The corona virus (Covid 19) is a different form of virus from its predecessors. Its lethality has dramatically surpassed the former corona viruses. The mechanisms of toxicity include Adult Respiratory Distress syndrome (ARDS) and often, hypertension with an excessive loss of potassium. Covid 19’s ability to dock on to the Angiotensin 2 Receptor activates the Angiotensin system causing an inhibition of the vasodilator bradykinin and a hypertensive crisis.

The ARDS toxicity is caused by the generation of oxygen radicals, especially the product, peroxynitrite which leads to excessive toxicity in the lungs. The enzymes responsible for the toxicity are predominantly xanthine oxidase (XO), generating superoxide radical and the enzyme NADPH Oxidase which generates a hydroxy radical. The superoxide radical from XO combines with nitric oxide from the enzyme inducible nitric oxide synthase (iNOS) and generates the peroxynitrite. The inducible nitric oxide synthase is inhibited by nicotinamide and works along with the xanthine oxidase inhibitors.

There are methods of reducing the toxicity from these enzymes, either naturally or synthetically. Earlier data showed in Influenza B viral infections that inhibiting xanthine oxidase would indeed help to save lives in animal models. The drug used then was a very low dose of allopurinol, a gout drug that inhibits xanthine oxidase. However the dosage was only equivalent to 30 mg of allopurinol instead of the usual 300 mg that would be given to an adult man.

There are, however, many natural inhibitors of xanthine oxidase, usually flavonoids, that are simple for daily consumption or as teas. One of them is cherry extract but also rose hips are helpful to reduce xanthine oxidase levels. If allopurinol is used only 30 mg for an adult dosage is safe.

Additional mechanisms of toxicity are related to binding sites for the virus. There are several routes of entry for the virus to invade and often multiple ones are incorporated. Including the Angiotensin 2 receptor mentioned below, Inflammasomes, Furins and Viroporins. Melatonin blocks the inflammasomes, Furins are blocked by chrysin from many herbs as well as propolis. Viroporins are blocked by the antiviral compound, adamantine.

The antiviral substances have many mechanisms. Some prevent the docking of the virus in the body, such as monolaurin (a compound from coconuts) and humic acid (in forms such as shilajit and often combined with fulvic acid for trace minerals) are also effective in preventing the invasion of the virus.

Further for protection are inhibitors for viral replication that block an enzyme called NFKappa B. These are usually antioxidants including Vitamin C, which is across-the-board helpful for the immune system.

Additional support for the immune system comes from substances that increase interferon. such as licorice and olive leaf. They are released from the lymphocytes which can be by sulfa groups such as from acetylcysteine and even substances found in garlic.

Last but no least, the enhancement of interferon by zinc is well-known and certainly warrants taking zinc on a daily basis for protection and additionally: selenium, thuja and lysine are antiviral.

All of these factors are important to protect against the toxicity and the susceptibility to infections from the COVID19. It is not yet known if the patients who suffered from hypertension were indeed in greater danger of toxicity if they received an angiotensin-converting enzyme. It is thought that an ACE inhibitor may open up more binding sites for the COVID virus, which seems to bind to the angiotensin 2 receptor. Whether or not a direct Angiotensin 2 receptor inhibitor (ARB) will help is also not yet known.

Pharmacologically, the drugs that appear to be successful clinically, are Remdesivir, working against the RNA polymerase, and the HIV antiviral Kaletra, a protease inhibitor. Recently quinine, hydroxychloroqine plus zithromax have been shown to be effective in reducing the mortality in viral infected patients and helping to reduce the duration of the illness.

The importance of preventing the oxygen radical storm from cytokines and down-regulate the toxicity is of paramount important, however, the decreasing of the multiple pathways of entry is equally important and therefore a combination of support appears to be necessary to help decrease the mortalities and the toxicities seen with this virus.

Prof(hon) Dr. med. univ. Dana F. Flavin, Medial Director, www.collmed.org

 

References:

http://www.meddean.luc.edu/lumen/MedEd/elective/pulmonary/ards/ards_f.htm

https://europepmc.org/article/med/2278607

https://deepblue.lib.umich.edu/bitstream/handle/2027.42/26777/0000333.pdf?sequence=1

https://www.researchgate.net/publication/20876689_Oxidant_stress_adult_respiratory_distress_syndrome

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4711060/

https://www.sciencedirect.com/science/article/abs/pii/088394418790116X

https://academic.oup.com/jb/article-abstract/150/2/173/2182545

https://tmu.pure.elsevier.com/en/publications/role-of-nadph-oxidaseros-in-pro-inflammatory-mediators-induced-ai

https://www.atsjournals.org/doi/abs/10.1164/ajrccm.155.2.9032182?journalCode=ajrccm

https://grantome.com/grant/NIH/R21-HL145216-01

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https://www.evolutamente.it/covid-19-pneumonia-inflammasomes-the-melatonin-connection/