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The mechanism of illness post Covid-19 infection and vaccination exposes a safe and effective therapy

Summary:

 

1. Covid-19: The big picture

2. Gp120 & CD4 receptors

3. The mechanism of illness post Covid-19 infection (long-Covid) and vaccination

    (Res

4. The mechanism of illness post Covid-19 infection (long-Covid)

    and vaccination (Detailed).

5. Gp120 induced CD4 deficiency explains the large number 

    of diverse Covid-19 symptoms, (brief examples).

6. As with HIV, so with SARS-CoV-2

7. Outlining a simple, safe and effective therapy for Covid-19

    post infection and vaccination.

8. Does dietary copper reduce the symptoms of Covid-19 illness?

9. The Covid-19 - cancer connection

10. A warning from the author

11. References

There are 2 very distinct phases to Covid-19 illness. I have separated these into Phase 1 and Phase 2. To restore health, BOTH must be addressed in chronological order. See the Get Well Fast Now Protocol 

  • Phase 1 of Covid-19 = induced CD4 deficiency symptoms.

  • Phase 2 of Covid-19 = induced kidney insufficiency/failure & dysfunctioning RAS (Renin-Angiotensin System). Resulting in impaired energy production, fluid loss and imbalance, lymphatic congestion and metabolic waste accumulation, impairing spike protein elimination that must pass through the kidneys, developing into interstitial acidosis, chronic inflammation and multiple tissue/organ damage and dysfunction.

1. Covid-19: the big picture

 

The hallmark of Covid-19 is a climate of disinformation, distractions and censorship, created by contradictions and confusion. In order to sift through the information, we need to clear everything we think we know about Covid-19, and go back to the very beginning. By looking at the information that has been censored, we are able to uncover the mechanism of illness post Covid-19 infection and vaccination, leading us straight to a safe, cheap and effective solution.

 

2. Gp120 and the CD4 receptors

 

If there is one thing that Covid-19 has taught us, it is that when information is violently censored, you can be sure it is directly over the target.

 

To understand the mechanism behind Covid-19 illness, we must first realize that the main point of entry for SARS-CoV-2 into cells is not ACE2, but CD4 receptors. Well documented, yet violently censored in official conversations, is the presence of the gp120 gene insert in the SARS-CoV-2 genome, which binds to CD4 cell receptors. It is interesting to note that the ACE2 theory was never censored, in my view ACE2 has served as a useful distraction, diverting attention from gp120. (ACE2 is affected by SARS-CoV-2, but at a later stage through the impaired function of the reninangiotensin-system, due to tissue damage in the kidney’s distal convoluted tubules and the neighboring macular densa cells.)

It is also important to note that the ACE2 theory does not always correspond to the location of tissue damage throughout the body, where gp120 does. But more importantly therapeutics targeting ACE2 do not significantly improve Covid-19 patient status, whereas a simple protocol that targets CD4 cells literally transforms the patient’s health from day 1, with a significant reduction in symptom severity and occurrence in under 1 week.

Example: There is an abundance of ACE2 receptors in the kidney’s proximal tubules and few ACE2 receptors in the kidney's distal tubules, yet more damage and SARSCoV-2 infiltration is detected in the kidney’s distal tubules. …in autopsy kidney samples, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) nucleoprotein was detected in ACE2+ or TMPRSS2+ renal tubular cells, whereas the RNAscope® Assay targeting the SARS-CoV-2 Spike gene was positive mainly in the distal tubular cells and seldom in the proximal tubular cells. In addition, the TMPRSS2 and kidney injury marker protein levels were significantly higher in the SARS-CoV-2-infected renal distal tubular cells, indicating that SARS-CoV-2-mediated AKI mainly occurred in the renal distal tubular cells.” (1) (AKI = acute kidney insufficiency). Kidney damage caused by SARS-CoV-2 occurs mostly in the distal tubules, where there are few ACE2 receptors, but CD4 cells are abundant

 

3. The mechanism of illness post Covid-19 infection (long-Covid) and vaccination (Resume).

 

• Covid-19 illness is mediated by gp120 binding to CD4 receptors on immune cells (T-lymphocytes, monocytes, macrophages, and dendritic cells), which enter tissues and organs carrying SARS-CoV-2 into the cells along with them.

