AstraZeneca Endotoxin contamination measurements - Please Help gather the data

Given the patterns of Deaths and Adverse Reactions to AstraZeneca jabs, the big unanswered Question is: - How much Endotoxin was in each Batch?

Calling all those who have collections of papers on the Chimpanzee Adenovirus AstraZeneca jab production and quality control measurements.

I would like to know Endotoxin levels in the genetically modified Human Embryonic Kidney (HEK) 293 cells and in all additives in the brew.

Ingredients of ChAdOx1 nCoV-19 jab are:

0.1mM EDTA

10mM Histidine

7.5% Sugar (has been know to have Endotoxin contamination)

0.5% Ethanol

0.1% Polysorbate 80.

European Medicines Agency Endotoxin Interest

In April 2021, the EMA issued a document¹ in which they discussed the severe and often Fatal phenomenon of VITT, Vaccine Indiced Thromboembolic Thrombocytopenia.² ³

They dismissed Endotoxin contamination without presenting any measurements:

Possible vaccine-specific pathogenic mechanisms for combined thromboembolic/thrombocytopenic effects:

The following 3 pathogenic mechanisms were considered:

Hypothetical mechanism #1: Issue is caused by the SARS-CoV-2 spike protein immunogen encoded by the chimpanzee adenovirus vector. This mechanism was considered unlikely, as the mode and pattern of SARS-CoV-2 spike antigen presentation (on the surface of muscle cells and fibroblasts at intramuscular injection sites, and by antigen-presenting cells in draining lymph nodes) is not vaccine-specific (is shared with mRNA vaccines, which also employ very similar Wuhan-based spike immunogens).

Hypothetical mechanism #2. Issue is caused by product impurities and/or excipients: This mechanism was considered un-likely, because (i) the vaccine excipients (detailed above) are not considered to be associated with thromboembolic risk, and (ii) the issue has to our knowledge not associated with certain batches of product (which would have been expected if the cause was eg contamination with endotoxin or other pro-thrombotic compounds).

Hypothetical mechanism #3. Issue is caused by the chimpanzee adenovirus vector:

Replication in-competent adenovirus vectors based on different serotypes of human adenoviruses are known to be able to cause thrombosis, secondary (consumptive) thrombocytopenia and disseminated intravascular coagulation, potentially leading to multiorgan failure and death, especially after intravenous injection of virus particles. This has been consistently described in preclinical models eg nonhuman primates and rabbits, and one fatality has also been reported in a phase 1 clinical trial [44-49].

The pro-thrombotic effects of adenovirus vectors are considered to be caused by a combination of the following pathways/sub-mechanisms [44-49]:

Binding of adenovirus to platelets, causing platelet activation and thrombosis.

• Specifically, aggregation and activation of platelets is mediated by so called RGD motifs in the pentn base of adenovirus particles, binding to alphaIIb/beta3 integrins on platelet surfaces [44].

• Interestingly, adenovirus particles can also bind platelet factor 4, the platelet antigen considered to be responsible for triggering heparin-induced thrombocytopenia [40, 41, 50].

• Thus, it is likely that antibody production against vector and/or platelet self antigens can might aggravate platelet activation, as is known from eg histamine-induced thrombocytopenia [40, 41].

• Binding of adenovirus particles to endothelial cells, causing endothelial activation and thrombosis.

• Systemic inflammatory response syndrome (SIRS; cytokine storm), which in itself activated platelets and endothelia.

• Auto-amplification loops, where initial adenovirus vector-mediated injury to thrombocytes and endothelia self-amplify (as is also known from eg heparin-induced thrombocytopenia and disseminated intravascular coagulations) [40, 41].

None of pathways/sub-mechanisms above require active adenovirus replication in platelets or endothelia (all are triggered by simple binding of virus vectors to cell surfaces).

Due to the overall similarity in the build of adenovirus particles, it is considered likely that the abovementioned pro-thrombotic effects are also shared by chimpanzee adenoviruses such as the ChAdOx1 vector employed in the AZ vaccine.

