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10.3389/fimmu.2021.679482 http://scihub22266oqcxt.onion/10.3389/fimmu.2021.679482 34177923!8221109!34177923     free     free     free Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Front+Immunol 2021 ; 12 (ä): 679482 Nephropedia Template TP {{tp|p=34177923|t=2021. SARS-CoV-2 ORF8 Forms Intracellular Aggregates and Inhibits IFNgamma-Induced Antiviral Gene Expression in Human Lung Epithelial Cells |pdf=|usr=}}{{34177923}} gab.com Text SARS-CoV-2 ORF8 Forms Intracellular Aggregates and Inhibits IFNgamma-Induced Antiviral Gene Expression in Human Lung Epithelial Cells JO: Front Immunol http://www.kidney.de/pget.php?&tw=1&pmid=34177923 #FOAvip Infection with the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes COVID-19, a disease that involves significant lung tissue damage. How SARS-CoV-2 infection leads to lung injury remains elusive. The open reading frame 8 (ORF8) protein of SARS-CoV-2 (ORF8(SARS-CoV-2)) is a unique accessory protein, yet little is known about its cellular function. We examined the cellular distribution of ORF8(SARS-CoV-2) and its role in the regulation of human lung epithelial cell proliferation and antiviral immunity. Using live imaging and immunofluorescent staining analyses, we found that ectopically expressed ORF8(SARS-CoV-2) forms aggregates in the cytosol and nuclear compartments of lung epithelial cells. Using in silico bioinformatic analysis, we found that ORF8(SARS-CoV-2) possesses an intrinsic aggregation characteristic at its N-terminal residues 1-18. Cell culture did not reveal any effects of ORF8(SARS-CoV-2) expression on lung epithelial cell proliferation and cell cycle progression, suggesting that ORF8(SARS-CoV-2) aggregates do not affect these cellular processes. Interestingly, ectopic expression of ORF8(SARS-CoV-2) in lung epithelial cells suppressed basal expression of several antiviral molecules, including DHX58, ZBP1, MX1, and MX2. In addition, expression of ORF8(SARS-CoV-2) attenuated the induction of antiviral molecules by IFNgamma but not by IFNbeta in lung epithelial cells. Taken together, ORF8(SARS-CoV-2) is a unique viral accessory protein that forms aggregates when expressing in lung epithelial cells. It potently inhibits the expression of lung cellular anti-viral proteins at baseline and in response to IFNgamma in lung epithelial cells, which may facilitate SARS-CoV-2 escape from the host antiviral innate immune response during early viral infection. In addition, it seems that formation of ORF8(SARS-CoV-2) aggregate is independent from the viral infection. Thus, it would be interesting to examine whether any COVID-19 patients exhibit persistent ORF8 SARS-CoV-2 expression after recovering from SARS-CoV-2 infection. If so, the pathogenic effect of prolonged ORF8(SARS-CoV-2) expression and its association with post-COVID symptoms warrant investigation in the future. Twit Text FOAVip SARS-CoV-2 ORF8 Forms Intracellular Aggregates and Inhibits IFNgamma-Induced Antiviral Gene Expression in Human Lung Epithelial Cells ????Front Immunol http://www.kidney.de/pget.php?&tw=1&pmid=34177923 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34177923 #FOAvip English Wikipedia <ref>{{Cite pmid|34177923}}</ref> SARS-CoV-2 ORF8 Forms Intracellular Aggregates and Inhibits IFNgamma-Induced Antiviral Gene Expression in Human Lung Epithelial Cells #MMPMID34177923 Geng H; Subramanian S; Wu L; Bu HF; Wang X; Du C; De Plaen IG; Tan XD Front Immunol 2021[]; 12 (ä): 679482 PMID34177923show ga Infection with the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes COVID-19, a disease that involves significant lung tissue damage. How SARS-CoV-2 infection leads to lung injury remains elusive. The open reading frame 8 (ORF8) protein of SARS-CoV-2 (ORF8(SARS-CoV-2)) is a unique accessory protein, yet little is known about its cellular function. We examined the cellular distribution of ORF8(SARS-CoV-2) and its role in the regulation of human lung epithelial cell proliferation and antiviral immunity. Using live imaging and immunofluorescent staining analyses, we found that ectopically expressed ORF8(SARS-CoV-2) forms aggregates in the cytosol and nuclear compartments of lung epithelial cells. Using in silico bioinformatic analysis, we found that ORF8(SARS-CoV-2) possesses an intrinsic aggregation characteristic at its N-terminal residues 1-18. Cell culture did not reveal any effects of ORF8(SARS-CoV-2) expression on lung epithelial cell proliferation and cell cycle progression, suggesting that ORF8(SARS-CoV-2) aggregates do not affect these cellular processes. Interestingly, ectopic expression of ORF8(SARS-CoV-2) in lung epithelial cells suppressed basal expression of several antiviral molecules, including DHX58, ZBP1, MX1, and MX2. In addition, expression of ORF8(SARS-CoV-2) attenuated the induction of antiviral molecules by IFNgamma but not by IFNbeta in lung epithelial cells. Taken together, ORF8(SARS-CoV-2) is a unique viral accessory protein that forms aggregates when expressing in lung epithelial cells. It potently inhibits the expression of lung cellular anti-viral proteins at baseline and in response to IFNgamma in lung epithelial cells, which may facilitate SARS-CoV-2 escape from the host antiviral innate immune response during early viral infection. In addition, it seems that formation of ORF8(SARS-CoV-2) aggregate is independent from the viral infection. Thus, it would be interesting to examine whether any COVID-19 patients exhibit persistent ORF8 SARS-CoV-2 expression after recovering from SARS-CoV-2 infection. If so, the pathogenic effect of prolonged ORF8(SARS-CoV-2) expression and its association with post-COVID symptoms warrant investigation in the future. |COVID-19/*immunology/virology[MESH] |Gene Expression Regulation[MESH] |HEK293 Cells[MESH] |Humans[MESH] |Immunity[MESH] |Interferon-gamma/metabolism[MESH] |Intracellular Space[MESH] |Lung/*pathology[MESH] |Protein Aggregation, Pathological[MESH] |Respiratory Mucosa/*physiology/virology[MESH] |SARS-CoV-2/*physiology[MESH]SARS-CoV-2 ORF8 Forms Intracellular Aggregates and Inhibits IFNgamma-I(epmc).pdf DeepDyve Pubget Overpricing