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

Mankgopo Magdeline Kgatle*, Ismaheel Opeyemi Lawal, Gabriel Mashabela, Tebatso Moshoeu Gillian Boshomane, Palesa Caroline Koatale, Phetole Walter Mahasha, Honest Ndlovu, Mariza Vorster, Hosana Gomes Rodrigues, Jan Rijn Zeevaart, Siamon Gordon, Pedro Moura-Alves, Mike Machaba Sathekge*

*此作品的通信作者

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28 引文 斯高帕斯(Scopus)

摘要

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.

原文英語
文章編號752380
期刊Frontiers in Immunology
12
DOIs
出版狀態已出版 - 08 10 2021

文獻附註

Publisher Copyright:
© Copyright © 2021 Kgatle, Lawal, Mashabela, Boshomane, Koatale, Mahasha, Ndlovu, Vorster, Rodrigues, Zeevaart, Gordon, Moura-Alves and Sathekge.

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