Antiviral Immunotherapy – Hope against Multiple Viruses

by Frank M. Jordan MBA (Beta 1,3/1,6 glucan related U.S. Patents issued and applied for as co-inventor and U.S. Federal Court certified Expert Witness on Beta 1,3/1,6 glucan)

Antiviral immunotherapy may save your life!  What is antiviral immunotherapy and how does it help protect you today, especially against COVID 19 or any of the variants/mutations? Your body is equipped with a natural or innate immune defense system from birth, with this innate immune defense being your first line of protection against what seeks to harm you, including viruses.

Within this immune defense system of about 20 trillion cells are specific cells on alert to identify the existence and replication or expansion of a virus.

Specifically, the antiviral immune system of humans recognizes viruses that invade our body as foreign, meaning not produced naturally by the body but outside the body. These viruses are also recognized as dangerous to our continued health. The body’s recognition of these two factors triggers the innate immune response. The innate immune response when triggered attempts to interrupt the viral life-cycle which in turn stops and defeats the viral threat. The theory of “trained immunity” may also influence the reaction of cells to a virus when the innate immune response is triggered.

But let’s slow down to better understand how viruses invade and work in the body and then what in fact are those innate defenses against viruses. Why are these innate defenses sometimes unsuccessful in their defense goal and can we enhance their defensive capabilities?

First, we must understand that viruses are different from our natural body cells in that they have no defined home or walls. Viruses act as parasites which invade and then reside in and take over the functions inside normal cells, including the genetic reproduction capabilities.

What components of our innate immune response stop a virus from multiplying in the body after invading a living healthy cell host?

When a virus attacks your body, the innate defense responds by the internal issuance of interferons and the defensive action of NK or natural killer cells. Often these innate immune mechanisms react rapidly to eliminate the invading virus, but not always.

What are interferons?  Interferons (IFN) biologically are a group of glycoproteins produced by different cell types in response to various stimuli, such as exposure to a virus, bacterium, parasite, or other antigen. These Interferons I, II and III if not inhibited can prevent viral replication and the spreading of a virus to adjacent healthy cells.  Interferons do not kill a virus, but rather stimulate a normal cell to release its own interferons to counter-attack and interfere (thus the name) with an invading virus.

An innate immunity factor also involves NK or natural killer cells in the body that can be activated rapidly without previous antigen exposure and are designed to naturally destroy cells infected with a virus. These act rapidly but often with poor specificity, similar to killer missiles launched but without specific targets. Your NK cells are also limited in number, especially as you age.

Viruses of many types (influenza, common cold, SARS-CoV-2, etc., tuberculosis ) induce the secretion of interferons by attacked healthy cells. Stay with me – the secreted interferon molecules communicate by signalling back on the infected host cell by a process called autocrine* signaling. This process induces the expression of interferon-stimulated genes called ISGs, that in turn code for hundreds of antiviral molecules. These antiviral molecules can inhibit virus, but not without an internal battle with the invading virus.

In a second critical action, the interferons bind to adjacent non-infected cells by what is termed paracrine* signaling and enable these non-infected cells to attain an antiviral state that stops invading virus from reproducing. The secreted interferons can also confer a systemic antiviral immunity by endocrine* signaling throughout the body. This interferon function can help stop a viral riot that can result in what is often known as a cytokine storm.

A critically important characteristic of interferon is their ability to inhibit the growth of many different viruses, including influenza virus, various herpes viruses, and SARS-CoV-2 and its variants and mutations. No booster is needed for each virus, variant and mutation. Interferon represents a universal antiviral immunotherapy booster!  Today we have no other universal antiviral medication for multiple different viruses for antiviral protection, natural or otherwise.

What causes a failure or inhibited success in the innate immune defense against a viral invasion? While frequently the innate immune response is successful in killing the invading virus, at times an especially virulent virus attacks in high volume, including SARS-CoV-2 which causes COVID-19. To disable the interferon, the virus will respond by producing various proteins that act as interferon antagonist [interferon enemy]. If the interferons are inhibited from defending the attacked cell, the virus replicates and infects nearby non-infected cells. If repetitive in great volume a so-called cytokine storm occurs that can be intensely dangerous to health.