 

• A CD4 deficiency is the cause of early Covid-19 symptoms; (chronic fatigue, myocarditis, renal (AKI/CKD), pulmonary/neurological/reproductive/immune impairment…)

 

Dietary copper is required by the thymus for CD4 cell maturation. When a person is copper deficient, CD4 cell levels are not restored and therefore CD4 deficiency symptoms listed above worsen. Correction of dietary copper levels restores CD4 numbers and function “1 week”, at which time all Covid-19 symptoms are greatly reduced in severity and occurrence. (HOWEVER, to restore health, SARS-CoV-2 spike protein still needs to be eliminated and tissue damage repaired.)

 

• SARS-CoV-2 “severely damages” the kidneys, deregulating RAS (ReninAngiotensin System), leading to impaired water-solute balance and reabsorption, a reduction in waste elimination and an ACE2 deficiency. This triggers chronic inflammation, interstitial acidosis, oedemas, tissue/organ dysfunction, a vast array of skin conditions as the skin (the body’s largest elimination organ) tries to alleviate kidney impairment by aiding in waste elimination through the pores of the skin

4. The mechanism of illness post Covid-19 infection (long-Covid) and vaccination (Detailed).

 

Unravelling the Covid-19 – CD4 connection

 

In January 2020, a group of Indian scientists published a paper titled, Uncanny similarity of unique inserts in the 2019-nCoV spike protein to HIV-1 gp120 and Gag, (2) (2019-nCoV was the original name given to Covid-19). The authors of the paper explained they discovered the presence of 4 unusual gene inserts in the genome of SARS-CoV-2 that were similar to genes unique to the HIV virus. Of capital importance, they confirmed these gene inserts are located on the virus binding site, which determines where and how the virus causes disease in the body. The paper states; “We found 4 insertions in the spike glycoprotein (S) which are unique to the 2019- nCoV and are not present in other coronaviruses. Importantly, amino acid residues in all the 4 inserts have identity or similarity to those in the HIV-1 gp120 or HIV-1 Gag. Interestingly, despite the inserts being discontinuous on the primary amino acid sequence, 3D-modelling of the 2019-nCoV suggests that they converge to constitute the receptor binding site. The finding of 4 unique inserts in the 2019-nCoV, all of which have identity /similarity to amino acid residues in key structural proteins of HIV1 is unlikely to be fortuitous in nature. This work provides yet unknown insights on 2019-nCoV and sheds light on the evolution and pathogenicity of this virus with important implications for diagnosis of this virus. (3) Stating further that the gp120 inserts “…fold to constitute the part of glycoprotein binding site that recognizes the host receptor”. (4) The host receptor of HIV’s gp120 is CD4, not ACE2, and understanding the location and role of CD4 cells “sheds light on the evolution and pathogenicity of this virus with important implications for diagnosis of this virus”.

 

Nobel Prize laurate, and discoverer of HIV, Professor Luc Montagnier, detected and confirmed the findings published in the Indian paper; HIV inserts gp120 and Gag are located in the SARS-CoV-2 genome.

 

Covid-19 mechanism of action – Gp120 & CD4 cells:

 

Covid-19 mechanism of action – Gp120 & CD4 cells: Transmembrane TNF-alpha (via α4β7 integrin) facilitates the gp120 gene on the SARS-CoV-2’s binding site to enter into CD4 cell receptors on the epithelium of immune cells such as macrophages, lymphocytes, monocytes and dendritic cells. This increases the release of Interferon 1 (IFN 1), as “release of type I IFNs is one of the most potent mechanisms of innate immunity against viruses and other intracellular pathogens.” (5) Which we witness in SARS-CoV-2 infiltrated immune cells, in response to increased TNF-alpha.

