COVID-19, the disease caused by SARS-CoV-2, is a novel coronavirus that was discovered in Wuhan China at the end of 2019. Unlike other pathogens such as bacteria, viruses are not alive and require a living host to replicate1. The virus consists of a spherical structure with lots of bulky spike proteins creating a crown-like shape (corona = crown in Latin), from which their name is derived2 (Figure 1). COVID-19 is what’s called a ‘zoonosis’, which means that this disease jumped species into humans with the origin still being debated but it most likely from bats3.
Figure 1. Coronavirus COVID-19 virus shape with crown-like spikes from which it derives it’s name.
Once in contact with humans the spikes of COVID-19 bind to specific receptors on lung and respiratory tract cells called ACE-24, which fuses the virus particle with the host cell, delivers the genetic code, and starts the infection cycle5. After entry, the released viral genetic material is decoded inside the infected cell, replicated and then released to infect other neighbouring cells (Figure 2)6. COVID-19 particles are composed of structural components that both encapsulate the genetic code material (nucleocapsid) and give the virus particles their structure (membrane and envelope proteins)7. To replicate itself, the virus also encodes an enzyme to copy its genetic code (polymerase), and factors to inhibit the host’s immune defences (accessory proteins). The accessory proteins are often important factors in determining the severity of disease as is the binding site affinity and ease of replication. What makes COVID-19 so infectious is that it has strong binding affinity for the ACE2 receptor, it can easily suppress host defences, has rapid replication ability and can be easily transmitted from host to host.
Figure 2. How COVID-19 infect cells and replicates itself.
Our immune system protects us in two ways; with weapons that are very rapidly deployed (the innate immune system) and others that take some time to start operating (the adaptive immune system). Very simply put, the rapid response slows down the propagation of a virus, but cannot entirely stop it. It uses a series of cells like basophils, eosinophils, neutrophils, mast cells or natural killer cells (Figure 3) that engulf and bombard the infected cells and virus with harsh oxidative species. Think of the innate immune system as the “shoot first and ask questions later approach”, it seeks and destroys often creating excess inflammation and collateral damage to surrounding cells caught in the cross-fire. The slower acting adaptive immune system is strategic and far more precise, it is very effective and usually lets us regain health by clearing the virus from our body8 . Following infection adaptive immunity slowly builds an army consisting of antibodies and cells (B and T cells) that search and destroy the invading pathogen, and specifically generates a memory of this invader that helps it to mount a faster and more vigorous response to a secondary infection with the same pathogen8 (Figure 3).
A characteristic of immunological defence and memory is the occurrence of neutralizing antibodies in the plasma of our blood. Antibodies are proteins that bind to the virus. If they are neutralizing they prevent the virus from attaching to cells it is trying to infect by blocking it’s spike proteins8(Figure 4). It is still early days to form a sound judgment of immunological memory as a means to prevent re-infection with the COVID-19 virus. However, neutralizing antibodies have been found in infected persons and there is reason to hope that immunological memory will indeed mitigate the risk of getting sick again with COVID-199.
COVID-19 can actively reduce the impact of the rapid immune response, allowing the virus to multiply before the slower arm of the immune response starts being protective. During this time people are at high risk for severe inflammation of internal organs, particularly the lungs. Symptoms of infection include a loss of smell and taste10, followed days later by fever, cough, shortness of breath, fatigue and gastrointestinal issues including diarrhoea11. In a worst-case scenario severe infection can lead to life-threatening acute respiratory distress syndrome (ARDS)12. In addition, the vast release of cytokines by the immune system in response to the viral infection and/or secondary infections can result in a cytokine storm and symptoms of sepsis that also can lead to death via organ failure, especially of the cardiac (heart), hepatic (liver) and renal (kidney) systems (Figure 5)13. The median incubation period after infection is 5.1 days, with total infection till recovery lasting anywhere from 14-27 days. 80% of those infected will only experience mild or no symptoms, 14% will experience severe symptoms and 5% may require hospitalisation11. The actual death rate is hard to calculate as it is linked to age and co-morbidities but is estimated to be between 1-3%, with high-risk groups experiencing much higher risk of even up to 10-15%13.
