Did we get Covid-19 disease mechanisms wrong? Part 1

The ACE2 receptor theory for Covid-19 doesn’t entirely hold up… perhaps an alternative theory does

Understanding how SARS-CoV-2 and the COVID-19 ‘vaccines’ trigger illness is vital if we are to help those who are suffering. This series of 3 articles presents an alternative or complementary hypothesis to the ACE2 theory. It is the work of Janine Gallizia, author of Get Well Fast. I am pleased to share these three articles by Janine and trust that they will inspire important discussions on the mechanism, prevention and treatment of Covid-19 symptoms and vaccine-related disease.

Series Foreword

By Janine Gallizia

If you have been following the long list of symptoms attributed to post Covid-19 infection or Covid-19 GMO injection, one thing has become apparent: the official theory of how SARS-CoV-2 gets into cells doesn’t seem to hold up.

The official theory identifies the ACE2 receptor as the main entry for SARS-CoV-2 into cells, where it replicates and causes infection. However, the ACE2 theory is unable to explain most of the symptoms of Covid-19, Long Covid, post Covid-19 vaccination or the sudden rise in incidence of cancer, heart and vascular diseases, blood clots, cognitive decline, nerve damage, Creutzfeldt-Jakob disease (CJD), mitochondrial dysfunction, auto-immune disease, infections, infertility, and HIV false-positives. Perhaps an alternative theory can.

In this series of articles, I offer an alternative theory, which I believe will provide significant insights into how to treat Covid-19 related illness.

The mechanism of Covid-19 related illness comprises three distinct phases: the trigger, the inhibitor and the collapse of cell signalling.

Part 1 : The Trigger

By Janine Gallizia

Let’s step back in time to early 2020, when an alternative theory about Covid-19 disease was proposed. At the time, this theory was violently shut down and even branded as conspiracy, despite its author being a Nobel Prize Laureate.

The theory of Covid-19 by Nobel Prize Laureate Professor Luc Montagnier

On January 30th 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”.¹ ‘2019–nCoV’ and ‘2019 novel coronavirus’ were the first names given to the virus that creates the symptoms of Covid-19. The virus has since been named SARS-CoV-2.

The scientists explained they had found traces of HIV amino acids in the SARS-CoV-2 spike protein, and that these proteins were found on the spike protein binding site, which enabled the virus to enter human cells, where it replicated and caused infection. Not all cells have the corresponding receptor that permits SARS-CoV-2 entry into cells. Understanding which cells are directly infiltrated by the virus allows greater understanding as to the disease process that follows. It also opens up therapeutic opportunities. This is what the authors said: (Note: All text highlighted and underlined in this paper was done by the author of this document).

“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.”²

Professor Luc Montagnier, Nobel Prize Laureate

The World Health Organization describes HIV infection on its website, stating:

“The human immunodeficiency virus (HIV) targets cells of the immune system, called CD4 cells, which help the body respond to infection. Within the CD4 cell, HIV replicates and in turn, damages and destroys the cell. Without effective treatment of a combination of antiretroviral (ARV) drugs, the immune system will become weakened to the point that it can no longer fight infections and diseases.”³

The normal CD4 count range in a healthy person is approximately 500 to 1500 cell/mm3. In untreated HIV infection the number of CD4 immune cells declines. With less than 200 CD4 cells/mm3, a diagnosis of AIDS usually follows.⁴ Thus, if an HIV-infected person maintains sufficient levels of CD4 immune cells to conserve immune function they can live a normal, long heathy life.

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Nobel Prize Laureate and discoverer of HIV, Professor Luc Montagnier, detected and confirmed the findings published in the Indian paper, saying on live French television that he too had identified HIV fragments in the SARS-CoV-2 spike protein, specifically on the spike protein binding site (furin cleavage site). If the Indian scientists were right, it meant that SARS-CoV-2 is able to enter the same human cells, in the same manner that HIV does. In support of this theory are the unexplained HIV false-positives that have been detected post Covid-19 illness and vaccination.