 

How the HIV and SARS-CoV-2 viruses are able to infiltrate tissues and organs that do not have CD4 cells was a mystery, until a paper was discovered published in the Journal of the American Society of Nephrology, in 2016, which explains “No one understood how HIV could affect kidney cells that lack the receptors expressed in T cells and white cells.” (6) (CD4 cell receptors). Until nephrologists discovered Transmembrane TNF-alpha facilitates gp120 entry into certain cell types, enabling HIV, (and therefore also SARS-CoV-2), to enter cells and replicate, saying; “like a Trojan horse, the macrophage sits atop the epithelial cell with HIV hidden inside, opening a doorway into the kidney cell for high levels of HIV-1 to enter.” (7)

 

As with HIV, so is SARS-CoV-2

 

This process of “local immune cell infiltration” is witnessed in Covid-19; “Tissue inflammation and local immune cell infiltration have been repeatedly observed and might have a critical role in kidney injury.” (8)

5. Gp120 induced CD4 deficiency explains the large number of diverse Covid-19 symptoms, (brief examples)

 

CD4 deficiency effects on the nervous system

“The Human Immunodeficiency Virus (HIV), which causes the disorder Acquired Immunodeficiency Syndrome (AIDS), primarily affects the immune system but also can lead to a wide range of severe neurological disorders, particularly if HIV goes untreated and progresses to AIDS. Many of the most severe neurological conditions can be prevented with antiretroviral therapy. HIV does not directly invade nerve cells (neurons) but puts their function at risk by infecting cells called glia that support and protect neurons. HIV also triggers inflammation that may damage the brain and spinal cord (central nervous system) and cause symptoms such as: Confusion and forgetfulness, inability to concentrate, behavioral changes, headaches, mood disorders (anxiety disorder and depression), movement problems (loss of movement control) including a lack of coordination and difficulty walking.” (9)

 

As with HIV, so with SARS-CoV-2.

The Medical News Today, published an article in 2022, titled: Nerve damage in long COVID may arise from immune dysfunction. Stating; “New research sheds light on neuropathies in long COVID, suggesting immune dysfunction may be to blame for the nerve damage.” (10)

 

Coincidently SARS-CoV-2 infection or post vaccination are: Confusion and forgetfulness, inability to concentrate, behavioral changes, headaches, mood disorders (anxiety disorder and depression), movement problems (loss of movement control) including a lack of coordination and difficulty walking.

 

• The journal Neurology, published a paper in 2022, titled: CSF-Derived CD4+ TCell Diversity Is Reduced in Patients With Alzheimer Clinical Syndrome. Outlines when CD4 cells which are abundant in the Central Nervous System are reduced, cognitive decline occurs. Also sparking nerve dysfunction including tremors, seizures and involuntary movements. (11)

 

CD4 deficiency in myocarditis

 

• The journal Frontiers in Immunology, published a paper in 2020, titled: Dysregulated CD4+ T Cells and microRNAs in Myocarditis, states “CD4+ T cells are key pathogenic factors underlying the development and progression of myocarditis”. (12)

 

• The Journal of Immunology Research, published a paper in 2018, titled “Regulatory Role of CD4+ T Cells in Myocarditis”. (13)

 

CD4 deficiency effect in immune impairment

 

• The journal Immunological Reviews, published a paper in 2013, titled; CD4(+) T-cell depletion in HIV infection: mechanisms of immunological failure, stating; “The hallmark of acquired immunodeficiency syndrome (AIDS) pathogenesis is a progressive depletion of CD4(+) T-cell populations in close association with progressive impairment of cellular immunity and increasing susceptibility to opportunistic infections (OI)” (14)

 

As with HIV, so with SARS-CoV-2.

