Q: Should I take any of the current vaccines against SARS-CoV-2/SARS-2/chinese CCP Coronavirus/Wuhan Plague/Kung Flu/COVID-19?
A: Only if you feel like being a guinea pig.
Q: If I'm pressured into taking one, which one would be the safest?
A: Ranking by known "safety" ("top safe" after BCG are still pretty unsafe) and what's rolled out:
BCG vaccine > [shit you should not take] > Novavax and other shit that just delivers the spike+adjuvant > J&J, Sputnik and other human adenovirus vector shit > Astrazeneca and other non-human adenovirus shit ~ other non-replicating viral vectors >>> [shit you seriously should not take] > inactivated shit > replicating viral vectors > any chinkshit > pfizer/moderna any mRNA shit > live attentuated shit
SARS-CoV-2 Vaccines Tracker
Some food for thought first:
Israel: Pfizer vaccines, for the elderly, killed during the 5-week vaccination period ~40 times more people than SARS-2 itself would have killed, and ~260 times more people than the disease among the younger age
>all to produce a green passport valid at most 6 months, and promote Pfizer sales
>mid-December until mid-February, 2337 among all 5351 COVID-19 deaths reported for Israel occurred, 43.7%. Among these, since January 19, 1271 COVID-19 deaths were reported
>The table provided by the Ministry of Health on February 10 states 660 COVID-19 deaths among the vaccinated, 51.9% of the deaths for that period.
>The deaths among those vaccinated should be added to the numerous AVC and cardiac events reported just after vaccination that are not included among COVID-19 deaths which about double the deaths among those vaccinated, whose numbers remain unknown and which we will try to find in the coming days
>way to pass these points across relate to the monthly COVID-19 deaths rates since the start of the pandemic and until mid-December, 3014 deaths, hence 3014/9 = 334.9 deaths per month.
>Monthly death rates since mid-December are 2337/2 = 1168.5 deaths per month, hence 3.5 times greater
Israel government, Pfizer lead illegal experiment on humans
> On January 6, the “Cooperation Agreement for the Collection of Epidemiological Information from the Real World” was signed, in which Pfizer promised the State of Israel vaccines that would vaccinate all residents except children and those who could not be vaccinated. In return for advancing Israel over other countries, the State of Israel will provide Pfizer with epidemiological information that will allow it to assess the effectiveness of the vaccine.
> The question that arose in the Israeli public was: what medical information the State of Israel would be given to Pfizer? What exactly would it be used for?
> Many allegations have been made about the risk of violating the privacy of the country’s residents, and the lack of transparency in not disclosing the contract. The Ministry of Health said that it would give Pfizer only general epidemiological information, but then why did Pfizer sign an agreement to obtain such information, which is exposed in any case. The Ministry of Health agreed to publish the full agreement. However, parts in the agreement are hidden under black marks. Why?
Oxford Kept SARS-2 Vaccine Trial Volunteers in Dark About Dosing Error, Letter Shows
>Pharmaceutical corporations given vaccine liability exemptions from governments
You can’t sue Pfizer or Moderna if you have severe SARS-CoV-2 vaccine side effects. The government likely won’t compensate you for damages either
>Under the PREP Act (USA), companies like Pfizer and Moderna have total immunity from liability if something unintentionally goes wrong with their vaccines.
>A little-known government program provides benefits to people who can prove they suffered serious injury from a vaccine
>That program rarely pays, covering just 29 claims over last 10 years
>while the pandemic continues, Moderna will not enforce our COVID-19 related patents against those making vaccines intended to combat the pandemic
CEO of Pfizer says everyone should "trust science" and to get the vaccine because its your loved ones that will pay for it if you don't.
>He was then asked why he hasn't had the vaccine yet. He said "he's also 59 and in relatively good health, so it's not entirely appropriate for him to receive the vaccine before other people who "need it more" ". If he was vaccinated on camera, he said "it might help increase the public's willingness to receive it", citing Pfizer's internal research. But he emphasized that "none of the executives and board members will cut the line."
[Actual vaccine efficacy based on data from samples with proper size?]
>the final vaccine efficacy percentage may vary
Also, some vaccines require 2 doses and some time for them to offer the designated/promised levels of protection
Doctors explain vaccine effectiveness after nurse gets SARS-2 after taking 1st dose
>Doctors tell ABC7 News that the first vaccine shot gives 50 percent immunity, which doesn't kick in for a week with the Pfizer vaccine and two weeks with the Moderna vaccine.
