期刊
ANNALS OF HUMAN GENETICS
卷 85, 期 6, 页码 221-234出版社
WILEY
DOI: 10.1111/ahg.12440
关键词
COVID-19; DNA methylation; epigenetic regulation; SARS-CoV-2
资金
- National Natural Science Foundation of China [81770029]
- Key Research Project of Shandong Province [2020SFXGFY031, 2020SFXGFY03-3, 2020SFXGFY04]
DNA methylation differences were found between healthy individuals and COVID-19 patients with varying disease severities, with key genes identified that may play a role in disease progression. Specific gene functions and pathways were enriched in signal transduction and the immune system.
In the early 2000s, emerging SARS-CoV-2, which is highly pathogenic, posed a great threat to public health. During COVID-19, epigenetic regulation is deemed to be an important part of the pathophysiology and illness severity. Using the Illumina Infinium Methylation EPIC BeadChip (850 K), we investigated genome-wide differences in DNA methylation between healthy subjects and COVID-19 patients with different disease severities. We conducted a combined analysis and selected 35 marker genes that could indicate a SARS-CoV-2 infection, including 12 (ATHL1, CHN2, CHST15, CPLX2, CRHR2, DCAKD, GNAI2, HECW1, HYAL1, MIR510, PDE11A, and SMG6) situated in the promoter region. The functions and pathways of differentially methylated genes were enriched in biological processes, signal transduction, and the immune system. In the Severe versus Mild group, differentially methylated genes, after eliminating duplicates, were used for PPI analyses. The four hub genes (GNG7, GNAS, PRKCZ, and PRKAG2) that had the highest degree of nodes were identified and among them, GNG7 and GNAS genes expressions were also downregulated in the severe group in sequencing results. Above all, the results suggest that GNG7 and GNAS may play a non-ignorable role in the progression of COVID-19. In conclusion, the identified key genes and related pathways in the current study can be used to study the molecular mechanisms of COVID-19 and may provide possibilities for specific treatments.
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