A paper titled, “False-Positive Human Immunodeficiency Virus Results in COVID-19 Patients” was published in January 2023 in the scientific review Cureus. This paper reflects on the similarity of HIV’s protein GP41 to the SARS-CoV-2 spike protein, suggesting that SARS-CoV-2 and HIV “use their membranes through the same mechanism”. The authors stated that: “HIV-1 gp41 and SARS-CoV-2 share several structural sequences and motifs, including the N-terminal leucine/isoleucine repeat sequence and the C-terminal leucine/isoleucine repeat motif. In addition, the helix structures of SARS-CoV-2 and HIV gp41 are very similar, suggesting that both viruses are able to fuse their membranes through the same mechanism.”⁵

The scientific journal Clinical Infectious Diseases published a paper in August 2023 that concluded: “Based on our findings, patients with active COVID-19 appear significantly more likely to have an FP fourth-generation HIV test.” (FP = false-positive). The authors also confirmed similarities between HIV proteins and the SARS-CoV-2 virus spike protein, quoting an earlier paper, and offering a potential explanation as to why HIV false-positive diagnostics are occurring in Covid-19 patients:

“Zhang et al confirmed that 4 insertions unique to the 2019 novel coronavirus spike protein that are part of the receptor binding site of the 2019 novel coronavirus share similarities with HIV-1 proteins… suggesting potential cross-reactivity between Ags [antigens] of the 2 viruses. Zhang et al showed that these insertions were short, 6-8 amino acid segments and considered the relationship to HIV-1 as ‘coincidental’ and not specific, shared by other viruses. However, due to the nature of the test, an exact amino acid sequence homology to HIV is not required to yield an FP test result, which requires only enough antigenic similarity for a detectable amount of false signal.”⁶

For a better understanding of Covid-19, we need to look more closely at HIV.

It is well recognized that the HIV virus enters human cells by infiltrating CD4 immune cells. If the scientists above are correct, HIV proteins GP41 and GP120 are located on the SARS-CoV-2 spike protein, making CD4 the corresponding receptor for SARS-CoV-2 entry into human cells.

On the left, SARS-CoV-2/HIV virus with the spike protein, which includes segments of GP41 and at the tip (binding site) is GP120. On the right, a CD4 T cell with transmembrane α4β7 integrin, which binds to GP120.  The diagram is not to scale.

Understanding why CD4 cell numbers are reduced should lead us to natural therapies to restore and maintain CD4 cell numbers. These therapies would work in both HIV and SARS-CoV-2 infected populations.

If SARS-CoV-2 and HIV share the same proteins, does SARS-CoV-2 decrease CD4 cells?

If SARS-CoV-2 and HIV share the same proteins, namely GP120 and GP41, then SARS-CoV-2 would ultimately also decrease the number of CD4 cells, specifically T-lymphocytes (CD4+T cells), in the Covid-19 infected and vaccinated public, leaving them immunosuppressed and susceptible to infections from other pathogens, just as in HIV.

If this theory is correct, we should see SARS-CoV-2 infiltration directly into CD4 cells, leading to CD4 cell death and a drastic reduction in CD4+ T immune cell numbers in Covid-19 patients.

The Zhang and others (2020) meta-analysis published in Journal of Infection entitled ‘CD4+T, CD8+T counts and severe COVID-19: A meta-analysis’ found that “Acute infection with SARS-CoV-2 is associated with lymphopenia in approximately 80% of patients. Furthermore, lymphopenia with the suppression of B, helper (CD4+) and cytotoxic (CD8+) T cell function, is an indicator of a poor clinical outcome.”⁷

Later in 2020, Peng and others published a paper entitled ‘Sharing CD4+ T Cell Loss: When COVID-19 and HIV Collide on Immune System’ in Frontiers in Immunology that made the direct connection between CD4 cell loss in both HIV and SARS-CoV-2.⁸

In 2021, two further scientific papers reported dramatic reductions in immune system cells in Covid-19 infection. In BMC Infectious Diseases, Wen and others published a study entitled ‘Clinical characteristics and predictive value of lower CD4+T cell level in patients with moderate and severe COVID-19: a multicenter retrospective study’. The authors conclude that “The study showed that the absolute numbers of T-lymphocytes, CD4+T cells, and CD8+T cells were decreased in almost all COVID-19 patients, with significantly lower numbers in patients with severe COVID-19.”⁹

The other 2021 study by Petrovic and others, published in Chest, the journal of the American College of Chest Physicians, concurs.¹⁰

A 2023 study by Brunetti and others published in Immunology and Inflammation hit the nail on the head. Entitled simply and clearly “SARS-CoV-2 uses CD4 to infect T helper lymphocytes”, the authors explain: “We demonstrated that SARS-CoV-2 spike glycoprotein (S) directly binds to the CD4 molecule, which in turn mediates the entry of SARS- CoV-2 in T helper cells. This leads to impaired CD4 T cell function and may cause cell death.”¹¹

The cascade of dysfunction triggered by SARS-CoV-2 to CD4 binding

The interaction of GP120 on SARS-CoV-2 with α4β7 integrin on CD4 cells triggers a cascade of dysfunctional cell signalling that causes downstream cell disruption and the cascade of Covid-19 illness symptoms.