New research looking at severe COVID cases has revealed high correlations with the presence of platelet-fibrin thrombi (blood clots) in small arterial vessels in the lungs14. Furthermore, one study from Italy demonstrated that the cause of death from autopsies of COVID patients who died was classified as hypoxemic respiratory failure from diffuse alveolar damage (DAD) due to multiple thromboembolisms (blood clots – Figure 6)15. What this tells us is that the virus is attacking the endothelial cells through oxidative processes leading to endothelial cell dysfunction (destruction of the blood vessel walls) and increased risk for thromboembolisms (blood clotting). This clinical finding is significant as it not only explains more about the mechanisms of disease progression but questions the way in which COVID is currently treated.
If this hypothesis is correct, this could suggest the benefit of using anti-thrombotic/coagulation regimens and, at the same time, utilising agents that could alter the inflammatory storm, thus protecting the blood vessel walls of the lungs and saving more lives16. In more simplistic terms, COVID-19 is more of a vascular disease than a lung disease and causes of death are more linked to blood clots of vessels in the lungs than traditional pneumonia. So should we be ventilating patients or should we be treating them with anti-inflammatories and anti-coagulants? Or both?
To understand why we are seeing such an increase of blood clotting in the lungs we need to look into the mechanisms of what is occurring post infection and understand the process of clotting in inflammation itself. Firstly, COVID-19 binds to cells via the ACE2 receptor site. The ACE2 receptor plays an important role of converting the inflammatory angiotensin II hormone (AT-II) to the anti-inflammatory angiotensin 1,7 (AT-1,7). AT-II is a pro-inflammatory hormone that promotes the production of reactive superoxide while AT-1,7 is anti-inflammatory and removes superoxide17. So we see a resulting accumulation of inflammatory AT-II and a deficiency of AT-1,7 (Figure 7). This shifts the cellular environment into a state of oxidative stress.
Secondary to this polymorphonuclear leukocytes (PMNs) like neutrophils, eosinophils, and basophils, from the innate immune system are stimulated to produce more superoxide to attack the viral infection18. The result of these interactions is a marked increase in production of superoxide. Superoxide is a reactive oxygen species (ROS) that induces damage to the endothelial cells that line the interior surface of blood vessels causing endothelial cell dysfunction19.
Figure 7. Proposed progression of COVID-19 infection leading to thrombosis.
Endothelial cells maintain the integrity and elasticity of our blood vessels. In addition they are involved in the production of nitric oxide that dilates the smooth muscle cells of the vessels and reduces blood pressure. Disruption of endothelial function reduces production of nitric oxide and can increase blood pressure, vascular stress and inflammation20. Once damaged the endothelial cells rupture to release large glycoproteins from the sub-endothelium layer called Von Willebrand factors (VWFs) that mediate adhesion and aggregation of platelets at sites of vascular injury21. VWFs are involved in blood coagulation and stimulate the accumulation of platelets through what is known as disulphide bond formation, eventually resulting in blood clotting and destruction of lung blood vessels22(Figure 8). Once blocked the blood vessels feeding the lungs struggle to oxygenate the blood to the body and the person becomes severely hypoxic (deficient in oxygen).
Infection follows 10 key pathophysiological steps:
Step 1: COVID-19 binds the host cells via the ACE2 receptor, this blocks ACE2 and reduces its expression in lung cells
-> ACE2 receptor levels decrease
Step 2: This reduction in ACE2 function therefore prevents the conversion of AT-II to AT-1,7
-> Production of AT-1,7 decreases
Step 3: Increased levels of AT-II promote increased production of superoxide
-> Superoxide levels increase
Step 4: Reduced levels of AT-1,7 cause an inability to effectively reduce superoxide and promotes an oxidative environment
-> Superoxide levels increase further
Step 5: PMNs from the innate immune system are stimulated to produce more superoxide to attack the viral infection
->Superoxide levels continue to increase
Step 6: Elevated levels of superoxide and other reactive oxygen species stimulate the production of cytokines that creates a cytokine storm
-> Cytokine levels increase, creating more inflammation
Step 7: Localised oxidative stress causes destruction and dysfunction of endothelial cells In the blood vessels.
