tetano
Editor, Senior Moderator
Front Immunol
. 2021 Oct 8;12:752380.
doi: 10.3389/fimmu.2021.752380. eCollection 2021.
COVID-19 Is a Multi-Organ Aggressor: Epigenetic and Clinical Marks
Mankgopo Magdeline Kgatle[SUP] 1 2 [/SUP], Ismaheel Opeyemi Lawal[SUP] 1 2 3 [/SUP], Gabriel Mashabela[SUP] 4 [/SUP], Tebatso Moshoeu Gillian Boshomane[SUP] 1 2 3 5 [/SUP], Palesa Caroline Koatale[SUP] 1 2 [/SUP], Phetole Walter Mahasha[SUP] 6 [/SUP], Honest Ndlovu[SUP] 2 [/SUP], Mariza Vorster[SUP] 2 [/SUP], Hosana Gomes Rodrigues[SUP] 7 [/SUP], Jan Rijn Zeevaart[SUP] 1 8 9 [/SUP], Siamon Gordon[SUP] 9 10 [/SUP], Pedro Moura-Alves[SUP] 11 [/SUP], Mike Machaba Sathekge[SUP] 1 2 4 [/SUP]
Affiliations
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.
Keywords: ACE2; COVID-19; SARS-CoV-2; TMPRSS2; cytokine storm; epigenetics; multi-organ; pro-inflammatory cytokines.
. 2021 Oct 8;12:752380.
doi: 10.3389/fimmu.2021.752380. eCollection 2021.
COVID-19 Is a Multi-Organ Aggressor: Epigenetic and Clinical Marks
Mankgopo Magdeline Kgatle[SUP] 1 2 [/SUP], Ismaheel Opeyemi Lawal[SUP] 1 2 3 [/SUP], Gabriel Mashabela[SUP] 4 [/SUP], Tebatso Moshoeu Gillian Boshomane[SUP] 1 2 3 5 [/SUP], Palesa Caroline Koatale[SUP] 1 2 [/SUP], Phetole Walter Mahasha[SUP] 6 [/SUP], Honest Ndlovu[SUP] 2 [/SUP], Mariza Vorster[SUP] 2 [/SUP], Hosana Gomes Rodrigues[SUP] 7 [/SUP], Jan Rijn Zeevaart[SUP] 1 8 9 [/SUP], Siamon Gordon[SUP] 9 10 [/SUP], Pedro Moura-Alves[SUP] 11 [/SUP], Mike Machaba Sathekge[SUP] 1 2 4 [/SUP]
Affiliations
- PMID: 34691068
- PMCID: PMC8531724
- DOI: 10.3389/fimmu.2021.752380
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.
Keywords: ACE2; COVID-19; SARS-CoV-2; TMPRSS2; cytokine storm; epigenetics; multi-organ; pro-inflammatory cytokines.