At the same time, it is considered likely that due to the sequence differences in the RGD loops between ChAdOx1and human adenoviruses [51], the risk profile of the AZ vaccine may in this respect differ from vaccines based on human adenoviruses.

As mentioned, while the pathways/sub-mechanisms above are triggered by binding of virus vectors to cell surfaces, the thromboembolic mechanisms thus triggered can proceed and propagate due to self-amplifying feedback mechanisms; likely for this reason, the relationship between dose of vector and toxicity is non-linear, with dramatic differences in scope and severity of toxicity noted with only modest increases of vector dose at higher doses [49].

Also, there is substantial subject-to-subject variation in the toxicity of adenovirus vectors in humans [51]. The causes for this are unknown, but may relate to known genetic polymorphisms in eg alphaIIb/beta3 integrins or Fc receptors on platelet surfaces.

It should be stressed that such pro-thrombotic effects of adenovirus vectors in humans is exceedingly rare [49].

For all the reasons above, it is concluded that if the AZ vaccine causes the observed thrombotic/thrombocytopenic events, this is most likely caused by the ChAdOx1 vector.

Note EMA “Hypothetical mechanism #2” that talks about the fact that Endotoxin variation could affect Batch to Batch variation, but they denied evidence of this.

Of course before we can describe “Bad Batches” we have to get actaula doses jabbed for each Batch to compare with Adverse Events Report Frequencies.

AstraZeneca Interest in Endotoxin

We know the company has a keen interest in Endotoxin, as seen in this Tweet, but their story is behind a paywall.⁴

TGA Measures Endotoxin in AstraZeneca

As found with other brands of Jabs, the Therapeutic Goods Administration claims to have measured Endotoxin for every batch released in Australia but keeps the actual results secret.⁵

I will list papers that have referred to Endotoxin in Adverse Reaction reports as we go.

Rhabdomyolysis and Multiorgan Failure

Cirillo and coworkers tried to work out what caused this reaction in one of their patients.⁶

Endotoxin Contamination in Commercial Spike

As I reported in an earlier article, Commercial Covid19 Spike rRBD protein obtained from ABP Biosciences is contaminated with Endotoxin, calling into question all Spikopathy studies of inflammation using this source material. This rRBD protein [Gln321-Ser591] was produced in HEK293 cells and had a stated purity > 95% as determined by SDS-PAGE and endotoxin < 1.0 EU per μg protein as determined by the LAL method.⁷

I went shopping for HEK293 Culture Medium brands and found Endotoxin specification < 2 EU/ml.

Vanderbilt University, close friend of Pfizer, Invitrogen, Gibco, Thermo Fisher Scientific and Life Sciences brands shows us E. coli contamination in these brews is a common problem.

See also the version of AstraZeneca made in India called Covishield.⁸

Please feel free to contribute information via the comments below or contact me privately via direct message on Twitter to keep your input confidential.

https://twitter.com/FluoridePoison

1. EMA 2021. Signal assessment report on embolic and thrombotic events (SMQ) with COVID-19 Vaccine (ChAdOx1-S [recombinant]) – Vaxzevria (previously COVID-19 Vaccine AstraZeneca) (Other viral vaccines)

2.

3.

4. Wong D, et al. 2022. https://www.europeanpharmaceuticalreview.com/article/173738/a-strategic-approach-to-optimisations-of-testing-bacterial-endotoxins/

5. https://www.tga.gov.au/batch-release-assessment-covid-19-vaccines

6. Cirillo E, et al. 2022. Case Report: Severe Rhabdomyolysis and Multiorgan Failure After ChAdOx1 nCoV-19 Vaccination. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8968726/

7. Tabynov K, et al. 2022. An adjuvanted subunit SARS-CoV-2 spike protein vaccine provides protection against Covid-19 infection and transmission. https://www.nature.com/articles/s41541-022-00450-8

8.