I and my wife are senior citizens and we both have underlying comorbidities. We both received the Moderna mRNA shots in Jan and Feb 2021.
We are now eligible to receive the booster shots but have several questions related to efficacy and protection duration of these booster shots to the Delta variant and the new Delta variant mutation reported in England.
This CDC information packet on Booster Shots is being updated
The questions we raise:
1. Even though boosters raise human monoclonal neutralizing antibodies (MNABs) based upon initial mRNA vaccine spikes, how effective are these initial MNABs against the Delta and future variant viruses, especially when longterm animal test data was not done because of EUA protocols?
2. What causes the waning efficacy from the original mRNA vaccine?
3. Could waning efficacy also be caused by Delta variant spike mutation which resists initial MNABs caused by Delta variant creating protective glycans( glycoproteins) which cover the receptor binding domain (RBD) and/ or other unknown causes?
4. How does the booster/3rd shot improve waning efficacy of first two shots if it generates more of the same MNABs?
5. How long does this reported “increased booster efficacy” last before a 4th, and 5th booster is recommended? Again longterm animal studies were not performed.
6. Using flu vaccines as an example, we would have expected a new mRNA vaccine which included the genome to produce Delta variant spike glycoproteins to generate human MNABs to neutralize delta variant spikes.
7. Are new mRNA vaccines which include Delta variant genome being made/tested? When can the public expect their release?
8.We also read that England has seen a new variant mutation occur from the Delta variant. Does that imply new and more mRNA vaccines?
9. When do these “temporary vaccine solutions” end?
10. More short term vaccine solutions which address current variant but do not address future mutant strains?
11. What if our body’s MNABs become ineffective against pathogenic viral infection because these viruses become resistant to anti viral vaccines/therapeutics similar to bacteria resistance due to overuse of antibiotics?
12. Why not include mutation in the problem definition and implement longterm , cost effective solutions which prevent infection, meet goals/objectives, are within CDC/FDA control, and don’t negatively impact “human Guinea pigs/lab Experimental animals use via emergency use authorization (EUA) protocols?
Gates foundation is heavily investing in pharmaceutical drugs/capsule which show 50% efficacy. The treatment, a pill called molnupiravir developed by US lab Merck, reduces the risk of hospitalization by half in COVID-19 patients who take it in their first few days of infection, the company has said, and could be even more effective at preventing deaths from the virus.
Other Repurposed Drugs
Coincidentally, that’s what Dr Zelenko claims by using zinc plus Hydroxychloroquine in the first 5 days of infection to prevent severe disease , hospitalization, and death.
N4-hydroxycytidine = molnupiravir ( another repurposed drug)
N4-Hydroxyctidine, or EIDD-1931, is a ribonucleoside analog which induces mutations in RNA virions. N4-hydroxycytidine was first described in the literature in 1980 as a potent mutagen of bacteria and phage. It has shown antiviral activity against Venezuelan equine encephalitis virus, and the human coronavirus HCoV-NL63 in vitro. N4-hydroxycytodine has been shown to inhibit SARS-CoV-2 as well as other human and bat coronaviruses in mice and human airway epithelial cells.
Remedesivir ( Adenosine homologue) and Hydroxychloriquine, both zinc ionophores, also interfere with viral RT enzyme and prevent viral reproduction. Hydroxychloriquine has been banned for Hospital use but Remdesivir is still accepted as a recommended CV19 disease treatment protocol in hospitals and maybe causing adverse side effects/deaths in treating this pandemic.
NIAID Funded Study on Remdesivir
WHO study on repurposed drugs used to treat CV19 disease
N4-hydroxycytidine also appears in the pharmaceutical Zinc20 database funded by a subsidiary of National Institute of Health (NIH). It is another ligand ( binds and transports blood serum metals like Zinc) aka zinc ionophore.
Excerpt from above article:Covid-19: Waning vaccine efficiency, high pre-symptomatic transmission behind Delta variant’s rapid spread – The Financial Express
The study also revealed that peak viral load even in vaccinated individuals was similar to that of unvaccinated people. Similar results have been found in studies conducted in Singapore and the US.
This means even fully-vaccinated people are at risk of spreading the Delta variant, making it even more difficult to break the chain.
A US CDC report this month said 469 Covid-19 cases were reported in Massachusetts following a large gathering in Provincetown, a beach town. Of these, nearly 75 per cent people were vaccinated.
Analyses have shown that vaccinated individuals showed his Ct values, similar to unvaccinated people. This indicated a high viral load.
Delta R0 is 6.4 vs initial SARS COV-2 which is 2-4. So it’s more infectious than SARS, MERS, Flu, Cold, Ebola.
Seems that the Delta variant has a mutation of two amino acids ,Argentine and Proline in S1 RBD which allows the enzyme
Furin to cleave the spike more efficiently and bind to ACE-2 bypassing MNABs detection .
I began reading the attached below article:
“Worse Than the Disease? Reviewing Some Possible Unintended Consequences of the mRNA Vaccines Against COVID-19 Stephanie Seneff1 and Greg Nigh 21Computer Science and Artificial Intelligence Laboratory, MIT, Cambridge MA, 02139, USA, E-mail:
PEG nano lipids can cause anaphylaxis and cardiac arrest. Actual percentage of those vaccinated is 2.4% which is 21x higher than reported in VAERS
ADE- antibody dependent enhancement antibodies created by spike protein , (via exposure to virus, similar viruses, or from vaccine) in insufficient numbers can bind to Fc receptor on cell’s surface ( not ACE-2 receptor) facilitating viral entry and enhancing infectivity.
S protein specific Antibodies may contribute to disease severity upon reexposure to SARS COV-2 infection.
*This sounds similar to what happened in development of mRNA vaccines for MERS/SARS COV1 where ferrets were vaccinated and then reexposed to virus in field 6+ months later resulting in cytokine storm.*
It has been reported that all three US vaccine manufacturers – Moderna, Pfizer, and Johnson & Johnson – are working to develop booster shots (Zaman 2021).
With tens of millions of young adults and even children now with vaccine-induced coronavirus spike protein antibodies, there exists the possibility of triggering ADE related to either future SARS-CoV-2 infection or booster injection among this younger population. Time will tell.
The mRNA vaccines ultimately deliver the highly antigenic spike protein to antigen-presenting cells. As such, monoclonal antibodies against the spike protein are the expected outcome of the currently deployed mRNA vaccines. Human spike protein monoclonal antibodies were found to produce high levels of cross-reactive antibodies against endogenous human proteins (Vojdani et. al., 2021; reviewed in more detail below).
Given evidence only partially reviewed here, there is sufficient reason to suspect that antibodies to the spike protein will contribute to ADE provoked by prior SARS-CoV-2 infection or vaccination, which may manifest as either acute or chronic autoimmune and inflammatory conditions.
We have noted above that it is not possible to distinguish an ADE manifestation of disease from a true, non-ADE viral infection. In this light it is important to recognize that, when diseases and deaths occur shortly after vaccination with an mRNA vaccine, it can never be definitively determined, even with a full investigation, that the vaccine reaction was not a proximal cause.
EJL *VAERS collects data but has not produced any causal reports. Why not?