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COVID-19 and Its Damage Outside the Lungs
COVID-19 and Its Damage Outside the Lungs
Written By: Nayada Deevisetpunt
Currently, there have been more than 13 million confirmed cases of COVID-19 and even more than 570,000 deaths globally. This illness was initially thought to be a respiratory infection; however, doctors are now recognizing that its effects are far more widespread outside the lungs.
Dr. Aakriti Gupta, one of the first cardiology specialists deployed to the COVID-19 intensive care unit at Columbia University, mentioned, “I observed that patients were clotting a lot, they had high blood sugars even if they did not have diabetes, and many were experiencing injury to their hearts and kidneys.” As a result, Gupta and her colleagues collaborated with other doctors across the United States to develop the first clinical guidelines on COVID-19’s nonrespiratory symptoms. The guidelines provide a summary on how the disease affects particular organ systems and even the clinical presentation and treatment of children and pregnant women with the disease.
One of the first things doctors treating patients with COVID-19 noticed was that the patient’s blood clotted very easily. Not only this, but some of the manifestations of this disease also include cardiovascular complications, kidney injury, liver injury, effects on the central nervous system, effects on the eyes, and dermatological (skin) complications. Four main mechanisms that could explain these widespread effects are direct damage to cells that the virus itself inflicts, damage to the endothelial cells that could result in blood clots and inflammation, dysregulation of the immune response, and disruption of the hormones regulating blood pressure and fluid balance (known as the renin-angiotensin-aldosterone system or RAAS).
In order to enter a host cell, the spike proteins on the virus must bind to the receptor on the cell’s surface. Prior to this, a protease (protein-degrading enzyme) must prime to the receptor called angiotensin converting enzyme 2 (ACE2). As a result, tissues that carry a considerable amount of ACE2 on their cell surfaces may be especially susceptible to COVID-19 infection and injury.
Moreover, doctors also found out that damage to the endothelial cells triggers inflammation and allows for the formation of blood clots (thrombosis). These clots impair the blood supply to tissues around the body; in fact, when they break free, they may lodge throughout the circulatory system and cause further blockages, tissue damage, and inflammation.
When a pathogen enters the cell, the immune cells release cytokines (signaling molecules) to recruit more immune cells to fight the infection. This could lead to an immune overreaction, or what is called “cytokine release syndrome”. In fact, a clinical trial has found that steroid dexamethasone, which suppressed the immune response, reduced deaths by one-third in patients on ventilators.
The final mechanism mentioned is the disruption of the RAAS. The RAAS function is to regulate physiological processes throughout the body, including fluid balance, blood pressure, and tissue growth. Since the role of the membrane-bound protein ACE2 is to break down the hormones angiotensin 1 and 2, the SARS-CoV-2 that invades host cells by binding to ACE2 could disrupt the normal regulatory function.
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