Brazil institute says CoronaVac efficacy above 50%, but delays full results
[List of current vaccines?]
[Side-effects? Adverse events?]
Some of the reported (including the ones where, supposedly, placebo or anything else were "reported" to be the cause):
Cases where Vaccine targets SARS-2 (COVID19) and Patient Died
>"Underreporting" is one of the main limitations of VAERS
>fewer than 1% of vaccine adverse events are reported. Low reporting rates preclude or slow the identification of “problem” drugs and vaccines that endanger public health.
>Guide to Interpreting VAERS Data
>VAERS Data Limitations
>"Underreporting" is one of the main limitations of passive surveillance systems, including VAERS. The term, underreporting refers to the fact that VAERS receives reports for only a small fraction of actual adverse events. The degree of underreporting varies widely.
Very huge page with all the latest available reports on effects from all the SARS-CoV-2 vaccines
[slightly outdated] A Long List of Recorded Adverse Reactions to the Experimental SARS-CoV-2 Vaccine in .pdf
Original official source where you can make your own query
Norway warns frail patients over 80 of vaccine risks after vaccine-related deaths
Israel has been hailed for its speedy and efficient mass inoculation program, which has vaccinated a staggering 20 percent of the country’s population since the drive began at the end of December. For a handful of Israelis, however, the initiative has led to some unexpected health scares. At least 13 people have reported mild facial paralysis after receiving the Pfizer/BioNTech jab, Israeli outlet Ynet reported, citing the Health Ministry, adding that officials believe the number of such cases could be higher.
51 adverse reactions reported & 1 person hospitalized in Delhi as India begins world’s largest Covid-19 vaccination program
Peru says china's Sinopharm may resume coronavirus vaccine trial after volunteer's illness
>The Peruvian health minister said on Wednesday that China’s Sinopharm could resume a trial for its coronavirus vaccine in the hard-hit Andean nation, just days after authorities suspended the tests to better understand why a volunteer had fallen ill.
>Health authorities announced over the weekend that the Sinopharm trial would be temporarily halted as a safety measure after a volunteer experienced decreased strength in his legs, among other symptoms.
>“We have had several meetings with Sinopharm and ... the suspension has been lifted today (Wednesday),” Health Minister Pilar Mazzetti said.
>Sinopharm Group Co Ltd, which is conducting its trials in Peru with some 12,000 volunteers, was about to complete the first stage of the trials in the next few days, and had plans to administer a second dose of its vaccine in the coming weeks.
>Peru’s government said on Tuesday negotiations with Sinopharm to purchase COVID-19 vaccines are “well advanced.”
Four team members at Advocate Condell Medical Center in Libertyville experienced reactions shortly after receiving the Pfizer SARS-CoV-2 vaccination. Their symptoms included tingling and elevated heartrates, the hospital said in a statement.
[USA] Fairbanks clinician is third Alaskan with adverse reaction to SARS-CoV-2 vaccine
2 Alaska Health Workers Got Emergency Treatment After Receiving Pfizer’s Vaccine
Four trial volunteers who got Pfizer's SARS-CoV-2 vaccine developed Bell's palsy - but FDA denies that the temporary facial paralysis was caused by the shot
Priest Dies After Participating In Moderna COVID Vaccine Trial
AstraZeneca SARS-2 vaccine trial volunteer has died
[OCT 13 2020] Johnson & Johnson’s coronavirus vaccine trial is paused after ‘adverse event’ in a participant
>“We must respect this participant’s privacy,” the company said in a statement late Monday. “We’re also learning more about this participant’s illness, and it’s important to have all the facts before we share additional information.”
Mild fever after taking the first shot of the mRNA-1273 vaccine. "Full-on COVID-like symptoms".
There were other participants who also experienced similar side-effects
Mild side effects after getting the first shot of the vaccine, while some reported side-effects after taking the second jab
>AstraZeneca [BTW they accidentally made the dosaging smaller]
At least 2 participants experienced transverse myelitis, which is an inflammatory syndrome that affects the spinal cord.
>Johnson & Johnson
Unexplained illness injection.