-> Endothelial cell dysfunction
Step 8: Endothelial cell dysfunction causes the release of Von Willebrand factors (VWFs) from the sub endothelial space
-> VWF levels increase in the blood
Step 9: VWFs and oxidative stress causes thrombosis of lung vessels leading to hypoxia and respiratory complications
->Thrombosis occurs in the lungs
Figure 8. As COVID-19 binds and down-regulates ACE2, we see a perfect storm of inflammation occurring that impacts on vascular function and leads to thrombosis and the over production of life-threatening blood clots.
In essence we see a massive over-production of oxidative species and the body rapidly becomes oxidatively stressed creating a cytokine storm. This storm after viral infection has been linked to dysfunction of the renin angiotensin system (RAS), which influences blood pressure and fluid/electrolyte balance, and enhances inflammation and vascular permeability in the airways23. In addition it heavily impacts the vascular system by disrupting the endothelial cells that line the blood vessels. So the progression of complications seems to be more closely related to vascular function than pulmonary function. Supporting the notion that we are dealing more with a blood vessel disease than a lung disease.
Our body has natural defences against cytokine storms and oxidative stress in the form of antioxidant enzyme systems. The antioxidant enzymes, superoxide dismutase (SOD), glutathione peroxidase (GPx) and catalase form the primary defence system against reactive species like superoxide and oxidative stress24. SOD converts superoxide (O2–) to hydrogen peroxide (H2O2)25, while GPx is responsible for the conversion of H2O2 and other organic peroxides, to harmless water and oxygen (Figure 9)26.GPx then recycles back to an active form using the co-factor glutathione (GSH), which itself is reduced back to an active form by GSH-reductase27. As a system these enzymes and molecules work together to maintain oxidative balance and to reduce the risk of endothelial cell dysfunction and further vascular complications.
Figure 9. Glutathione peroxidase (GPx) with its co-factor glutathione remove harmful oxidants and return oxidative balance to the cells, preventing further severe complications from infection.
Those at high risk for complications with COVID are people that are already experiencing oxidative stress from other chronic health conditions. High risk groups include those with Hypertension, Cardiovascular disease, Diabetes, Chronic respiratory disease, Cancer, Renal disease, and Obesity (Figure 10)28. In all these conditions patients already have high levels of oxidative stress, elevated superoxide and inactive or insufficient levels of protective enzymes like GPx and glutathione. In addition, levels and activity of these cellular defence systems decrease with age29, which leaves the elderly already in this category and a possible reason why they face mortality rates much higher than younger people. In fact one recent study30 demonstrated that glutathione deficiency is the most plausible explanation of why people with established risk factors have severe clinical manifestations of COVID-19 infection and increased risk of death. The authors observed that patients with moderate-to-severe infection had lower levels of glutathione (GSH), higher levels of ROS (reactive oxygen species e.g. superoxide) and greater ROS/GSH ratios than patients with a mild illness. This also suggests that COVID-19 cannot actively replicate at higher levels of cellular glutathione, and a lower viral load is manifested by milder clinical symptoms. So could the glutathione system be the key determinant of COVID-19 outcome – an underprepared glutathione system leaves people at higher risk while a balanced and boosted glutathione system promotes quicker recovery and reduced severity of symptoms.
Figure 10. Risk factors for COVID complications based on their ability to create inflammation, reduce cellular levels of glutathione and upset endothelial cell function.
NAC – N-acetylcysteine is a natural precursor to glutathione and mucolytic agent that breaks down thick mucus by reducing disulphide bonds in coagulants31. Supplementation with NAC has been shown to build levels of glutathione in the body32 and in pulmonary cases to loosen thick mucus and improve respiratory outcomes33. Recent case studies from a New York hospital demonstrated that supplementation with glutathione, N-acetyl-cysteine (NAC) and alpha lipoic acid may represent a novel treatment approach for addressing “cytokine storm syndrome” and respiratory distress in patients with COVID-19 pneumonia34. Patients that were classified as in a severe or life-threatening state found improvements within an hour of treatment from high doses of glutathione precursors. This study is supported by previous studies assessing the effectiveness of NAC in acquired pneumonia and similar respiratory issues in which patient symptoms rapidly improved with NAC supplementation35.
