Why Vitamin D3 is important in the prevention of severe respiratory viral disease

Vitamin D3, which is also known as cholecalciferol, represents a hormone that is produced by our organism as soon as the skin is exposed to UV radiation from the sun. Basically, there is a series of chemical reactions taking place in the skin before the vitamin is produced and taken into the system. Higher amounts found in the body are associated with a greater immunity against infectious pathogens, including the novel coronavirus, whilst lower amounts are generally associated with a weaker immunity and higher susceptibility to develop severe illness as a result of infection.

There is a number of misconceptions, which tend to be taken by mainstream journalistic and scientific agencies as evidence that Vitamin D3 has only a little efficacy against the novel disease. Diverse clinical study results show that hospital patients in the intensive care unit and those who are intubated due to COVID-19 complications did not display symptom improvement. The reason why this is likely the case is that the natural drug tends to be much more effective as a prophylactic and early therapeutic agent than a late therapeutic one. This is not new information, since many doctors and scientists, like Dr. Pierre Kory from the FLCCC alliance or Dr. Philip McMillan from Vejon Health, who worked very hard to save lives of COVID-19 patients by discovering and publishing treatment schemes with promising results, have warned the mainstream scientists and journalists, as well as the general public, that early treatment is crucial and that preventing is much easier than treating severe symptoms. It is important to acknowledge that over 80% of COVID-19 patients, in hospitals around the world, were also found to be Vitamin D3 deficient.

Important information about Interferons I and III

I believe the reason why Vitamin D3 can significantly prevent disease is the likely firm association between a high concentration of Vitamin D3 in the body and the ability of infected cells to robustly produce Type I Interferons (interferon-α and interferon-β), which represent the frontline workers of the immune system. Children and teenagers usually have a more alert Interferon I-based immunity and this may explain why they are the least likely to develop morbidity following infection. Type I Interferons are responsible with regulating inflammation and decreasing the viral load, and many clinical trials involving Interferon I-based therapy have shown the immuno-stimulating agents to be highly effective against various pathogens. Effectiveness of these interferons that were used at the right time and in the right amounts reached even diseases caused by radiation poisoning, the avian influenza strain (H5N1), the Human Immunodeficiency Virus (HIV) and a number of important sub-types of malignant tumours. 

A delayed production of Interferon I not only does not help improve symptoms usually, but can sometimes aggravate the disorder as well. Because this delay allows a sharper increase of the viral load, a latter intervention would only contribute to an over-sensitised and exaggerated interferon signalling. I believe this is why Vitamin D3 does not improve severe symptoms on more occasions. Another motive is more obvious, which is the fact that treating hyper-inflamed and damaged tissues in the bronchi and the lungs requires more than just a regular dosage of Vitamin D3 and other antioxidants.
The novel coronavirus is capable of camouflaging itself by producing a number of non-structural proteins (for example, nsp1, nsp10 and nsp16) to down-regulate and often even impair the synthesis of Type I Interferons, and this represents an important reason why many people end up in hospitals and in the Intensive Care Units as a result of infection. The non-structural protein 1 of the rotavirus and the porcine epidemic diarrhea virus was shown to impair Type III Interferon synthesis as well, and, given that interferon-lambda was only discovered in 2003, we strongly believe this is also the case with SARS-CoV-2 as well, and that would further highlight the need to resolve the gaps created by the pathogen in the first and second-line immune defences. As a result, adding a more significant quantity of interferon-lambda to the combination of interferon-alpha and beta might bring visible improvements to the potential interferon-based vaccine. Viruses might have adapted to the hidden powers of the innate immune system and started producing proteins that would impair such hidden powers that were developed as a result of human evolution against various strong pathogens. Likewise, we require to develop a counter-evolutionary response in order for humans to remain on the positive side of natural selection. Additionally, the likely reason why there is now a higher number of children and teenagers that have been admitted to the hospital following infection with the Omicron variant, in spite of the ten-fold lower mortality rate of the disease for the general population, is because it is more capable of down-regulating the synthesis of Type I Interferon than the previous variants.

A clear sign that the non-structural protein 1 produced by the (A)H5N1 and (A)H1N1 influenza strains, as well as the novel coronavirus, represents a problematic agent when it comes to suppressing first and second-line antiviral immune defenses is a clinical study involving swine that were infected with genetically attenuated Influenza viruses. These viruses had an induced deletion kind of mutation on the gene specifying the non-structural protein 1, and they were shown to be much easier to be tackled and disposed of by the immune system of the infected swine. Likewise, the ability of these Influenza A and SARS-CoV-2 viral variants to produce proteins that suppress first and second-line immune defenses represents nothing but a peak evolutionary response of certain pathogens against the hidden power that our innate immune systems display when exposed to pathogens with trickier infective and virulent mechanisms. Losing this sort of evolutionary battle would likely be caused by the loss of another evolutionary battle in the realm of psychology; human intelligence and manipulation of the masses to trust information that is in reality intellectually modest.

