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Spike Protein Bloodwork

I am on the email list for what is known as the [C19D] group (Covid-19). Here is an interesting article from that feed.

This image of a lab test is quite revealing.

What stands out in this test result is what Dr. Carter and I see daily, even in those who did not get the jab but reported symptoms from SARS. Notice that WBCs came down over time, but we do not know the treatment. Importantly, even though the WBCs improved into a normal range, the ABSOLUTE LYMPHOCYTES remain abnormally low. Ideally, they should be between 1.5 and 1.9 - not 0.5 or 1.0.

I'm no expert on HIV, but Dr. Carter is. When the absolute lymphocytes are below 1.5, levels of various viruses, especially EBV, are high. The "CD" tests - noted in bold in the image, are affordable but much more expensive than a basic CBC with differential. In this latter test, you get all the markers below the CD4/CD8 Ratio.

IMHO, the absolute lymphocyte levels are adequate to predict the CD4/CD8 Ratio Profile. I have never seen an abnormal ratio when the lymphocyte levels are normal. As stated above, EBV, HSV, and other virals like CMV are elevated in all cases.

This person also had a co-morbid bacterial infection based on an initial WBC of 10.5 and very high absolute neutrophils. However, the more recent labs STILL indicate low-grade stealth bacterial infections. The neutrophils (absolute) should be between 2.0 and 2.8. Even though the WBCs are almost normal (4.0 - 5.7), the absolute neutrophils, at 3.8, are elevated.

The neutrophil-to-lymphocyte ratio should be between 1.1 and 1.5. This NLR marker is a good indication of the burden of stealth infection. However, it should always be interpreted in conjunction with the other CBC with different markers. No one marker is ever 100% predictive. Informative- YES - predictive with accuracy and precision - NO.

NLR before: 18.4 (severe cancer risk level)

NLR after: 3.8 (better but far from optimal)

Also, note that platelet counts rebounded as the WBC value improved. I often see low platelet counts when lymphocyte levels are low, and I also have consistently seen platelet values rebound.

Now, in over 100 cases, I have seen dramatic improvement in these abnormal values with the Brownstein Protocol and Mega IGG 2000. In a severe case like the one above - the 05/05/2023 lab values, I would also add Hydroxychloroquine, Ivermectin, and possibly methylene blue.


Here is a portion of the article linked above discussing the impact of the Spike on the gut.

Multiple components of the gut immune system are affected, resulting in a diminished or dysfunctional gut immunological barrier. Antiviral peptides, inflammatory mediators, immune cell chemotaxis, and secretory immunoglobulins are important parameters that are negatively affected in SARS-CoV-2 infection. Mucosal CD4+ and CD8+ T cells, Th17 cells, neutrophils, dendritic cells, and macrophages are activated, and the number of regulatory T cells decreases, promoting an overactivated immune response with increased expression of type I and III interferons and other proinflammatory cytokines. The changes in the immunologic barrier could be promoted in part by a dysbiotic gut microbiota, through commensal-derived signals and metabolites. On the other hand, the proinflammatory intestinal environment could further compromise the integrity of the intestinal epithelium by promoting enterocyte apoptosis and disruption of tight junctions.

Exhaustion/depletion of CD4+ T cells, a hallmark of HIV infection, is also observed in SARS-CoV-2 infection. The resulting dysregulation of CD4+ T cells in the gut may contribute to intestinal epithelial barrier dysfunction and leaky gut, which promotes systemic inflammation (35). Accordingly, IL-17 producing Th17 cells are overactivated in SARS-CoV-2 infection (36).

Alterations in gut immunological barrier in SARS-CoV-2 infection and their prognostic potential

There is much evidence that the Spike Protein alone may be inducing these responses.

Studies have reported the occurrence of gastrointestinal (GI) symptoms, primarily diarrhea, in COVID-19. However, the pathobiology regarding COVID-19 in the GI tract remains limited. This work aimed to evaluate SARS-CoV-2 Spike protein interaction with gut lumen in different experimental approaches. Here, we present a novel experimental model with the inoculation of viral protein in the murine jejunal lumen, in vitro approach with human enterocytes, and molecular docking analysis. Spike protein led to increased intestinal fluid accompanied by Cl− secretion, followed by intestinal edema, leukocyte infiltration, reduced glutathione levels, and increased cytokine levels [interleukin (IL)-6, tumor necrosis factor-α, IL-1β, IL-10], indicating inflammation.

Additionally, the viral epitope caused disruption in the mucosal histoarchitecture with impairment in Paneth and goblet cells, including decreased lysozyme and mucin, respectively. Upregulation of toll-like receptor 2 and toll-like receptor 4 gene expression suggested potential activation of local innate immunity. Moreover, this experimental model exhibited reduced contractile responses in jejunal smooth muscle. In barrier function, there was a decrease in transepithelial electrical resistance and alterations in the expression of tight junction proteins in the murine jejunal epithelium. Additionally, paracellular intestinal permeability increased in human enterocytes.

Finally, in silico data revealed that the Spike protein interacts with cystic fibrosis transmembrane conductance regulator (CFTR) and calcium-activated chloride conductance (CaCC), inferring its role in the secretory effect. Taken together, all the events observed point to gut impairment, affecting the mucosal barrier to the innermost layers, establishing a successful experimental model for studying COVID-19 in the GI context.

SARS-CoV-2 Spike protein triggers gut impairment since mucosal barrier to innermost layers: From basic science to clinical relevance

And, perhaps more disturbingly, the gut may be a reservoir (along with many other locations) for persistent Spike production after natural infection.

SARS-CoV-2 viral rebound in the gut, possibly resulting from viral persistence, has also been associated with lower levels and slower production of receptor-binding domain IgA and IgG antibodies51. There are major differences in antibody creation, seroreversion and antibody titre levels across the sexes, with women being less likely to seroconvert, being more likely to serorevert and having lower antibody levels overall52,53, even affecting antibody waning after vaccination54.

Several reports have pointed towards possible viral persistence as a driver of long COVID symptoms; viral proteins and/or RNA has been found in the reproductive system, cardiovascular system, brain, muscles, eyes, lymph nodes, appendix, breast tissue, hepatic tissue, lung tissue, plasma, stool and urine55–60. In one study, circulating SARS-CoV-2 spike antigen was found in 60% of a cohort of 37 patients with long COVID up to 12 months after diagnosis compared with 0% of 26 SARS-CoV-2-infected individuals, likely implying a reservoir of active virus or components of the virus16. Indeed, multiple reports following gastrointestinal biopsies have indicated the presence of virus, suggestive of a persistent reservoir in some patients58,61.


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