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231225s2020 xx |||||o 00| ||eng c |
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|a 10.1016/j.clim.2020.108410
|2 doi
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|a pubmed24n1028.xml
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|a (DE-627)NLM308612779
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|a (NLM)32276140
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|a (PII)S1521-6616(20)30239-4
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|a DE-627
|b ger
|c DE-627
|e rakwb
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|a eng
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| 100 |
1 |
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|a Sawalha, Amr H
|e verfasserin
|4 aut
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| 245 |
1 |
0 |
|a Epigenetic dysregulation of ACE2 and interferon-regulated genes might suggest increased COVID-19 susceptibility and severity in lupus patients
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|c 2020
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| 336 |
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|a Text
|b txt
|2 rdacontent
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| 337 |
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|a ƒaComputermedien
|b c
|2 rdamedia
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| 338 |
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|a ƒa Online-Ressource
|b cr
|2 rdacarrier
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| 500 |
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|a Date Completed 23.06.2020
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|a Date Revised 19.10.2023
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|a published: Print-Electronic
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|a UpdateOf: medRxiv. 2020 Apr 04;:. - PMID 32511654
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|a Citation Status MEDLINE
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|a Copyright © 2020 Elsevier Inc. All rights reserved.
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|a 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, NFκB, 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
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| 650 |
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4 |
|a Journal Article
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| 650 |
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4 |
|a Research Support, N.I.H., Extramural
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| 650 |
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4 |
|a Research Support, Non-U.S. Gov't
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| 650 |
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4 |
|a ACE2
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| 650 |
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4 |
|a COVID-19
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| 650 |
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4 |
|a Epigenetics
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| 650 |
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4 |
|a Interferon
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| 650 |
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4 |
|a Lupus
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| 650 |
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4 |
|a Methylation
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| 650 |
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4 |
|a SARS-CoV-2
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| 650 |
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7 |
|a CD11a Antigen
|2 NLM
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| 650 |
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7 |
|a Cytokines
|2 NLM
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| 650 |
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7 |
|a Interferon Regulatory Factors
|2 NLM
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| 650 |
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7 |
|a NF-kappa B
|2 NLM
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| 650 |
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7 |
|a Receptors, KIR
|2 NLM
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| 650 |
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7 |
|a Spike Glycoprotein, Coronavirus
|2 NLM
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| 650 |
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7 |
|a spike protein, SARS-CoV-2
|2 NLM
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| 650 |
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7 |
|a Peptidyl-Dipeptidase A
|2 NLM
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| 650 |
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7 |
|a EC 3.4.15.1
|2 NLM
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| 650 |
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7 |
|a ACE2 protein, human
|2 NLM
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| 650 |
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7 |
|a EC 3.4.17.23
|2 NLM
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| 650 |
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7 |
|a Angiotensin-Converting Enzyme 2
|2 NLM
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| 650 |
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7 |
|a EC 3.4.17.23
|2 NLM
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| 700 |
1 |
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|a Zhao, Ming
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Coit, Patrick
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Lu, Qianjin
|e verfasserin
|4 aut
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| 773 |
0 |
8 |
|i Enthalten in
|t Clinical immunology (Orlando, Fla.)
|d 1999
|g 215(2020) vom: 15. Juni, Seite 108410
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnns
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| 773 |
1 |
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|g volume:215
|g year:2020
|g day:15
|g month:06
|g pages:108410
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| 856 |
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|u http://dx.doi.org/10.1016/j.clim.2020.108410
|3 Volltext
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|a GBV_USEFLAG_A
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|a SYSFLAG_A
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|a GBV_NLM
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|a GBV_ILN_11
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| 912 |
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|a GBV_ILN_24
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| 912 |
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|a GBV_ILN_350
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| 951 |
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|a AR
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| 952 |
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|d 215
|j 2020
|b 15
|c 06
|h 108410
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