 

• The journal of Frontiers in Immunology published a paper in 2020, titled; Sharing CD4+ T Cell Loss: When COVID-19 and HIV Collide on Immune System. Stating: “Like for HIV, lymphopenia and drastic reduction of CD4+ T cell counts in COVID-19 patients have been linked with poor clinical outcome.” (15)

 

CD4 deficiency effect in respiratory impairment

 

• The journal of Clinical Immunology published a paper in 2021, titled; Expansion of Cytotoxic CD4+ T cells in the lungs in severe COVID-19. Stating; “We establish here that cytotoxic CD4+ T cells (CD4+CTLs) are prominently expanded in the COVID-19 lung infiltrate. CD4+CTL numbers in the lung increase with disease severity and progression is accompanied by widespread HLA-DR expression on lung epithelial and endothelial cells, increased apoptosis of epithelial cells and tissue remodeling.” (16)

 

CD4 deficiency effect in kidney insufficiency

 

• In the journal Nephrology Dialysis Transplantation, a paper was published in 2006, titled: Distal renal tubular acidosis in association with HIV infection and AIDS. (17)

 

As with HIV, so with SARS-CoV-2.

 

MedRxiv published a paper in April, 2020, by a group of scientists working in Wuhan, China, titled: Human Kidney is a Target for Novel Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) Infection. The authors stated “SARS-CoV-2 mediated ARF may be one of the major causes of multiorgan failure and eventual death in COVID-19 patients” (18)

 

The paper conclusion reads: “SARS-CoV-2 induces ARF in COVID-19 patients. Viruses directly infect human kidney tubules to induce acute tubular damage. The viruses not only have direct cytotoxicity, but also initiate CD68+ macrophage together with complement C5b-9 deposition to mediate tubular pathogenesis.” (19) Concluding: “SARS-CoV-2 induces ARF in COVID-19 patients.” (20) (ARF = Acute Renal Failure).

 

• The journal Frontiers in Cell and Developmental Biology published a paper in 2021, titled; SARS-CoV-2 Causes Acute Kidney Injury by Directly Infecting Renal Tubules. The authors state: “The renal distal tubule was highly damaged in severe COVID-19 patients.” (21)

6. As with HIV, so with SARS-CoV-2

 

If gp120 in HIV and SARS-CoV-2 have the same mechanism of action, entering the same cells via the same CD4 receptors, inducing the same CD4 deficiency, which leads to the same CD4 deficient symptoms, we should see an overlap in symptoms, which we do. Perhaps more importantly however, we should also see the same therapeutic effect if a treatment is found. To explain the solution for SARS-CoV-2, based on his position as one of the world’s leading HIV and Covid-19 experts, I will allow the manof-the-hour, Dr Anthony S Fauci himself explain the solution.

 

Dr Anthony Fauci, ex-Director of NIAID, who is coincidently the same leading figure behind HIV & SARS-CoV-2 research, knows the importance of the role of gp120 in HIV, stating on his NIAID webpage; “Understanding the complexities and significance of the signalling processes that gp120 mediates will enhance our understanding of HIV-1 pathogenesis and may facilitate the discovery of new strategies for the treatment and prevention of HIV-1 disease.” (22)

 

Dr Anthony S Fauci is so convinced that gp120’s interaction with the active glycoprotein Alpha(4)beta(7) integrin / α4β7 located on CD4 cells allowing gp120 to infiltrate immune cells is the cause of HIV pathogenicity (and therefore also of SARS-CoV-2), that he, and his colleagues, applied for and were granted, a patent in September, 2016 for any agent used that “affects the interaction of HIV GP120 and α4β7integrin.” (α4β7 being a “glycoprotein found on activated CD4 + T cells”.) (23)

 

The title of this Patent: 9441041, is “Use of antagonists of the interaction between HIV GP120 and α4β7 integrin”. Filed: September 21, 2015. Date of Patent: September 13, 2016. Assignee: The United States of America, as Represented by the Secretary, Department of Health and Human Services. Inventors: James Arthos, Diana Goode, Claudia Cicala, Anthony S. Fauci. (24)

 

The patent itself reads; “Methods are provided for the treatment of a HIV infection. The methods can include administering to a subject with an HIV infection a therapeutically effective amount of an agent that interferes with the interaction of gp120 and α4β7 integrin, such as a α4β1 or α4β7 integrin antagonist, thereby treating the HIV infection.” (25)

 

In other words, the authors of the patent: 9441041, which include Dr Anthony S Fauci, claim rights on any “agent that interferes with the interaction of gp120 and α4β7 integrin”, as they believe that “a therapeutically effective amount” of any such agent will be effective in treating the HIV infection.” As in HIV, so as SARS-CoV2, as the mechanism of infection and pathogenicity are the same.

