New Research: Good News, Bad News on Covid Jabs

Good news - 50% of shots may be duds. Bad news - the other 50% do cause heart inflammation, whether you feel it or not. The more jabs your get, the slimmer are your chances of avoiding a "live" jab.

New research on the effects of Covid-19 mRNA “vaccines” on human body keeps coming in, 3 years too late, but very interesting.

Firstly, “Detection of recombinant Spike protein in the blood of individuals vaccinated against SARS-CoV-2: Possible molecular mechanisms” (Wiley Online Library, 2023.08.31). The Jab-manufactured (recombinant) S spike protein differs from the virial infection-produced (natural) S spike in that the recombinant S spike contains two proline substitutions to “stabilize the S spike in the open configuration”, as they say. So, the study tested for the manufactured PP-Spike in the serum of post-jab subjects and in the serum of unvaccinated infected subjects. None of the unvaccinated infected subjects were tested positive for PP-Spike. The kicker: 50% of the “vaccinated” subject tested positive for the PP-Spike, for 69 to whopping 187 days after the jab.

Hence my title of this post: the good news is that 50% of “vaccinated” subjects possibly received a “placebo” with non-functional mRNA; the bad news is, the other 50% became long-term S spike-generating machines. How is this possible? Only two ways, according to the study authors: either the mRNA code gets imbedded in your cells’ DNA, or in the DNA of the bacteria that you permanently host. Either way, you have a lasting (or permanent?) fountain of PP-Spike inside of you.

In their own words:

Experimental design: Mass spectrometry examination of biological samples was used to detect the presence of specific fragments of recombinant Spike protein in subjects who received mRNA-based vaccines.

Results: The specific PP-Spike fragment was found in 50% of the biological samples analyzed, and its presence was independent of the SARS-CoV-2 IgG antibody titer. The minimum and maximum time at which PP-Spike was detected after vaccination was 69 and 187 days, respectively.

Figure 1, D,E: (D) Time from the day of vaccination completion to the discovery of vaccine mRNA-induced Spike protein “PP”. (E) quantification of the antibody titer of the 20 vaccinated cases.

According to the authors [15] and in general, the vaccine messenger RNA nanoparticle molecules should be picked up by the immune cells in the lymph nodes after injection into the muscle. Recently, other authors have isolated vaccine messenger RNA sequences from peripheral plasma after 28 days after injection [24]. The question of whether or not the vaccine RNA can be integrated into the lymphocyte or other body cells is much debated. Nonetheless, the observation of the protein produced, as presented in this manuscript, goes beyond the purely cognitive aspect and defines a method to verify not only the persistence of the vaccine RNA but the quantification of the product, that is, the protein that is supposed to induce antibody production, in order to verify the correct half-life and a possible need to update the vaccine status. Using mass spectrometry examination of biological samples, we detected the presence of specific fragments of recombinant Spike protein in about 50% of subjects who received mRNA-based vaccines. In some cases, we found the PP-Spike marker in vaccinated individuals more than 30 days after the vaccine, indicating that it is possible to detect vaccine “Spike” protein even sometime after vaccination and in any organic tissue (data in preparation). Based on the results obtained, hypotheses can be made for possible molecular mechanisms of persistence of “Spike PP.” In particular, three hypotheses are possible and are shown in Figure 3.

1. It is possible that the mRNA may be integrated or re-transcribed in some cells.

2. It is possible that pseudo-uridines at a particular sequence position, as described in the article, induce the formation of a spike protein that is always constitutively active. But it seems very remote as a hypothesis.

3. It is possible that the mRNA-containing nanoparticle will be picked up by bacteria normally present at the basal level in the blood. In fact, the existence of blood microbiota in clinically healthy individuals was proven during the last 50 years. Indeed, indirect evidence by radiometric analyses suggested the existence of living microbial forms in erythrocytes [25]. In addition, the observation of the PP-Spike marker in individuals vaccinated more than 30 days after the vaccine in about 50% of subjects could also be explained by the wide biodiversity of eukaryotic and prokaryotic microbiota identified in blood by next-generation sequencing technologies [25].

