Cellular Immunity Hampered After Vaxx for High Risk Recipients

Paradoxically, the modRNA transfections are the least effective for the least amount of time for recipients most vulnerable to SARS-COV-2 infection who are also most likely to develop immune tolerance to the spike protein, which increases their risk over baseline. This doesn’t really become apparent until we stop looking at spike specific antibody titer levels and examine cellular immune responses instead.

A serological study that assessed the T-cell responses of fully vaxxed elderly participants who received XBB1.5 booster and had no infections in the 6 months prior to recruitment (n = 18) in Jan-March 2024 and compared them to virus naive healthcare workers who received the primary series and provided samples between March and April 2021 (n = 15), found, through peripheral blood mononuclear cells, that the elderly recipients had a lower median T cell response to the the BA2.86 subvariant compared to the virus naive healthcare workers who had only received the primary series at the time their sample was collected. Elderly participants also had no significant helper T cell reactivity to the 2023 variants despite receiving the latest booster, while virus naive healthcare workers had a reduced response to the later variants compared to the Wuhan variant. The authors suggest spike specific IgG4 antibody proliferation may have a mechanistic role in inhibiting the humoral response of elderly booster recipients. 17/18 booster recipients had cardiovascular disease and 4/18 had diabetes.

Diabetics Develop Immune Tolerance to the Spike Protein After Multiple modRNA transfections.

The COVAC-DM study, a prospective cohort study comparing the cellular immune response of diabetics and non-diabetic controls to SARS-COV-2 4-16 weeks after receiving the primary series and 2-4 weeks after the first booster administered between April 2021 and March 2022, found through peripheral blood mononuclear cells, that only 20% of participants with type 2 and 30% of participants with type 1 had detectable spike specific helper T cells and cytotoxic T cells compared to 80% of controls. Even diabetics with spike specific T cells had an unfocused cytokine phenotype production with an increase in interleukin 13 specifically (an anti-inflammatory cytokine) and a severely impaired recall T cell response compared to controls. Diabetics with spike specific helper T cells and cytotoxic T cells still exhibited an immune tolerance response with increased interleukin 10 and 13 proliferation. Diabetics also had fewer effector memory cells compared to controls suggesting a more rapid memory T cell decay. After the booster, only 33% of type 1 diabetics and 22% of type 2 diabetics had detectable spike specific helper T cells compared to 79% of controls, with a much lower frequency of an effector memory phenotype and a much higher frequency of anti-inflammatory cytokine producing cells (e.g. 10, 13, 21). Although diabetics had similar spike specific cytotoxic T cells compared to controls, after the booster, they produced anti-inflammatory cytokines more frequently than controls suggesting an immune tolerance response to the spike protein.

Vaxx Spike Protein Causes Programmed Cell Death of T-cells

A recent peripheral blood mono-nuclear cell study, published in the Journal of Allergy and Clinical Immunology, discovered that the circulating receptor binding domain spike protein in vaxxed participants triggered a cascade of programmed T cell death through elevated Angiotensin II that induced white blood cells to release free radicals. As I mentioned in a prior post last year, Vitamin D3 indirectly inhibits angiotensin II synthesis through the renin-angiotensin system and also increases Angiotensin-converting enzyme 2 expression. This is why Vitamin D insufficiency is a risk factor for acute respiratory disease while sufficiency is a mitigating factor after SARS-COV-2 infection.

Immune Tolerance Induced in less than 6 months

A target trial emulation study conducted among Veterans Health Admin patients between October 2023 and May 2024 (n = 1,174,274) found, through 7 sequential 2 week trials wherein XBB1.5 booster recipients were matched 1:1 with eligible unvaxxed patients assigned to the index date of the other participant’s booster shot, that there were more documented infections in the booster group (n = 8,028) than in the unvaxxed group (n = 7,946) through an average follow up time of 176 days (less than 6 months). Although COVID-19 associated hospitalizations and deaths were slightly higher in the unvaxxed group this difference rapidly declined over 4 months (120 days). 40% of participants had diabetes, about 35% had coronary heart disease and over a quarter had chronic kidney disease.

It has become very apparent over the past 4 years that vaxx induced immunity is restricted by the innate immunity of the recipient which is why the public health focus should be on reducing the risk factors that make the latter worse instead of pushing for more frequent boosters. We are already at bi-annual boosters recommendations. Whats next? Quarterly? Monthly?

Metabolic syndrome increases COVID-19 Disease Severity: Even with the Vaxx

A murine mouse model study found that mice with metabolic syndrome established after 12 weeks of a high fat diet and vaxxed with two 5 microgram modRNA doses not only evidenced immune imprinting towards the ancestral variant in serum sample, same as the wildtype control mice, but also diminished neutralization capacity against both the ancestral variant and delta variant compared to the wildtype control mice. Of course, this experiment only examined spike specific antibody serum levels and not the much more important cellular immune response.