 

In hindsight this makes Dr Fauci’s farewell speech when he stepped down from his post at NIAID more intriguing, when he said “My career and my identity has really been defined by HIV.” (26) This may have sounded strange to many people after Fauci’s role in coordinating the entire worldwide Covid-19 response from insisting on mandatory face masks, lockdowns and his influence behind the use of the Covid-19 emergency use of mRNA vaccinations.

7. Outlining a simple, safe and effective therapy for Covid-19 post infection and vaccination.

 

There are 2 effective therapies for SARS-CoV-2 that I know of, one being Suramin, which inhibits the binding of gp120 with CD4 as confirmed in the journal of Antimicrobial agents and chemotherapy, for the American Society for Microbiology, in 1991, stating: “We have shown that suramin can directly inhibit the binding of the human immunodeficiency virus type 1 gp120 envelope protein to immobilized CD4.” (27)

 

However, Suramin is used as an injectable, and would be ideal in an emergency setting, but less so for the general public. There is however a natural molecule that increases CD4 cell synthesis, number and function in a matter of days, eliminating the CD4 deficiency symptoms we attach to Covid-19, and that is dietary copper (Cu1).

 

CD4 cell maturation is copper dependent, therefore when a person is deficient in dietary copper (Cu1), CD4 synthesis ceases, meaning the CD4 deficiency continues, therefore so do the CD4 deficiency symptoms.

 

The Journal Nutrition published a key paper in 1993, titled: Copper repletion restores the number and function of CD4 cells in copper-deficient rats. The authors state; “Copper is essential for the optimal function of the cellular and humoral branches of the immune system” (28), as copper “is required for maturation and signal-mediated proliferation of lymphocytes.” (29) The maturation of T-lymphocytes occurs in the thymus and requires copper to take place. Stating that the “activities of Cu-deficient neutrophils were restored to normal when rats were fed diet containing adequate Cu for 1 wk.” (30) (1 week). The thymus plays a key role in Covid-19 severity and health restoration due to its role in the maturation and proliferation of CD4 cells.

 

A great paper in the Annual Review of Immunology, in 1991 sums up the gp120-CD4 relationship perfectly, stating: “Infection by the human immunodeficiency virus (HIV) leads to progressive destruction of the CD4+ subset of T lymphocytes, resulting in immunodeficiency and AIDS. The selectivity of CD4+ cell destruction is due to the specific binding of gp120, the external envelope glycoprotein of HIV, to CD4, initiating viral entry. Binding of gp120 to CD4 on the cell surface may also lead to CD4+ cell depletion by inappropriate immune targeting, and may interfere with CD4+ cell function and ontogeny by disrupting CD4-mediated cell signaling. The CD4-gp120 interaction is thus an obvious target for AIDS therapeutics.” (31)

 

As with HIV, so with SARS-CoV-2

 

Despite all this information, perhaps the most important information, is that increased dietary copper (Cu1), significantly reduces the severity and occurrence of Covid-19 symptoms in just a few days. As witnessed so far on 70+ people post Covid-19 infection & vaccination

8. Does dietary copper reduce the symptoms of Covid-19 illness?

 

“Based on available data, we hypothesize that enrichment of plasma copper levels will boost the innate and adaptive immunity in people. Moreover, owing to its potent antiviral activities, Cu may also act as a preventive and therapeutic regime against COVID-19.” (32)

 

“…serum Cu and SELENOP levels contribute to a good prediction of survival. Adjuvant supplementation in patients with diagnostically proven deficits in Cu or Se may positively influence disease course, as both increase in survivors and are of crucial importance for the immune response and antioxidative defense systems.” (33)

