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10.1073/pnas.2024202118 http://scihub22266oqcxt.onion/10.1073/pnas.2024202118 34021074!8201919!34021074     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=34021074&cmd=llinks): Failed to open stream: HTTP request failed! 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The ORF8 protein of SARS-CoV-2 mediates immune evasion through down-regulating MHC-Iota |pdf=|usr=}}{{34021074}} gab.com Text The ORF8 protein of SARS-CoV-2 mediates immune evasion through down-regulating MHC-Iota JO: Proc Natl Acad Sci U S A http://www.kidney.de/pget.php?&tw=1&pmid=34021074 #FOAvip COVID-19, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has become a global pandemic and has claimed over 2 million lives worldwide. Although the genetic sequences of SARS-CoV and SARS-CoV-2 have high homology, the clinical and pathological characteristics of COVID-19 differ significantly from those of SARS. How and whether SARS-CoV-2 evades (cellular) immune surveillance requires further elucidation. In this study, we show that SARS-CoV-2 infection leads to major histocompability complex class Iota (MHC-Iota) down-regulation both in vitro and in vivo. The viral protein encoded by open reading frame 8 (ORF8) of SARS-CoV-2, which shares the least homology with SARS-CoV among all viral proteins, directly interacts with MHC-Iota molecules and mediates their down-regulation. In ORF8-expressing cells, MHC-Iota molecules are selectively targeted for lysosomal degradation via autophagy. Thus, SARS-CoV-2-infected cells are much less sensitive to lysis by cytotoxic T lymphocytes. Because ORF8 protein impairs the antigen presentation system, inhibition of ORF8 could be a strategy to improve immune surveillance. Twit Text FOAVip The ORF8 protein of SARS-CoV-2 mediates immune evasion through down-regulating MHC-Iota ????Proc Natl Acad Sci U S A http://www.kidney.de/pget.php?&tw=1&pmid=34021074 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34021074 #FOAvip English Wikipedia <ref>{{Cite pmid|34021074}}</ref> The ORF8 protein of SARS-CoV-2 mediates immune evasion through down-regulating MHC-Iota #MMPMID34021074 Zhang Y; Chen Y; Li Y; Huang F; Luo B; Yuan Y; Xia B; Ma X; Yang T; Yu F; Liu J; Liu B; Song Z; Chen J; Yan S; Wu L; Pan T; Zhang X; Li R; Huang W; He X; Xiao F; Zhang J; Zhang H Proc Natl Acad Sci U S A 2021[Jun]; 118 (23): ä PMID34021074show ga COVID-19, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has become a global pandemic and has claimed over 2 million lives worldwide. Although the genetic sequences of SARS-CoV and SARS-CoV-2 have high homology, the clinical and pathological characteristics of COVID-19 differ significantly from those of SARS. How and whether SARS-CoV-2 evades (cellular) immune surveillance requires further elucidation. In this study, we show that SARS-CoV-2 infection leads to major histocompability complex class Iota (MHC-Iota) down-regulation both in vitro and in vivo. The viral protein encoded by open reading frame 8 (ORF8) of SARS-CoV-2, which shares the least homology with SARS-CoV among all viral proteins, directly interacts with MHC-Iota molecules and mediates their down-regulation. In ORF8-expressing cells, MHC-Iota molecules are selectively targeted for lysosomal degradation via autophagy. Thus, SARS-CoV-2-infected cells are much less sensitive to lysis by cytotoxic T lymphocytes. Because ORF8 protein impairs the antigen presentation system, inhibition of ORF8 could be a strategy to improve immune surveillance. |*Antigen Presentation[MESH] |*Immune Evasion[MESH] |Animals[MESH] |Autophagy/genetics/immunology[MESH] |COVID-19/genetics/*immunology[MESH] |Chlorocebus aethiops[MESH] |Down-Regulation/*immunology[MESH] |HEK293 Cells[MESH] |Histocompatibility Antigens Class I/genetics/*immunology[MESH] |Humans[MESH] |Lysosomes/genetics/immunology/virology[MESH] |Mice[MESH] |Mice, Transgenic[MESH] |SARS-CoV-2/genetics/*immunology[MESH] |Vero Cells[MESH]The ORF8 protein of SARS-CoV-2 mediates immune evasion through down-re(epmc).pdf DeepDyve Pubget Overpricing