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10.1073/pnas.2024202118

http://scihub22266oqcxt.onion/10.1073/pnas.2024202118
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34021074!8201919!34021074
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suck abstract from ncbi


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pmid34021074      Proc+Natl+Acad+Sci+U+S+A 2021 ; 118 (23): ä
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  • 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]


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