 

Dietary chlorophyll, is a formulation derived from sodium copper chlorophyllin (SCC). “Therapeutic doses of SCC have been demonstrated to provide an effective clinical treatment for leukopenia. On this basis, we propose that taking SCC at the onset of symptoms or, for immunocompromised patients, at the time of diagnosis, could reverse the lymphopenia observed during COVID-19. It is envisaged that in symptomatic individuals SCC treatment could control leukocyte homeostasis, specifically of lymphocytes, thereby preventing their progressive reduction that is associated with severe disease outcomes. By first restoring and then maintaining adequate peripheral blood levels of CD4+ and CD8+ T lymphocytes this would enable the immune system of an SCC-treated COVID-19 patient to respond appropriately to resolve SARS-CoV-2 infection. Additionally, it may produce a synergistic effect as SCC is known to block expression of the pro-inflammatory cytokine IL-6. Hence, importantly, such SCC therapy would avoid triggering the characteristically excessive inflammation that causes lasting lung epithelial cell damage and cytokine storm events which often precipitate a fatal outcome of COVID-19.” (34)

 

And finally…

 

The EPA (the American Environmental Protection Agency) published an official press release regarding copper’s effect on Covid-19, February 2021“Today, the U.S. Environmental Protection Agency (EPA) is announcing that certain copper alloys provide long-term effectiveness against viruses, including SARS-CoV-2, the virus that causes COVID-19. As a result of EPA’s approval, products containing these copper alloys can now be sold and distributed with claims that they kill viruses that come into contact with them”. The document continues to state “EPA expects these products to eliminate 99.9 percent of SARS-CoV-2, the virus that causes COVID19, within two hours.” (35)

 

9. The Covid-19 – cancer connection

 

Why are cancer incidences rising post Covid-19?

 

Scientific censorship did not begin with Covid-19. In 1956 a brilliant paper was published in Science, by Nobel Prize laureate and 51- time Nobel Prize nominee; Dr Otto Heinrich Warburg, titled On the Origin of Cancer Cells. (36)

 

Warburg explained the 2 phases required for the transformation of normal cells into cancer cells. (Below is a very brief outline. To learn the full mechanism behind cancer I suggest you read my book GET WELL FAST.

 

Phase 1:

The cell’s struggle to survive and maintain its structure, leading to the death of cells due to a lack of energy. Warburg wrote; the “struggle for existence by the injured cells to maintain their structure, in which a part of the cells perish from lack of energy.” Which occurs due to kidney dysfunction/damage, as the kidneys regulate body fluids. Triggering the dehydration (hypertonic state) which ultimately reduces ATP production, as intracellular water is vital to ensure the Krebs cycle, and produce cellular energy. Kidney dysfunction is a major factor in cancer development before cancer occurs:

 

A paper published in Journal of the American Society of Nephrology, in 2009, titled: Association of CKD and Cancer Risk in Older People, (CKD = Chronic Kidney Disease), confirms that for every 10-ml/min/1.73m2 decrease in kidney filtration (GFR), the risk of cancer increases by 29%. (37) This refers to any kind of cancer, not just kidney cancer. Covid-19 patients are seeing a massive reduction in GFR, often losing between 20-50-ml/min/1.73m2. Triggering the first phase required to trigger cancer development.

 

Phase 2:

Some cells are able to survive this situation by switching energy production from respiration energy (from oxygen) to fermentation energy (from glycose). Warburg stated “… while another part succeed in replacing the irretrievably lost respiration energy by fermentation energy.” (38)

 

Cellular respiration is oxygen dependent, which is why Warburg said cancer cells require a state of hypoxia (lack of oxygen) and fermentation to be develop. Stating further: “To prevent cancer it is therefore proposed first to keep the speed of the blood stream so high that the venous blood still contains enough oxygen; second, to keep high the concentration of hemoglobin in the blood; third, to add always to the food, even in healthy people, the active groups of the respiratory enzymes.” (39)

 

Nobel Prize laureate Dr Hartmut Michel discovered the respiratory enzyme Warburg referred to was cytochrome c oxidase, which is copper dependent! The production of heme to make hemoglobin and the transport of iron, which enables the red blood cells to transport oxygen are also copper dependent! SARS-CoV-2 induces a deficiency of copper through the loss of CD4 cells. Ensuring the second phase required to trigger cancer development.