Side effects of the Moderna and Pfizer SARS-CoV-2 vaccines
>Neither company reported side effects that affected less than 2% of participants in their press releases but more detailed data will be released.
>Pfizer reported 3.8% of the recipients felt fatigue and 2% experienced headache, based on preliminary data from its Phase 3 trial. These symptoms are classified as Grade 3 or “severe” adverse events because they can interfere with daily activity.
>Moderna reported more Grade 3 side effects. There was fatigue in 9.7% of recipients, muscle pain in 8.9%, joint pain in 5.2%, headache in 4.5%, pain in 4.1%, and redness at the injection site in 2%.
[Efficacy of vaccines by type?]
Current subunit/vector vaccines present only the spike protein to the immune system of the recipient, which would not be enough to prime the immunity for clearance properly:
>9 identified T cell epitopes were derived from the ORF1ab (n=4), S protein (n=3), membrane protein (n=1), and nucleoprotein (n=1). Strikingly, the CD8 T cell responses specific for the epitopes derived from ORF1ab were of significantly higher magnitude compared to the CD8 T cell responses towards the spike, membrane and nucleoprotein combined, was not due to increased relative expression of ORF1ab compared to other proteins
But inactivated vaccines offer higher risks of autoimmune problems due to more proteins being present that could trigger pathogenic priming, and live attenuated virus vaccines also can replicate, act with the most virulence and possibly mutate back to more virulent/pathogenic form (may as well just get infected with the real virus, but only after souping up on prohyplaxis).
Pathogenic priming likely contributes to serious and critical illness and mortality in COVID-19 via autoimmunity
>Homology (similarity) between human and viral proteins is an established factor in viral- or vaccine-induced autoimmunity.
>Immunogenic peptides in viruses or bacteria that match human proteins are good candidates for pathogenic priming peptides
>If all of the parts of the epitopes that are homologous to human proteins are excluded from consideration due to risk of pathogenic priming, the remaining immunogenic parts of the epitopes may be still immunogenic and remain as potentially viable candidates for vaccine development
Epitope mimicry analysis of SARS-COV-2 surface glycoproteins and envelope proteins and human lung proteins
IgA autoantibodies target pulmonary surfactant in patients with severe COVID
>we established a prospective observational cohort to study lung specific autoantibodies (auto-Abs). Incubation of plasma from severe COVID-19 patients with healthy human lung tissue revealed the presence of IgA antibodies binding to surfactant-producing pneumocytes. Enzyme-linked immunosorbent assays (ELISA) and protein pull-downs using porcine surfactant confirmed the presence of auto-Abs binding to surfactant proteins in severe COVID-19 patients. Mass spectrometry and ELISAs with recombinant proteins identified IgA auto-Abs that target human surfactant proteins B and C. In line with these findings, lungs of deceased COVID-19 patients showed reduced pulmonary surfactant
[Molecular Mimicry] between SARS-CoV-2 spike glycoprotein and mammalian proteomes: implications for the vaccine
>Of the 33 peptides from SARS-CoV-2 that mimic the human reference proteome, 20 peptides are not found in any previous human-infecting coronavirus (SARS, MERS, or seasonal HCoVs)
>Such a peptide commonality is unexpected and highly improbable from a mathematical point of view
[Human–viral molecular mimicry] Benchmarking evolutionary tinkering underlying human–viral molecular mimicry shows multiple host pulmonary–arterial peptides mimicked by SARS-CoV-2
Coronavirus associated molecular mimicry common to SARS-CoV-2 peptide
New-Onset IgG Autoantibodies in Hospitalized Patients with COVID
Distinct Autoimmune Antibody Signatures Between Hospitalized Acute COVID Patients, SARS-CoV-2 Convalescent Individuals, and Unexposed Pre-Pandemic Controls
An Autoantigen Atlas from Human Lung HFL1 Cells Offers Clues to Neurological and Diverse Autoimmune Manifestations of SARS-2
SARS-CoV2 infection as a trigger of humoral response against apolipoprotein A-1
>Anti-Spike domain 1 (SD1) IgGs, anti-apoA-1 IgGs and against mimic peptides, as well as cytokines were assessed by immunoassays on a case-control (n=101), an intensive care unit (ICU; n=126) with a 28-days follow-up, and a general population cohort (n=663) with available samples in the pre and post-pandemic period.
