated PEDV replication in Vero E6 cells. We further showed that PEDV infection increased SOCS1 expression by decreasing host miR-30c-5p expression. MiR-30c-5p suppressed SOCS1 expression through targeting the 3' untranslated region (UTR) of SOCS1. The inhibition of IFN-lambda elicited ISGs expression by SOCS1 was specifically rescued by overexpression of miR-30c-5p. Collectively, our findings identify a new strategy by PEDV to escape IFN-lambda-mediated antiviral immune responses by engaging the SOCS1/miR-30c axis, thus improving our understanding of its pathogenesis. äThe Coronavirus PEDV Evades Type III Interferon Response Through the (epmc).pdf DeepDyve Pubget Overpricing