   

   Figure3. Possible molecular mechanisms of persistence of “Spike PP”.

For a discussion of this article, watch this 12-minute Del Bigtree podcast with Jefferey Jaxen on Rumble (starting at 7:20):

Secondly, “SARS-CoV-2 spike protein induces endothelial inflammation via ACE2 independently of viral replication”(Nature, 2023.08.28):

Here we investigated whether spike protein binding to ACE2 induces inflammation in endothelial cells and determined the role of ACE2 in this process. Human endothelial cells were exposed to SARS-CoV-2 spike protein, S1 subunit (rS1p) and pro-inflammatory signaling and inflammatory mediators assessed. ACE2 was modulated pharmacologically and by siRNA. Endothelial cells were also exposed to SARS-CoV-2. rSP1 increased production of IL-6, MCP-1, ICAM-1 and PAI-1, and induced NFkB activation via ACE2 in endothelial cells.rS1p increased microparticle formation, a functional marker of endothelial injury. ACE2 interacting proteins involved in inflammation and RNA biology were identified in rS1p-treated cells. Neither ACE2 expression nor ACE2 enzymatic function were affected by rSP1. Endothelial cells exposed to SARS-CoV-2 virus did not exhibit viral replication. We demonstrate that rSP1 induces endothelial inflammation via ACE2 through processes that are independent of ACE2 enzymatic activity and viral replication.

Results: SARS-CoV-2 recombinant S1 protein induces endothelial inflammation and cell damage independently of viral infection.

rS1p induces endothelial cell inflammation and injury. Proteomic analysis of rS1p-treated endothelial cells. Human endothelial cells (hMEC) were stimulated with rS1p (0.66 μg/mL) for 5 h and 24 h for assessment of IL-6 (C) and MCP-1 (D) mRNA expression; IL-6 (E) and MCP-1 (F) production. Data are expressed as ± SEM; *p < 0.05 control (Ctl) (non-stimulated cells) vs. rS1p stimulated cells after student’s t-test.

So, harboring PP-Spike is surely inducing endothelial inflammation and damage, whether you notice it or not.

Thirdly, we also have another corroboration of myocardial inflammation in this most recent study, “Assessment of Myocardial 18F-FDG Uptake at PET/CT in Asymptomatic SARS-CoV-2-vaccinated and Nonvaccinated Patients” (Radiology, 2023.09.19):

Purpose: To assess myocardial 18Fluorine-fluorodeoxyglucose (18F-FDG) uptake on PET/CT in asymptomatic SARS-CoV-2 vaccinated patients compared to nonvaccinated patients.

Results: The study included 303 nonvaccinated patients (mean age, 52.9 years ± 14.9 [SD]; 157 females) and 700 vaccinated patients (mean age, 56.8 years ± 13.7 [SD]; 344 females). Vaccinated patients had overall higher myocardial FDG uptake compared to nonvaccinated patients (median SUVmax, 4.8 [IQR: 3.0-8.5] vs median SUVmax, 3.3 [IQR: 2.5-6.2]; P < .0001). Myocardial SUVmax was higher in vaccinated patients regardless of sex (median range, 4.7-4.9 [IQR: 2.9-8.6]) or patient age (median range, 4.7-5.6 [IQR: 2.9-8.6]) compared to corresponding nonvaccinated groups (sex median range, 3.2-3.9 [IQR: 2.4-7.2]; age median range, 3.3-3.3 [IQR: 2.3-6.1]; P range, <.001-.015). Furthermore, increased myocardial FDG uptake was observed in patients imaged 1-30, 31-60, 61-120, and 121-180 days after their second vaccination (median SUVmax range, 4.6-5.1 [IQR: 2.9-8.6]) and increased ipsilateral axillary uptake was observed in patients imaged 1-30, 31-60, 61-120 days after their 2nd vaccination (median SUVmax range, 1.5-2.0 [IQR: 1.2-3.4]) compared to the nonvaccinated patients (P range, <.001-<.001).