>Linear sequence homologies and antibodies cross-reactivity between apoA-1, TLR2, and Spike epitopes were identified.
>Apolipoprotein serum levels related to metabolic syndrome in patients with schizophrenia
>Serum apolipoprotein A1: a predictor and prognostic biomarker in acute ischemic stroke
Neutralizing IFNL3 Autoantibodies in Severe SARS-2 Identified Using Molecular Indexing of Proteins by Self-Assembly
>we present Molecular Indexing of Proteins by Self Assembly (MIPSA), a technique that produces ORFeome-scale libraries of proteins covalently coupled to uniquely identifying DNA barcodes for analysis by sequencing.
>We used MIPSA to profile circulating autoantibodies from 55 patients with severe COVID-19 against 11,076 DNA-barcoded proteins of the human ORFeome library.
>MIPSA identified previously known autoreactivities, and also detected undescribed neutralizing interferon lambda 3 (IFN-λ3) autoantibodies.
>At-risk individuals with anti-IFN-λ3 antibodies may benefit from interferon supplementation therapies, such as those currently undergoing clinical evaluation
[Will I still be spreading the virus after being inoculated?]
Still no evidence to suggest otherwise
Moderna chief medical officer: Vaccinated adults could still infect the unvaccinated
UK: Coronavirus vaccine won't free you from self-isolation, says Government
>The jabs provide Covid-19 immunity but scientists are yet to prove this prevents recipients from carrying and spreading the virus.
[For how long does the immunity from vaccines last?]
~6 months for humoral/antibody immunity, like from being infected naturally
>The Pfizer vaccine is thought to offer up to six months of immunity to Covid-19
>Images have now been shared of a card patients will receive to prove they have received the jab - which has proved to be effective in 95 per cent of cases and offers up to six months of immunity
Vaccines (or being naturally infected) should still provide cellular immunity (lower limit for how long exactly - unknown, presumably at least around up to 6 years for B cells, 17 years for T cells, as in SARS-CoV-1 survivors cellular immunity lasted for this long)
>patients who recovered from SARS have T cells that are specific to epitopes within different SARS-CoV proteins that persist for 11 years after infection11. Here, we collected PBMCs 17 years after SARS-CoV infection and tested whether they still contained cells that were reactive against SARS-CoV and whether these had cross-reactive potential against SARS-CoV-2 peptides. PBMCs from individuals who had resolved a SARS-CoV infection (n = 15) were stimulated directly ex vivo with peptide pools that covered the N protein of SARS-CoV (N-1 and N-2), NSP7 and NSP13 (Fig. 3a). This revealed that 17 years after infection, IFNγ responses to SARS-CoV peptides were still present and were almost exclusively focused on the N protein rather than the NSP peptide pools
Although in effectiveness of cellular immunity against T-cell resistant mutations of SARS-CoV-2 is unknown
>D614G strain with a I472V mutation on it that is also fast growing in the US and Europe. Not only antibody resistant but also more infectious, and there are are now studies underway that might indicate that it's also T-cell resistant
[Is vaccines' efficacy affected by virus mutating?]
>As reinfection occurs with other strains, this is especially bad news for vaccine development as it means there won't be any protection from reinfection provided for other strains by the antibodies created on the original virus vaccine
The Potential for SARS-CoV-2 to Evade Both Natural and Vaccine-induced Immunity
Analysis of SARS-CoV-2 spike glycosylation reveals shedding of a vaccine candidate
>COVID-19 virulence may be more severe in Europe and North America due to coinfection with different SARS-CoV-2 strains leading to genomic recombination which might be challenging for current treatment regimens and vaccine development
SARS-CoV-2 will evolve quickly to evade widely deployed spike RBD-targeting monoclonal antibodies, requiring combinations with at least three antibodies to suppress viral immune evasion
>D614G strain with a I472V mutation on it that is also fast growing in the US and Europe. Not only antibody resistant but also more infectious, and there are are now studies underway that might indicate that it's also T-cell resistant
[Specialists' concerns about this] Monitor for COVID-19 vaccine resistance evolution during clinical trials
[Enhanced Respiratory Disease (ERD)? Antibody-Dependent Enhancement (ADE)? ]
>ERD describes severe clinical presentations of respiratory viral infections associated with medical interventions (especially vaccines). Similar clinical presentations can occur as a result of natural infections, and so ERD is detected during preclinical and clinical trials by comparing the distribution of disease severities between the intervention and placebo study arms. ERD can be associated with a broad range of molecular mechanisms, including FcR-dependent antibody activity and complement activation (that is, ADE), but also to other antibody-independent mechanisms such as tissue cell death, cytokine release and/or local immune cell activation.