Below is the first phase of the mechanism of illness after Covid-19 infection and vaccination. [This is complex. If you find this passage difficult to grasp, you can jump to the next heading.]

Phase one of the HIV and SARS-CoV-2 mechanism:

1. The α4β7 integrin is located on the surface of CD4+ T immune cells and binds to transmembrane protein MAdCAM-1 (Mucosal Addressin Cell Adhesion Molecule-1) on the endothelial cells in the gut, to ensure immune surveillance and response against pathogens present in the gut. “MAdCAM-1 is a transmembrane protein, is mainly expressed by intestinal endothelial cells and plays a crucial role in the immigration of T-lymphocytes into tissues in the gastrointestinal tract. MAdCAM-1 has an IgA-like [immunoglobulin] domain and serves as a ligand of L-selectin and an α4β7 integrin, both of which are involved in lymphocyte homing in Peyer's plaques.”¹² Peyer's patches are lymphoid follicles consisting mostly of B lymphocytes and T lymphocytes. They are found in the mucus membrane that lines the small intestine, and are an important part of the ‘first response’ immune reaction to pathogenic microorganisms and antigens entering the intestinal tract.

2. The α4β7 integrin on the surface of CD4+ T cells plays a key role in both the initial cell attachment and transport of both HIV and SARS-CoV-2 throughout the body. In the case of both viruses, the α4β7 integrin binds to the virus glycoprotein GP120, allowing both viruses to infiltrate CD4 immune cells. The α4β7 integrin on the surface of the CD4 immune cells then binds to MAdCAM-1 with HIV or SARS-CoV-2 hidden inside the immune cell. The infected CD4 cells then carry the viruses into the mucosal tissues, like a Trojan horse, where the viruses then replicate and are disseminated throughout the body. 

3. Both HIV and SARS-CoV-2 initial viral replication massively occurs in the lymphatic system in the gut-associated lymphoid tissue (GALT). An excellent paper published in the scientific journal Current HIV/AIDS Reports in 2018, written by a group of scientists, including Anthony Fauci, who presided over HIV and SARS-CoV-2 research in his position of Director of the U.S. National Institute of Allergy and Infectious Diseases (NIAID) stated: “A defining feature of acute HIV infection is high-level viral replication in gut-associated lymphoid tissue (GALT).” Several studies “demonstrated that HIV infection in humans leads to a similar loss of gut CD4+ T cells in the very early stages of infection. This gut-tropic aspect of acute HIV infection is believed to play a central role in the development of immune deficiencies that define HIV disease. The rapid loss of CD4+ T cells is accompanied by damage to the structural integrity of the gut, which has been linked to chronic systemic immune activation.”¹³ It is from the gut that infiltrated CD4 cells travel throughout the body, infecting every system.

4. Integrins act as bridges between the extracellular matrix (ECM) and the cytoskeleton inside the cell. They bind to specific ligands in the ECM, such as fibronectin and collagen, and other cell surface molecules, allowing cells to stick to the ECM, providing structural support and facilitating various cellular processes. Integrins are involved in many biological processes such as maintaining tissue integrity, regulating cell behaviour, mediating interactions between cells and their surrounding environment, cell migration, tissue development, immune responses, wound healing, and platelet aggregation leading to blood clotting. Integrins act like the maestro of a symphony creating a cascade of downstream cell signalling that directly alters the function of cells and is also directly linked to cancer development. “Integrins are a family of transmembrane receptors that connect the extracellular matrix and actin skeleton, which mediate cell adhesion, migration, signal transduction, and gene transcription. As a bi-directional signaling molecule, integrins can modulate many aspects of tumorigenesis, including tumor growth, invasion, angiogenesis, metastasis, and therapeutic resistance.”¹⁴

In summary: The interaction of GP120 and α4β7 integrin triggers a cascade of dysfunctional cell signalling that causes downstream cell disruption and the cascade of Covid-19 illness symptoms. Importantly, activation of α4β7 integrin is a reversible process.