Figure. 3: Qualitative and quantitative assessment of myocardial 18Fluroine-fluorodeoxyglucose (18F-FDG) uptake in vaccinated and nonvaccinated patients. (A) Bar plot showing the number of patients (N) who received each myocardial FDG uptake visual score (0-3) stratified by vaccination (vaccine [-], n = 303; vaccine [+], n = 700). Myocardial FDG uptake visual scores were higher in the vaccinated group compared to the unvaccinated group (Mann-Whitney U test, P < .001). (B) Boxplot showing the myocardial FDG uptake as measured by SUVmax in nonvaccinated (vaccine [-], n = 303) and vaccinated (vaccine [+], n = 700) patients. The myocardial SUVmax was higher in the vaccinated group (median, 4.8 [IQR: 3.0-8.5]) than in the unvaccinated group (median, 3.3 [IQR: 2.5-6.2]; P < .001). Horizontal bars in the boxplot represent the median SUVmax value and whiskers represent the interquartile range. The diamond in the box represents average. Mann-Whitney U test was used to compare median SUVmax values between groups.

Figure 4: Boxplots showing 18Fluroine-fluorodeoxyglucose (18F-FDG) uptake in the (A) axillary and (B) myocardium of patients stratified by the interval of time between SARS-CoV-2 vaccination and PET/CT imaging. (A) Compared to the unvaccinated group (Dose 0, median SUVmax, 1.2 [IQR: 1.0-1.4]), the axillary SUVmax was higher in patients imaged after their 1st dose (median, 1.6 [IQR: 1.3-3.2]; P <.001). Patients imaged ≤30 days (median, 2.0 [IQR: 1.6-3.4]), 31-60 days (median, 1.7 [IQR: 1.5-1.9]), and 61-120 days (median, 1.5 [IQR: 1.2-1.7]) after their 2nd dose also showed increased axillary SUVmax values compared to the unvaccinated group (P range, <.001-<.001). There was no difference observed in axillary SUVmax between unvaccinated patients and patients imaged 121-180 days (median, 1.2 [IQR: 1.0-1.5]; P = .99) or >180 days (median, 1.1 [IQR: 0.9-1.3]; P = .20) after their 2nd dose. (B) Boxplot showing myocardial SUVmax for nonvaccinated (Dose 0) and vaccinated groups. The myocardial SUVmax was higher in patients imaged after their 1st dose (median, 6.2 [IQR: 3.8-8.8]; P=.004) as well as in patients imaged 1-30 days (median, 5.1 [IQR: 3.2-8.6]), 31-60 days (median, 4.8 [IQR: 3.0-7.7]), 61-120 days (median, 4.6 [IQR: 3.2-8.5]), and 121-180 days (median, 5.1 [IQR: 2.9-8.2]) after their 2nd dose compared to the unvaccinated group (median, 3.3 [IQR: 2.5-6.2]; P range, <.001-<.001). There was no difference observed in myocardial SUVmax between unvaccinated patients and patients imaged >180 days after their 2nd dose (median, 4.5 [IQR: 2.7-9.3]; P = .15). For both boxplots, horizontal bars represent the median SUVmax value and whiskers represent the interquartile range. The diamond in the box represents average. Kruskal-Wallis test with post ad -hoc Dwass, Steel, Critchlow-Fligner multiple comparison analysis was used to compare median SUVmax values between groups.

Conclusion: Compared to nonvaccinated patients, asymptomatic patients who received their 2nd vaccination 1-180 days prior to imaging showed increased myocardial FDG uptake on PET/CT.

The inflammation markers clearly show ongoing inflammation after a jab (1st or 2nd), highest within 30 days post 2nd jab, returning to normal (unjabbed) levels only after 180 days or so.

To add some context, myocardial FDG uptake on PET/CT is an established diagnostic technique to actually see where (which organs of your body) the inflammation is ongoing (here, here, here).

Long story short, 50% of the Covid-19 jab mRNA-injected subjects for sure have myocardial and other endothelial inflammation for the duration of the PP-Spike production in their bodies, which is up to more than half a year on end.

Weigh your risks and benefits when considering your next new-and-improved Covid-19 booster shot?