>ADE can be broadly categorized into two different types based on the molecular mechanisms involved:
>ADE via enhanced infection. Higher infection rates of target cells occur in an antibody-dependent manner mediated by Fc–FcR interactions. ADE via enhanced infection is commonly measured using in vitro assays detecting the antibody-dependent infection of cells expressing FcγRIIa, such as monocytes and macrophages. The link between in vitro ADE assay results and clinical relevance is often implied, rather than directly observed. Dengue virus represents the best documented example of clinical ADE via enhanced infection.
>ADE via enhanced immune activation. Enhanced disease and immunopathology are caused by excessive Fc-mediated effector functions and immune complex formation in an antibody-dependent manner. The antibodies associated with enhanced disease are often non-neutralizing. ADE of this type is usually examined in vivo by detecting exacerbated disease symptoms, including immunopathology and inflammatory markers, and is most clearly associated with respiratory viral infections. RSV and measles are well-documented examples of ADE caused by enhanced immune activation.
>ERD and ADE (of the second type described above) are often identified by clinical data, including symptom prevalence and disease severity, rather than by the specific molecular mechanisms that drive severe disease. The presence of complex feedback loops between different arms of the immune system makes it very difficult (although not impossible) to conclusively determine molecular mechanisms of ADE and ERD in human and animal studies, even if the clinical data supporting ADE and ERD are quite clear. Many different measurements and assays are used to track ADE and ERD, which can vary based on the specific virus, preclinical and/or clinical protocols, biological samples collected and in vitro techniques used.
>Respiratory ADE is a specific subset of ERD.
Vaccine researchers, for some reason, don't want to conduct trials/studies or don't want to release detailed data on this and on how it would affect the health of humans who took the vaccine, so there's that.
]Available info on ADE with SARS-CoV-2]
The functions of SARS-CoV-2 neutralizing and infection-enhancing antibodies in vitro and in mice and nonhuman primates
>we isolated NAbs against the receptor-binding domain (RBD) and the N-terminal domain (NTD) of SARS-CoV-2 spike from individuals with acute or convalescent SARS-CoV-2 or a history of SARS-CoV-1 infection. Cryo-electron microscopy of RBD and NTD antibodies demonstrated function-specific modes of binding. Select RBD NAbs also demonstrated Fc receptor-γ (FcγR)-mediated enhancement of virus infection in vitro, while five non-neutralizing NTD antibodies mediated FcγR-independent in vitro infection enhancement. However, both types of infection-enhancing antibodies protected from SARS-CoV-2 replication in monkeys and mice. Nonetheless, three of 31 monkeys infused with enhancing antibodies had higher lung inflammation scores compared to controls. One monkey had alveolar edema and elevated bronchoalveolar lavage inflammatory cytokines. Thus, while in vitro antibody-enhanced infection does not necessarily herald enhanced infection in vivo, increased lung inflammation can occur in SARS-CoV-2 antibody-infused macaques
>ADE in respiratory infections is included in a broader category named enhanced respiratory disease (ERD), which also includes non-antibody-based mechanisms such as cytokine cascades and cell-mediated immunopathology
[2 types of ADE in vitro:]
[1. "Classic", Fc-dependent ADE, as an example noted here for one of the monoclonal antibodies (MW05)]
>results indicate that FcγRIIB is the major FcγR contributing to the enhancement of SARS-CoV-2 infection mediated by MW05
[2. "Unique" to SARS-CoV-2 ADE"]
An infectivity-enhancing site on the SARS-CoV-2 spike protein is targeted by SARS-2 patient antibodies
