Abstract
Evidence is emerging that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can infect various organs of the body, including cardiomyocytes and cardiac endothelial cells in the heart. This review focuses on the effects of SARS-CoV-2 in the heart after direct infection that can lead to myocarditis and an outline of potential treatment options. The main points are: (1) Viral entry: SARS-CoV-2 uses specific receptors and proteases for docking and priming in cardiac cells. Thus, different receptors or protease inhibitors might be effective in SARS-CoV-2-infected cardiac cells. (2) Viral replication: SARS-CoV-2 uses RNA-dependent RNA polymerase for replication. Drugs acting against ssRNA(+) viral replication for cardiac cells can be effective. (3) Autophagy and double-membrane vesicles: SARS-CoV-2 manipulates autophagy to inhibit viral clearance and promote SARS-CoV-2 replication by creating double-membrane vesicles as replication sites. (4) Immune response: Host immune response is manipulated to evade host cell attacks against SARS-CoV-2 and increased inflammation by dysregulating immune cells. Efficiency of immunosuppressive therapy must be elucidated. (5) Programmed cell death: SARS-CoV-2 inhibits programmed cell death in early stages and induces apoptosis, necroptosis, and pyroptosis in later stages. (6) Energy metabolism: SARS-CoV-2 infection leads to disturbed energy metabolism that in turn leads to a decrease in ATP production and ROS production. (7) Viroporins: SARS-CoV-2 creates viroporins that lead to an imbalance of ion homeostasis. This causes apoptosis, altered action potential, and arrhythmia.
Highlights
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which causes coronavirus disease 2019 (COVID-19), is threatening the entire world in one of the worst global pandemics, with over 200 million cases and an estimated 4.4 million deaths as of August 2021, and with new, more-threatening virus variants emerging according to theWorld Health Organization (WHO) [1].The virus mainly causes respiratory infection, which in severe cases causes viral pneumonia and acute respiratory distress syndrome (ARDS)
Severe COVID-19 cases have been associated with myocardial injury, arrhythmia, acute coronary syndrome, venous thromboembolism, and micro- and macro-thromboses, which are associated with high mortality [2,3,4,5]
After viral RNA export from the double-membrane vesicles (DMVs), the viral RNA, along with viral structural proteins, are assembled in single-membrane compartments made from the ER-to-Golgi intermediate compartment (ERGIC), and the newly assembled virions are excreted via the secretory pathway into the extracellular space [86,89,90]
Summary
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which causes coronavirus disease 2019 (COVID-19), is threatening the entire world in one of the worst global pandemics, with over 200 million cases and an estimated 4.4 million deaths as of August 2021, and with new, more-threatening virus variants emerging according to the. There are indications that SARS-CoV-2 can directly infect cardiomyocytes and cardiac endothelial cells This poses a possible risk of causing myocarditis or other complex heart diseases. Other viruses frequently causing myocarditis, such as enteroviruses like coxsackievirus B3 (CVB3) that infect cardiomyocytes and parvovirus B19 (PVB19) that infects cardiac endothelial cells, are shown to hijack the biological processes of the host cell to their advantage while damaging the heart [31,32,33] These include, among others, the immune system, viral replication, the autophagosomal pathway, cell death, energy metabolism, and ion homeostasis, which all play a significant role in myocardial function [31]. Our understanding of SARS-CoV-1 can help in understanding analogous actions of SARS-CoV-2, as data for the new SARS-CoV-2 are still incomplete [37]
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