COVID-19 Is a Multi-Organ Aggressor: Epigenetic and Clinical Marks
Mankgopo Magdeline Kgatle, Ismaheel O. Lawal, Gabriel T. Mashabela, Tebatso M.G. Boshomane, Palesa Caroline Koatale, Phetole Walter Mahasha, Honest Ndlovu, Mariza Vorster, Hosana Gomes Rodrigues, Jan Rijn Zeevaart, Siamon Gordon, Pedro Moura‐Alves, Mike Sathekge
Abstract
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.