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Proactively Stopping a Virus Before Severe Disease Manifests

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Specific Nutrients May Improve Your Innate Interferon Response


An article published in Progress in Cardiovascular Diseases proposes the use of nutritional supplements to enhance the body’s type 1 interferon immune response to influenza and coronaviruses.

“Activation of toll-like receptor 7 (TLR7) by single-stranded viral RNA trapped within endosomes provides a key stimulus to type 1 interferon induction by RNA viruses,” authors Mark F. McCarty and James J. DiNicolantonio wrote.

Based on this and other research findings, the researchers identified the antioxidant compounds lipoic acid, ferulic acid and sulforaphane as nutrients that may enhance TLR7-mediated induction of type 1 interferon.

Spirulina or a protein in spirulina extracts known as phycocyanobilin may also improve this response.

N-acetylcysteine (NAC) increases the production of glutathione and could also help protect TLR7 from damage due to oxidation.

Other medical literature has found that another mechanism of type 1 interferon response, the activation of mitochondrial antiviral-signaling protein (MAVS), can be upregulated by a high dose of glucosamine.

The provisional daily dosage suggestions for nutraceuticals that might aid control of RNA viruses including influenza and coronavirus were as follows:

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In mid-february, Dr. DiNicolantonio followed up in stating “Therefore, it is clear that certain nutraceuticals have antiviral effects in both human and animal studies. Considering that there is no treatment for the new coronavirus…we welcome further studies to test these nutraceuticals as a strategy to help provide relief in those infected with encapsulated RNA viruses.”

In theory, if one could detect initial infection with the SARS/Cov2 virus and mount an immediate type 1 interferon response, then the virus could be eradicated before serious COVID-19 disease manifested.


The delayed interferon response can be a factor that enables viruses to infect many cells and replicate out of control before the body’s adaptive immune system can mount an effective response.

This is because the cell's of the human body function a lot like assembly lines in factories and viral replication is essentially a hijacking of the assembly line. In the context of this example, using interferon therapy is a lot like cutting the power to the factory. Where applied ideally no viral products could continue to be viably produced. 

Interferon acts broadly to shut down cellular activity in the body and as a consequence it does come with noticeable side-effects that may outweigh its usefulness. 

Whether or not interferon will be beneficial all depends on one crucial variable, time! 

Upon initial exposure to an individual infected with COVID-19 it is more then likely that no more then a small handful of cells would become infected from the typical mechanism of a successful transmission.


Knowing that viral replication is an exponential function, it is only a short matter of time before a few infected cells become millions or billions of infected cells.

By this point, your immune system will be in crisis mode, producing loads of interferon and other anti-viral defenses. Generally speaking, if your immune system is incapable of or too late too put up these defenses, you may succumb to the virus, but where the immune system overdoes the response, you may succumb to your own immune system. 

But if interferon were to be given in what are known to be tolerable doses, immediately upon exposure to the virus, the infection could be stopped in its tracks.  


However, once systemic viral infection sets in, then excessive production of interferons may contribute to the “cytokine storm” while simultaneously turning down critical antiviral responses (such as inducing premature apoptosis of T-cells and depleting vital lymphocytes).


That’s why tamping down severely excessive inflammatory responses by targeting specific factors like IL-6 may be so important once COVID-19 progresses. This is important to clarify, interferon is an inflammatory factor, but it is only a net damage to your body when produced excessively, namely when it is too late and an infection has already run its course, when applied early it is a great net positive and should help prevent a great deal more inflammation then it will cause.

A study published on May 15, 2020, however, indicated that administration of the interferon-alpha drug in nebulized form (inhaled into the lungs) along with an anti-viral drug called (arbidol) reduced the duration of detectable SARS/Cov-2 (virus) in the upper respiratory tract with a concomitant reduction in IL-6 and C-reactive protein inflammatory markers.  

The full text to this is open label study of 77 hospitalized patients in Wuhan can be reviewed here.

Getting Through to Your Doctor When You Need to the Most


When pleading with your doctor for an unapproved cocktail of drugs they have limited or no previous clinical experience with, it helps far and above the theoretical to have clinical data handy that include dosages and outcomes for your doctor to review. 

A study published in The Lancet on May 8, 2020 found a triple drug combination of interferon-alpha, ribavirin, and lopinavir-rotonavir was more effective in alleviating symptoms and shortening the duration of viral shedding and hospital stay in patients with mild to moderate COVID-19 than lopinavir-rotonavir alone.

Here is link to full text article:

The New England Journal of Medicine picked up on this research and wrote the following summary on May 16 2020:

"A combination of three antivirals — Kaletra (which is lopinavir plus ritonavir) and ribavirin — when given early and with interferon significantly reduces viral shedding, disease symptoms, and hospital stay in  patients with COVID-19 when compared with a control regimen of Kaletra alone. The drugs are active against other coronaviruses, but the key factors seem to be interferon and promptness of treatment.

When the triple-drug combo was administered without interferon 7 days or more after the onset of symptoms, the results were no better than with Kaletra alone. Prof. Ivan Hung, the lead author on the report, explains that the researchers were afraid of prompting a cytokine “storm” if interferon was given after 6 days of symptoms — they’re not sure that that reluctance was well founded now. In any case, no patients died in either group.

The study was conducted in Hong Kong and has just been published in The Lancet. (An earlier study by another group published in the New England Journal of Medicine found no special benefit from Kaletra alone — a result seemingly confirmed by this study in The Lancet.)

In case you'd rather listen then read the study. Here is a link to the podcast:

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