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suck abstract from ncbi


10.1016/j.clim.2020.108410

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suck abstract from ncbi


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pmid32276140      Clin+Immunol 2020 ; 215 (ä): 108410
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  • Epigenetic dysregulation of ACE2 and interferon-regulated genes might suggest increased COVID-19 susceptibility and severity in lupus patients #MMPMID32276140
  • Sawalha AH; Zhao M; Coit P; Lu Q
  • Clin Immunol 2020[Jun]; 215 (ä): 108410 PMID32276140show ga
  • Infection caused by SARS-CoV-2 can result in severe respiratory complications and death. Patients with a compromised immune system are expected to be more susceptible to a severe disease course. In this report we suggest that patients with systemic lupus erythematous might be especially prone to severe COVID-19 independent of their immunosuppressed state from lupus treatment. Specifically, we provide evidence in lupus to suggest hypomethylation and overexpression of ACE2, which is located on the X chromosome and encodes a functional receptor for the SARS-CoV-2 spike glycoprotein. Oxidative stress induced by viral infections exacerbates the DNA methylation defect in lupus, possibly resulting in further ACE2 hypomethylation and enhanced viremia. In addition, demethylation of interferon-regulated genes, NFkappaB, and key cytokine genes in lupus patients might exacerbate the immune response to SARS-CoV-2 and increase the likelihood of cytokine storm. These arguments suggest that inherent epigenetic dysregulation in lupus might facilitate viral entry, viremia, and an excessive immune response to SARS-CoV-2. Further, maintaining disease remission in lupus patients is critical to prevent a vicious cycle of demethylation and increased oxidative stress, which will exacerbate susceptibility to SARS-CoV-2 infection during the current pandemic. Epigenetic control of the ACE2 gene might be a target for prevention and therapy in COVID-19.
  • |*Epigenesis, Genetic[MESH]
  • |*Genetic Predisposition to Disease[MESH]
  • |*Pandemics[MESH]
  • |Angiotensin-Converting Enzyme 2[MESH]
  • |Betacoronavirus/immunology/pathogenicity[MESH]
  • |CD11a Antigen/genetics/immunology[MESH]
  • |COVID-19[MESH]
  • |Coronavirus Infections/complications/epidemiology/*genetics/immunology[MESH]
  • |Cytokines/genetics/immunology[MESH]
  • |DNA Methylation[MESH]
  • |Disease Progression[MESH]
  • |Host-Pathogen Interactions/genetics/immunology[MESH]
  • |Humans[MESH]
  • |Interferon Regulatory Factors/genetics/immunology[MESH]
  • |Lupus Erythematosus, Systemic/complications/epidemiology/*genetics/immunology[MESH]
  • |NF-kappa B/genetics/immunology[MESH]
  • |Oxidative Stress/genetics/immunology[MESH]
  • |Peptidyl-Dipeptidase A/*genetics/immunology[MESH]
  • |Pneumonia, Viral/complications/epidemiology/*genetics/immunology[MESH]
  • |Protein Binding[MESH]
  • |Receptors, KIR/genetics/immunology[MESH]
  • |SARS-CoV-2[MESH]
  • |Signal Transduction[MESH]
  • |Spike Glycoprotein, Coronavirus/genetics/immunology[MESH]


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