>we screened a series of anti-spike monoclonal antibodies from COVID-19 patients, and found that some of antibodies against the N-terminal domain (NTD) dramatically enhanced the binding capacity of the spike protein to ACE2, and thus increased SARS-CoV2 infectivity. Surprisingly, mutational analysis revealed that all the infectivity-enhancing antibodies recognized a specific site on the surface of the NTD. The antibodies against this infectivity-enhancing site were detected in all samples of hospitalized COVID-19 patients in the study. However, the ratio of infectivity-enhancing antibodies to neutralizing antibodies differed among patients. Furthermore, the antibodies against the infectivity-enhancing site were detected in 3 out of 48 uninfected donors, albeit at low levels. These findings suggest that the production of antibodies against SARS-CoV-2 infectivity-enhancing site could be considered as a possible exacerbating factors for COVID-19 and that a spike protein lacking such antibody epitopes may be required for safe vaccine development, especially for individuals with pre-existing enhancing antibodies
Antibody-dependent enhancement and SARS-CoV-2 vaccines and therapies
>Evidence of ADE in coronavirus infections in vitro
>Findings to date argue against macrophages as productive hosts of SARS-CoV-2 infection
Monocytes and macrophages, targets of SARS-CoV-2: the clue for SARS-2 immunoparalysis
>SARS-CoV-2 efficiently infects monocytes and macrophages without any cytopathic effect
>“our data show that the presence of an intrauterine bacterial infection results in the infiltration of ACE2 expressing maternal macrophage and neutrophils into and across the placental tissues.These ACE2 expressing immune cells have the potential to transport the virus to the placenta in cases of COVID-19 infection in pregnancy and increase the risk of placental infection and vertical transmission of the virus to the fetus.
>monocytes and macrophages can either be infected by, or phagocytize, SARS-CoV-2
[Any additional detailed, sourced info?]
Reminder on the current SARS-CoV-2 vaccines being leaky, as in:
Scenario of Marek's disease in chicken:
But it's not just chicken, it also has this effect on influenza:
Rundown on the mRNA vaccines in general
And some detailed info on mRNA vaccines can be found in papers, like in Moderna's mRNA vaccine paper:
tl;dr of the Oxford's ChAdOx1 nCoV-19 vaccine (AZD1222) vaccine
1) no info if it can prevent asymptomatic transmission
2) 62-90% "efficacy"
3) no data for >55 year olds
4) is not clear what should be the correct dosage; the Low Dosage/Standard Dosage has better numbers than SD/SD for some unknown reason
5) it looks like it can avoid severe cases, but then again VERY SMALL SAMPLE SIZE
6) one of the brazilian patients died - supposedly murdered
Sinovac: Interim Results of a Phase 1–2a Trial of Ad26.COV2.S SARS-CoV-2 Vaccine
>single dose as well apparently
Sinovac vaccine results are a workshop in medical transparency:
91.2% >> (interim) Turkish data
65.3% >> (interim) Indonesian data
100% >> Chinese media headlines (against severe infections)
50.4% >> final Brazil data, delayed by confidentiality clause
Human adenovirus-vectored vaccines may be of limited use in the long term, as the human body develops immunity against the adenovirus
>the presence of preexisting Ad immunity and the rapid development of Ad vector immunity still pose significant challenges to the clinical use of these vectors. Innate inflammatory response following Ad vector administration may lead to systemic toxicity, drastically limit vector transduction efficiency and significantly abbreviate the duration of transgene expression
Pfizer's coronavirus vaccine should be "safe" for most Americans, but 5 groups may want to wait for more data before getting shots
>1.Children under 16
>2.Pregnant people (do they mean pregnant women?)
>3.People who are HIV-positive and others with weakened immune systems must be particularly careful
>4.People with severe allergies to the vaccine's ingredients must hold off
>5.People who previously had COVID-19 are in a gray area
>5.People who previously had COVID-19 are in a gray area
In Summer there was an estimate that, compared to official stats, 10x more Americans have been infected
[Pfizer leak] [!]