Why is this relevant to Covid-related disease?

A 2018 paper by Sivro and others published in Science Translational Medicine, confirmed the importance of integrin α4β7 in HIV cell entry and disease outcome.¹⁵

In SARS-CoV-2 just as in HIV, the interaction of GP120 on the virus spike protein with integrin α4β7 on CD4 cells, including lymphocytes (such as T cells and B cells) and natural killer cells, reduces the numbers of CD4 cells and, thus, predicts both HIV and SARS-CoV-2 acquisition and disease progression outcomes.

HIV and SARS-CoV-2 progression are directly correlated with the number of CD4 cells. HIV patients who maintain sufficient CD4 immune cell numbers are able to live healthy, symptom-free lives. “For decades, the CD4 cell count measurement has been used to understand the progression of the human immunodeficiency virus (HIV) disease”.¹⁶

In 2023, Huang and others explained how integrin α4β7 expression on peripheral blood CD4+ T cells predicts acquisition and disease progression outcomes of SARS-CoV-2. In a paper published in Signal Transduction and Targeted Therapy, they state:

“T-cell infection by SARS-CoV-2 and associated immune responses are correlated with disease severity and prognosis of COVID-19. Lymphopenia is associated with increased disease severity in COVID-19. Significantly lower circulating T and B cell counts were observed in patients who died from COVID-19 compared with survivors. Moreover, SARS-CoV-2 infection causes aberrant lymphocyte activation and dysfunction.”

The authors also confirmed that the ACE2 theory cannot explain the reduction observed in CD4 cell numbers:

“Angiotensin-converting enzyme 2 (ACE2) and some other reported S protein receptors are barely expressed in lymphocytes”, concluding “Collectively, these results indicate that T cell integrins mediate SARS-CoV-2 cell entry, which can be enhanced by integrin activation. In summary, our study demonstrates that integrins act as SARS-CoV-2 receptors on T cells and mediate entry and dysregulation of T cells by SARS-CoV-2.”¹⁷

Similarly, a paper in the Journal of Biological Chemistry confirms that integrins allow SARS-CoV-2 virus direct entry into cells independently of ACE2 receptors.¹⁸

What Anthony Fauci knew

The world’s leading scientist overseeing HIV and SARS-CoV-2 research, Dr Anthony S. Fauci, also knew of the important role α4β7 integrin plays in the acquisition and disease progression of HIV, as illustrated in U.S. Patent number: 9441041. 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, for the “Use of antagonists of the interaction between HIV GP120 and α4β7 integrin”.¹⁹

Conclusion of Part 1

The ACE2 receptor is not the most compatible receptor for SARS-CoV-2, as ACE2 is not compatible with GP120 located on the SARS-CoV-2 spike protein binding site. The cascade of dysfunction that occurs in the body in every single organ and system – cardiovascular system, respiratory system, nervous system, digestive system, the reproductive system, kidneys, liver and heart – after Covid-19 infection or injection, seems more likely to be triggered by the interaction of GP120 with integrin α4β7.

I suggest that SARS-CoV-2 enters CD4 immune cells, in the same manner as HIV, via integrin α4β7 interaction with GP120. The α4β7 integrin on the surface of the CD4 immune cells then binds to MAdCAM-1 with SARS-CoV-2 hidden inside the immune cell. The infected CD4 cells then carry the virus into the mucosal tissues, like a Trojan horse, where SARS-CoV-2 then replicates and is disseminated all throughout the body, triggering the same drastic reduction in CD4 cells, and the cascade of disease symptoms seen in Covid-19.

How does it do this?

The interaction of GP120 and α4β7 integrin triggers a cascade of dysfunctional cell signalling that causes downstream cell disruption and the cascade of Covid-19 illness symptoms. I state again, the activation of α4β7 integrin is a reversible process.

The disruption in the cell signaling pathways via integrin expression is a major aspect (but not the only aspect), explaining how SARS-CoV-2 leads to the rise in incidences of many chronic diseases, which leads us on to the second phase of the Covid-19 mechanism of illness and Part 2 of this series.

Thank you for your interest and support.

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19. 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 https://patents.justia.com/inventor/anthony-s-fauci