WARNING: SARS-CoV-2 initiates the 2 phases required for normal cells to transform into cancer cells, as such there will be a massive rise of cancer if the mechanism of cancer is not understood, and addressed.

To read the entire cancer mechanism and understand how to prevent and halt this situation, please read my book GET WELL FAST

https://www.getwellfastnow.com/shop

 

10. WARNING: There are 4 phases required to restore health.

Each phase needs to be completed in order

for the protocol to work correctly.

The GET WELL FAST NOW protocol is FREE here:

11. References:

 

(1) Front. Cell Dev. Biol., 31 May 2021 https://doi.org/10.3389/fcell.2021.664868 SARSCoV-2 Causes Acute Kidney Injury by Directly Infecting Renal Tubules. Zhaohui Chen, Junyi Hu, Lilong Liu, Rong Chen, Miao Wang, Ming Xiong, Zhen-Qiong Li, Yi Zhao, Hong Li, Chuhuai Guan, Jie Zhang, Liang Liu, Ke Chen and Yu-Mei Wang

(2) Uncanny similarity of unique inserts in the 2019-nCoV spike protein to HIV-1 gp120 and Gag https://www.biorxiv.org/content/10.1101/2020.01.30.927871v1.full

(3) Uncanny similarity of unique inserts in the 2019-nCoV spike protein to HIV-1 gp120 and Gag https://www.biorxiv.org/content/10.1101/2020.01.30.927871v1.full

(4) Uncanny similarity of unique inserts in the 2019-nCoV spike protein to HIV-1 gp120 and Gag https://www.biorxiv.org/content/10.1101/2020.01.30.927871v1.full

(5) Kuka, Mirela et al. “The role of type I interferons in CD4+ T cell differentiation.” Immunology letters vol. 215 (2019): 19-23. doi:10.1016/j.imlet.2019.01.013 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7234836/

(6) ‘Trojan horse’ macrophage TNF-alpha opens door for HIV-1 to enter kidney epithelial cells, causing nephropathy. November 18, 2016. https://innovationdistrict.childrensnational.org/trojan-horse-macrophage-tnf-alphaopens-door-hiv-1-enter-kidney-epithelial-cells-causing-nephropathy/

(7) ‘Trojan horse’ macrophage TNF-alpha opens door for HIV-1 to enter kidney epithelial cells, causing nephropathy. November 18, 2016. https://innovationdistrict.childrensnational.org/trojan-horse-macrophage-tnf-alphaopens-door-hiv-1-enter-kidney-epithelial-cells-causing-nephropathy/

(8) Legrand, M., Bell, S., Forni, L. et al. Pathophysiology of COVID-19-associated acute kidney injury. Nat Rev Nephrol 17, 751–764 (2021). https://doi.org/10.1038/s41581- 021-00452-0

(9) AIDS and HIV, Neurological Complications of. (NIH) National Institute on Neurological Disorders and Stroke. NIH website. https://www.ninds.nih.gov/healthinformation/disorders/aids-and-hiv-neurological-complications

(10) Annie Lennon on March 11, 2022. Medical News Today. Nerve damage in long COVID may arise from immune dysfunction. https://www.medicalnewstoday.com/articles/nerve-damage-in-long-covid-mayarise-from-immune-dysfunction