SARS-CoV-2 Vaccine Leaked Data
Russians have hacked into EMA and leaked a bunch of emails and documents
QRDs (special thanks for anons from /plg/ - Pfizer Leak General https://archive.4plebs.org/pol/search/subject/plg/):
>effectiveness not 95% as it's being marketed
>BNT162b2 when the drug product was stored at the recommended frozen temperature of -70±10 °C for up to 1 month, and accelerated temperatures of 2-8 °C for up to 2 weeks and 25±2 °C for up to 10 days. ('09. Applicant-Rapps-EMA CMC TC - 26.11.2020/Annex 1 - Draft 3.2.P.2.2 Drug Product.pdf' page 20)
>mRNA gets degraded/damaged quickly at room-ambient temperatures outside of freezers, only 76% of the mRNA is left intact in perfect lab conditions before inoculation/getting into the cells through lipid nanoparticles, which, in turn, may possibly result in being translated as trash RNA (as mRNA is compromised in structure). Often it'll be recycled for its components (building blocks) or very rarely will it produce a protein that is misfolded and serves no purpose and eventually be degraded as well
[more on lipid nanoparticles]
tl;dr toxic, inflammatory, may mess up the "timing" of your immune response towards a real infection, resulting in either unproductive response, or a damaging and inflammatory one
The mRNA-LNP platform's lipid nanoparticle component used in preclinical vaccine studies is highly inflammatory
>we present evidence that LNPs used in many preclinical studies are highly inflammatory in mice.
>Intradermal injection of these LNPs led to rapid and robust inflammatory responses, characterized by massive neutrophil infiltration, activation of diverse inflammatory pathways, and production of various inflammatory cytokines and chemokines.
>The same dose of LNP delivered intranasally led to similar inflammatory responses in the lung and resulted in a high mortality rate. In summary, here we show that the LNPs used for many preclinical studies are highly inflammatory.
>Thus, their potent adjuvant activity and reported superiority comparing to other adjuvants in supporting the induction of adaptive immune responses could stem from their inflammatory nature.
>Furthermore, the preclinical LNPs are similar to the ones used for human vaccines, which could also explain the observed side effects in humans using this platform
>damaged RNA almost serves no purpose unless it's being broken down into its basic components. There are checklists within the cells that make sure the damaged RNA doesn't get translated into an unusable protein, such as ribosomes not allowing the structure through (no proteins are made), certain regions on the RNA form earlier stop codons (if it does go through the ribosome, the protein being manufactured stops at an early stage), and there are proteins within the cell that proof-read the sequences and if anything's wrong they take care of it (either by disposal or recycling)
>if there was a way the mRNA did produce a functional protein that does something bad there's no way to test for it right now, and that's because there haven't been enough cases with adverse effects to call for that type of testing. To test for that, you'd collect the individuals who did react negatively and simply run protein assays (you compare their protein levels in their blood to a control) and determine what's elevated and what's not. As for the long term effects of the byproducts, I don't think there are any longitudinal studies to warrant any adverse effects since these seem to be novel ingredients made specifically for this vaccine's solution
>liver, lymphatic and nerve inflammation in rat models
>60% enlarged spleen in rat models
>reduced number of mature and immature red blood cells in rat models
>large amount of unclassified cells in blood in rat models, among them:
>1) possibly formation of stem cells in response to organ trauma
>2) possibly also LARGE unspecified cells. Large cells can mean a few things (people refer to ovum as large cells as they are visible with the naked eye as well as being the largest cell in the body phagocytes are also large cells though): large cell is a term used in oncology, it does not refer to a particular type of cell; rather it refers to cells that are larger than would be normally expected for that type. It is frequently used when describing lymphoma and lung cancer. The phrase giant cell is also frequently used, especially with carcinoma. The leaked paper does not go into any greater detail describing these "large cells" so no definitive conclusions can be drawn for now
>surfactants in the vaccine solution may be the cause of inflammation (these are triggering your immune system and other organ systems as a result):
>ALC-0315 (acetamide side-chain in ALC-0315 could be a possible culprit in the unspecified cell formation, since acetamides are known carcinogens) are there to prevent the solution from clumping in on itself, ensuring everything in the vaccine solution remains 'itself'. These two components have an interesting metabolic cycle (how they get degraded in the body) where they must first undergo degradation in the liver (and this is why there's enlargement of livers and associated organs/tissue (spleens, bone marrow, immune cell count)) in which the by-product is turning out to be somewhat toxic (however, this was not common)
>ALC-0159 (more concerning because of the biotransformations it undergoes. Since this compound has an acetamide moiety (side group) and it is known to be a carcinogen, it may be the cause of the adverse side-effects the studies are seeing because of the metabolic pathways it undergoes. Also, ALC-0159 is shown to be more stable in your body with a 120min mark (>82% remaining) in liver microsomes and 240min (>87% remaining) in hepatocytes, and that's probably why we're seeing toxicity within the liver and associated organ/tissue systems))
>carcinogenous metabolite that needs further investigation
EMA quality review of toxicology (page 46)
[pfizer leak 2.0] - official documents from pfizer than partially confirm the points brought up above
Zero clues on how stable their mRNA, aside from the fact that the payload may be degraded up to 50%
>risk of autoimmune problems from modRNA - brought up
>needed research and data to assess safety - not
>re-presenting the spike triggers the inflammation
>re-presenting the RBD does not
Almost like the RBD is not of natural origin and is there to stay in the virus, with it not aggravating the pathology too much and not being susceptible to become deleted/changed
Accumulation of surfactans in the liver (and other organs maybe?)
