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  • Endoplasmic reticulum stress and NF-kB activation in SARS-CoV-2 infected cells and their response to antiviral therapy #MMPMID34390301
  • Bartolini D; Stabile AM; Vacca C; Pistilli A; Rende M; Gioiello A; Cruciani G; Galli F
  • IUBMB Life 2022[Jan]; 74 (1): 93-100 PMID34390301show ga
  • Unfolded protein response (UPR) and endoplasmic reticulum (ER) stress are aspects of SARS-CoV-2-host cell interaction with proposed role in the cytopathic and inflammatory pathogenesis of this viral infection. The role of the NF-kB pathway in these cellular processes remains poorly characterized. When investigated in VERO-E6 cells, SARS-CoV-2 infection was found to markedly stimulate NF-kB protein expression and activity. NF-kB activation occurs early in the infection process (6 hpi) and it is associated with increased MAPK signaling and expression of the UPR inducer IRE-1alpha. These signal transduction processes characterize the cellular stress response to the virus promoting a pro-inflammatory environment and caspase activation in the host cell. Inhibition of viral replication by the viral protease inhibitor Nelfinavir reverts all these molecular changes also stimulating c-Jun expression, a key component of the JNK/AP-1 pathway with important role in the IRE-1alpha-mediated transcriptional regulation of stress response genes with anti-inflammatory and cytoprotection function. The present study demonstrates that UPR signaling and its interaction with cellular MAPKs and the NF-kB activity are important aspects of SARS-CoV-2-host cell interaction that deserve further investigation to identify more efficient therapies for this viral infection.
  • |*SARS-CoV-2/drug effects/pathogenicity[MESH]
  • |Adenosine Monophosphate/analogs & derivatives/pharmacology[MESH]
  • |Alanine/analogs & derivatives/pharmacology[MESH]
  • |Animals[MESH]
  • |Antiviral Agents/*pharmacology[MESH]
  • |COVID-19/*drug therapy/*metabolism/virology[MESH]
  • |Caspase 9/metabolism[MESH]
  • |Chlorocebus aethiops[MESH]
  • |Cytopathogenic Effect, Viral/drug effects[MESH]
  • |Endoplasmic Reticulum Stress/*drug effects[MESH]
  • |Humans[MESH]
  • |MAP Kinase Signaling System/drug effects[MESH]
  • |Models, Biological[MESH]
  • |NF-kappa B/*metabolism[MESH]
  • |Nelfinavir/pharmacology[MESH]
  • |Unfolded Protein Response/drug effects[MESH]
  • |Vero Cells[MESH]

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  • suck abstract from ncbi

    93 1.74 2022