(11) American Academy of Neurology. January 2022. Chaitanya Joshi, Karthigayini Sivaprakasam, Scott Christley, Sara Ireland, Jacqueline Rivas, Wei Zhang, Danielle Sader, Rebecca Logan, Doris Lambracht-Washington, Roger Rosenberg, Munro Cullum, Brian Hitt, Quan-Zhen Li, Robert Barber, Benjamin Greenberg, Lindsay Cowell, Rong Zhang, Ann Stowe, Ryan Huebinger, Brendan Kelley, Nancy Monson. CSF-Derived CD4+ T-Cell Diversity Is Reduced in Patients With Alzheimer Clinical Syndrome. First published November 30, 2021, DOI: https://nn.neurology.org/content/9/1/e1106

(12) Wang J, Han B. Dysregulated CD4+ T Cells and microRNAs in Myocarditis. Front Immunol. 2020 Mar 25;11:539. doi: 10.3389/fimmu.2020.00539. PMID: 32269577; PMCID: PMC7109299. https://pubmed.ncbi.nlm.nih.gov/32269577/

(13) Vdovenko D, Eriksson U. Regulatory Role of CD4+ T Cells in Myocarditis. J Immunol Res. 2018 Jun 21;2018:4396351. doi: 10.1155/2018/4396351. PMID: 30035131; PMCID: PMC6032977. https://pubmed.ncbi.nlm.nih.gov/30035131/

(14) Okoye AA, Picker LJ. CD4(+) T-cell depletion in HIV infection: mechanisms of immunological failure. Immunol Rev. 2013 Jul;254(1):54-64. doi: 10.1111/imr.12066. PMID: 23772614; PMCID: PMC3729334.https://pubmed.ncbi.nlm.nih.gov/23772614/ (15) Peng X, Ouyang J, Isnard S, Lin J, Fombuena B, Zhu B, Routy JP. Sharing CD4+ T Cell Loss: When COVID-19 and HIV Collide on Immune System. Front Immunol. 2020 Dec 15;11:596631. doi: 10.3389/fimmu.2020.596631. PMID: 33384690; PMCID: PMC7770166. https://pubmed.ncbi.nlm.nih.gov/33384690/

(16) Kaneko N, Boucau J, Kuo HH, Perugino C, Mahajan VS, Farmer JR, Liu H, Diefenbach TJ, Piechocka-Trocha A, Lefteri K, Waring MT, Premo KR, Walker BD, Li JZ, Gaiha G, Yu XG, Lichterfeld M, Padera RF, Pillai S. Expansion of Cytotoxic CD4+ T cells in the lungs in severe COVID-19. medRxiv [Preprint]. 2021 Mar 26:2021.03.23.21253885. doi: 10.1101/2021.03.23.21253885. Update in: Clin Immunol. 2022 Apr;237:108991. PMID: 33791730; PMCID: PMC8010762. https://pubmed.ncbi.nlm.nih.gov/33791730/

(17) Chris M. Laing, Rhys Roberts, Shaun Summers, Jon S. Friedland, Liz Lighstone, Robert J. Unwin, Distal renal tubular acidosis in association with HIV infection and AIDS, Nephrology Dialysis Transplantation, Volume 21, Issue 5, May 2006, Pages 1420–1422, https://doi.org/10.1093/ndt/gfk055 https://academic.oup.com/ndt/article/21/5/1420/1822178?login=false

(18) Bo Diao, Chenhui Wang, Rongshuai Wang, Zeqing Feng, Yingjun Tan, Huiming Wang, Changsong Wang, Liang Liu, Ying Liu, Yueping Liu, Gang Wang, Zilin Yuan, Liang Ren, Yuzhang Wu, Yongwen Chen. Human Kidney is a Target for Novel Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) Infection. MedRxiv. doi: https://doi.org/10.1101/2020.03.04.20031120

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(20) Bo Diao, Chenhui Wang, Rongshuai Wang, Zeqing Feng, Yingjun Tan, Huiming Wang, Changsong Wang, Liang Liu, Ying Liu, Yueping Liu, Gang Wang, Zilin Yuan, Liang Ren, Yuzhang Wu, Yongwen Chen. Human Kidney is a Target for Novel Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) Infection. MedRxiv. doi: https://doi.org/10.1101/2020.03.04.20031120

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