Many viruses, like SARS-CoV-2, invade extremely fast and with high volume viral replication. If not stopped or slowed down the viruses result in a severe infection and an innate overwhelmed viral immune system.

A second viral immune defense in the body is described as the adaptive or cell-mediated immune response, which features production of antibodies after evaluation of virus antigens that recognize and neutralize the attacking virus. Additional components are CD8 cytotoxic T cells; a T lymphocyte, or white immune cell, that directly attacks and destroys infected cells.

The adaptive immune response is a positive addition to your immune arsenal, but unfortunately can require several critical days to become protective, while an invading virus multiplies in the body in the interim. The innate immune system during these critical days attempts to delay replication of the virus until the adaptive immune response can become fully functional.  Success in this delay attempt is speculative at best. 

Visualize one fire truck (innate) at a five alarm multi-story fire attempting to help to keep the fire from spreading while waiting for the additional needed fire trucks (adaptive) including a hook-and-ladder truck capable of successfully fighting the multi-story fire. If the fire can be held in check until the additional trucks arrive, the building may not burn down.

A major negative factor in the current Pandemic involving SARS-CoV-2 related viruses is the ability of these viruses to inhibit the interferon antiviral response. This causes interference or failure of the paracrine interferon signaling to non-infected adjacent cells; thus inhibiting the interferon benefit of stopping virus replication and spread to other cells.

Certain natural biological defense modifiers and antiviral immunotherapy products, including beta 1,3/1,6 glucan, have demonstrated promise in blocking the ability of SARS-CoV-2 to disable interferon benefits. Success in this area would provide benefits in milder illnesses of shorter duration and reduce hospitalizations related to multiple viruses prevalent today and could save lives. Multiple studies involving beta 1,3/1,6 glucan are underway or reported with a review under the non-commercial website www.betagucan.org for beta glucan, Covid-19, trained immunity and interferon suggested for further information.

**Note: The key difference between “Autocrine” and “Paracrine” signalling is “Autocrine signalling” refers to the action of secretions by a cell on the same cells they secreted or produced.  “Paracrine signalling” refers to the action of secretions such as interferons on the cells nearby the original production cells. “Endocrine signalling” involves cells distributing secretions into the extracellular environment in the body.

Research:

Cell Rep, 2020 May 19;31(7):107634. doi: 10.1016/j.celrep.2020.107634.

β-Glucan Induces Protective Trained Immunity against Mycobacterium tuberculosis Infection: A Key Role for IL-1

Simone J C F M Moorlag ¹, Nargis Khan ², Boris Novakovic ³, Eva Kaufmann ², Trees Jansen ¹, Reinout van Crevel ¹, Maziar Divangahi ⁴, Mihai G Netea 

• PMID: 32433977 PMCID: PMC7242907 DOI: 10.1016/j.celrep.2020.107634

Abstract

“β-glucan is a potent inducer of epigenetic and functional reprogramming of innate immune cells, a process called “trained immunity,” resulting in an enhanced host response against secondary infections. We investigate whether β-glucan exposure confers protection against pulmonary Mycobacterium tuberculosis (Mtb) infection. β-glucan induces trained immunity via histone modifications at gene promoters in human monocytes, which is accompanied by the enhanced production of proinflammatory cytokines upon secondary Mtb challenge and inhibition of Mtb growth. Mice treated with β-glucan are significantly protected against pulmonary Mtb infection, which is associated with the expansion of hematopoietic stem and progenitor cells in the bone marrow and increased myelopoiesis. The administration of β-glucan may be used as a novel strategy in the treatment of mycobacterial infections and possibly as an adjuvant to improve anti-tuberculosis vaccines.

Netea, M.G., Domínguez-Andrés, J., Barreiro, L.B. et al. Defining trained immunity and its role in health and disease. Nat Rev Immunol 20, 375–388 (2020). https://doi.org/10.1038/s41577-020-0285-6

Quote: “…trained immunity represents the concept of long-term adaptation of innate immune cells rather than a particular transcriptional or functional program: indeed, different stimuli (for example, B-glucan, ..can induce different trained immunity programs). … Although trained immunity is controlled by distinctive mechanisms and is less specific and of shorter duration than adaptive immune memory, both fulfil the same principal function: a quicker and stronger response against pathogens and improved survival of the host.”

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