Figure 1: A more specific timeline of Interferon-alpha and Interferon-beta synthesis in the early stages of Herpes Simplex Virus 2 (HSV-2) infection (Amanda J. Lee and Ali A. Ashkar, 2018)

Given that interferon-β is generally produced around 40 hours before interferon-α is produced, possibly in slightly smaller amounts, and that it is interferon-β that stimulates the recruitment of Natural Killer Cells, which in turn stimulate the production of Type II Interferon (interferon-γ), I believe that a low-dose Interferon I-based therapeutic approach would reach its maximum potential if scientists used a combination of interferon-α and interferon-β, with a slightly higher quantity of the latter. Natural Killer Cells induce the programmed death of virally infected cells and require the activation by interferon-β to be able to recognise the infected cell and induce its death. Type II Interferon plays a further role in balancing immune responses and stimulating their antiviral mechanisms. Namely, interferon-gamma is secreted by infected cells to stimulate neighbouring cells to produce antiviral signals, and when the production rate of interferon-gamma is lower, there is a weaker ability of infected cells to prepare other cells against the pathogen. Overall, this problem leads to a negative domino effect, which perfectly explains why people actually become hospitalised, why a number of them unfortunately die, and why early treatment is actually important.

Interferon I and III-based immunisation and early treatment: the breakthrough we have all been looking for?

Since Type I Interferons simulate cellular infection and stimulate the development of a complete, healthy immune response, which involves rigorous anti-inflammatory and anti-pathogenic mechanisms, I believe that low-dose Interferon I and III-based nasal sprays should be trialed as a possible vaccine. Such nasal sprays could also contain a small amount of nitric oxide (NO) so the antiviral effects would be even more precise and further match the flexibility of the pathogen. The reason why this might be low-dose interferon-based nasal spray a potential vaccine for specific time frame is that a viral infection is simulated weeks to a few months before the actual infection, and likewise, signals are transmitted to neighbouring cells and immune components as if the cell became infected with the virus, and not only received an exogenous amount of interferon-alpha, beta and lambda. This might be a vaccine on a different dimension, and the level of focus is an intracellular one, from the moment pattern recognition receptors transmit signals of infection to the IFNA1, IFNA2 and IFNB1 genes, and likely even IFNL1, IFNL2 and IFNL3 genes, to the moment the mRNA encoding the interferons underwent the translation process, since the viral non-structural proteins impair the signalling of certain pattern recognition receptors and also bind to the ribosome and cut the mRNA that specifies the interferons.

With regards to classical methods of immunisation, I would like to mention that the option of using a UV-attenuated SARS-CoV-2 specimen with a deletion in the genes encoding the non-structural proteins 1 and 16 could have been a great vaccination candidate, had around 1% of the mRNA not been reverse transcribed by HIV-1/LINE-1 Reverse Transcriptases and a part of it inserted into coding DNA, and had the spike protein not acted as a superantigen, caused hyper-inflammation via Toll-Like Receptor 4 signalling, weakened genes implicated in DNA repair and antibody gene rearrangement, entered the lymphatic system and caused damage to the endothelium, crossing the endothelial barrier and entered the bloodstream. The main problem seems to be the great level of toxicity the spike protein has been displaying, especially through instances of severe disease and significant adverse reactions developed after the administration of spike protein-based vaccines. The dosage could involve a daily puff in each nostril, and the duration of the prophylactic session could last from two weeks to a month. If it is an early therapeutic approach, the spray could be administered only if symptoms are generally mild and weakening as a result of previous dosages. Likewise, this vaccine candidate would be of a long-term kind with regards to its dose administration.

An interferon-based approach would also directly support mucosal immunity, which has involvements in IgA antibody responses, support the development of an immune response from the most remote areas, to systemic areas where needed, and could outcompete the ability of the virus to self-camouflage. Moreover, interferon-lambda, which is part of the Type III Interferon class, also tends to be complementary with interferon-alpha with regards to inflammation. Specifically, interferon-alpha sometimes stimulate a few pro-inflammatory genes more than necessary, whilst interferon-lambda tends to be more restrictive against inflammation. Likewise, this is another sign that adding interferon-lambda to the interferon-alpha and interferon-beta-based nasal spray would make the effects of the compound more precise and accurate, and overall bring even better results, although interferon-alpha and interferon-beta alone have still brought amazing results with regards to therapy and immunisation.
Perhaps, if we paid more attention to the scientists developing methods of improving natural immunity, we would have had significantly fewer complications, medically, financially and societally.

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