Further to this NAC may be highly beneficial in reducing blood clots during COVID-19 infection by preventing cross-linking of platlet von Willebrand Factor (VWF) multimers and restoring blood flow to areas previously blocked36. This is due to the ability of NAC to act as a disulphide reducing agent that can prevent VWF proteins from cross linking during coagulation (Figure 11)37. This dual approach of reducing oxidative damage and preventing the formation of life-threatening blood clots may explain the positive results seen in the study outlined above in which patients saw rapid reductions in complications with supplementation of NAC. Based on these findings authors of both studies31,34 suggest that NAC should be used as a preventative against COVID-19 infection to reduce risk of complications and poor health outcomes. In addition, evidence supports the use of Lipoic acid (a glutathione precursor also used in the study) and supplementation of glutathione peroxidase (GPx) through increased Selenium intake.
Figure 11. NAC has the unique ability to cleave disulphide bonds to prevent coagulation of mucus as a mucolytic for respiratory issues (left). Secondly it can act as a direct antioxidant or indirectly by boosting natural glutathione production (right).
We have formulated an all-in-one nutraceutical that ticks all these boxes and acts as a potent antioxidant glutathione booster through building cellular glutathione, GPx and by reducing mucous build up and coagulation through NAC to reduce the risk of complications if infected. It is a preventative that will boost natural immunity and prepare the body should COVID-19 infection unfortunately occur. GPx Cell Protect is a unique formula of essential natural products that the body requires to build and recycle GPx and your cellular defence systems from inflammation. GPx Cell Protect will increase your circulating levels of GPx and allow it to recycle more rapidly, ensuring it stays active for longer. The result is a significant reduction in the impact of oxidative stress, increased energy and better immunity against colds, flu and viral infections like COVID-19.
COVID-19 is a novel coronavirus that infects cells via the ACE2 receptors
ACE2 down regulation causes a perfect storm of inflammation leading to endothelial cell damage and vascular complications, including life-threatening thrombosis (blood clotting) in the lungs
Those at higher risk for COVID-19 complications include people with inflammatory co-morbidities like heart disease, diabetes, insulin resistance, obesity, metabolic syndrome, high blood pressure and old age
Some new studies have shown that glutathione deficiency is a determinant of complication severity and poor health outcomes with COVID-19
Supplementation with N-acetylcysteine (NAC) in a clinical setting was able to improve symptoms within an hour of administration for severely ill COVID-19 patients
NAC works as a mucolytic by cleaving disulphide bonds to reduce risk of thrombosis and as an antioxidant to build cellular glutathione and reduce vascular inflammation and oxidative stress
Supplementing the glutathione system with NAC, lipoic acid and Selenium may be a novel way to prevent and reduce the severity of COVID-19 complications
GPx Cell Protect is a novel all in one NAC, GPx and glutathione booster that can help build immunity towards viral infections and reduce the risk of complications
Video Key Timestamps:
2:04 What is COVID-19?
5:00 How does the body’s immune system respond to infection?
10:26 How does COVID-19 kill?
15:38 How does COVID-19 create life-threatening blood clots?
36:56 How does the body protect from superoxide and oxidative stress?
41:31 Why are some people at higher risk for complications with COVID?
46:40 Is NAC a potential treatment option or preventative to help protect against COVID-19?
53:49 What are some natural products that can be used to help reduce risk for severe covid complications?
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- Pulmonary post-mortem findings in a large series of COVID-19 cases from Northern Italy. Luca Carsana, et al.medRxiv 2020.04.19.20054262.
- Saba L, Sverzellati N. Is COVID Evolution Due to Occurrence of Pulmonary Vascular Thrombosis?. J Thorac Imaging. 2020;10.1097/RTI.0000000000000530.
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- Heather K. Lehman, Brahm H. Segal, The role of neutrophils in host defense and disease, Journal of Allergy and Clinical Immunology, 2020,ISSN 0091-6749.
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- J. Deanfield, A. Donald, C. Ferri et al., “Endothelial function and dysfunction. Part I: methodological issues for assessment in the different vascular beds: a statement by the working group on endothelin and endothelial factors of the European society of hypertension,” Journal of Hypertension, vol. 23, no. 1, pp. 7–17, 2005. (c) Escher R, Breakey N, Lämmle B. Severe COVID-19 infection associated with endothelial activation [published online ahead of print, 2020 Apr 15]. Thromb Res. 2020;190:62.
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Written by Dr Corin Storkey Founder and Director of Seleno Health. www.selenohealth.com
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