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COVID-19 Is a Multi-Organ Aggressor: Epigenetic and Clinical Marks

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FRONTIERS IN IMMUNOLOGY
卷 12, 期 -, 页码 -

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FRONTIERS MEDIA SA
DOI: 10.3389/fimmu.2021.752380

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ACE2; COVID-19; cytokine storm; epigenetics; multi-organ; pro-inflammatory cytokines; SARS-CoV-2; TMPRSS2

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Severe cases of COVID-19 may be influenced by metabolic and epigenetic mechanisms, including DNA methylation and histone/chromatin alterations. These epigenetic phenomena may lead to enhanced viral replication, resulting in severe symptoms and fatalities.
The progression of coronavirus disease 2019 (COVID-19), resulting from a severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, may be influenced by both genetic and environmental factors. Several viruses hijack the host genome machinery for their own advantage and survival, and similar phenomena might occur upon SARS-CoV-2 infection. Severe cases of COVID-19 may be driven by metabolic and epigenetic driven mechanisms, including DNA methylation and histone/chromatin alterations. These epigenetic phenomena may respond to enhanced viral replication and mediate persistent long-term infection and clinical phenotypes associated with severe COVID-19 cases and fatalities. Understanding the epigenetic events involved, and their clinical significance, may provide novel insights valuable for the therapeutic control and management of the COVID-19 pandemic. This review highlights different epigenetic marks potentially associated with COVID-19 development, clinical manifestation, and progression.

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