Lipid nanoparticles overstimulating inflammation
Toxicity and accumulation of surfactants in the liver, again
If you want to be vaccinated with something with known risks, efficacy and safety, then consider getting a BCG jab instead
BCG vaccination confers protection from SARS-2 via cross-reactive SARS-CoV-2-specific T cell responses
BCG vaccine demonstrates effectiveness after 40 years (cross-reactivity with SARS-CoV-2 would last ~5 years after (re)vaccination)
>Since the delayed cell-mediated immune response, historically measured as immunoreactivity to tuberculin (tuberculin sensitivity test or TST) and presumably, the concomitant “trained immunity” conferred by BCG vaccination at childbirth wanes rapidly within first few years of childhood in the absence of “booster” Mycobacterium spp. exposures [12,15,16], the prevalent actual “trained immunity” and heterologous cell-mediated immunity correlate of any population could be a better evaluable predictive parameter of populations’ response to COVID-19 infections
Reactions to the BCG vaccine are uncommon and generally mild.
>The most common side effects include fever, headache and swollen glands.
>More serious complications, such as abscesses or bone inflammation, are rare.
>Most children develop a sore at the injection site. Once healed, the sore may leave a small scar. This is normal and nothing to worry about.
BCG revaccination boosts adaptive polyfunctional Th1/Th17 and innate effectors in IGRA+ and IGRA– adults
No cross-reactivity from BCG-induced antibodies with SARS-CoV-2, thus no chance of ADE effect from it:
Common childhood vaccines do not elicit a cross-reactive antibody response against SARS-CoV-2
>we tested whether BCG, Pneumococcal, Rotavirus, Diphtheria, Tetanus, Pertussis, Hepatitis B, Haemophilus influenzae, Hepatitis B, Meningococcal, Measles, Mumps, and Rubella vaccines provide cross-reactive neutralizing antibodies against SARS-CoV-2 in BALB/c mice. Results indicated that none of these vaccines provided antibodies capable of neutralizing SARS-CoV-2 up to seven weeks post vaccination. We conclude that if such vaccines have any role in COVID-19 immunity, this role is not antibody-mediated.
Vaccination against tuberculosis has influence on the epidemiology of SARS-2
>analysis of statistical data was conducted by experts from St Petersburg University
>incidence of COVID-19, the course of acute interstitial pneumonia caused by infection, and the mortality rate from it are associated with being vaccinated with bacilli Calmette-Guerin (BCG) according to the national vaccination schedule. The mortality rate turned out to be lower in those countries and areas where national vaccine immunization programmes have taken place for a long time or continue today, especially if revaccinations were practiced.
>BCG vaccine activates a local immune response on the mucous membranes. It is through them that acute respiratory disease caused by SARS-CoV-2 spreads
>BCG vaccine serves as a trigger for a 'trained' immune system response that activates monocytes, macrophages and natural killer cells - that power in the non-antigen-specific protective rogrammes of the body. Also, gamma-interferon, produced after BCG vaccination, and other mediators may ultimately attenuate the course of COVID-19.
>'The causative agent of the new coronavirus infection and BCG have common peptides, which means that induction of cross-immunity is possible. Large clinical trials of the BCG vaccine and trials of its use for the prevention of the new coronavirus infection are currently underway, for example, in the Netherlands and Australia'
>BCG vaccination could reduce the infection caused by SARS-2 and MCV2 vaccine years increases the total infection rate. This study identified high economic characteristics and not having universal BCG coverage as the independent risk factors of mortality by the multivariate analysis.
Trained immunity’ from Mycobacterium spp. (environmental or BCG) exposure predicts protection from SARS-2
Good job on reading it all.