In a recent paper titled COVID-19 Vaccine Frontrunners and Their Nanotechnology Design, the authors make the introductory statements:
Moderna reached clinical trials 63 days after their sequence selection. It is striking that an unestablished nanotechnology formulation reached clinical testing almost a full month before established approaches (ie, inactivated and live-attenuated vaccines) entered clinical trials.
It is also of note that in previous severe coronavirus outbreaks of SARS-CoV and MERS-CoV clinical trials were not reached until 25 and 22 months after the outbreaks began.
The improved speed into clinical trials is hopeful, but despite the rapid progress, there are still reasons for concern.
The fact is, vaccine development does not happen overnight. They must be preventative but also risk-free. Most substances are given to unwell patients, but vaccines are dispensed to healthy individuals and so necessitate an extremely high protective promise.
The current SARS CoV 2 vaccines are emergency use drugs and have bypassed usual developmental methodology. It is important to note, because it has previously been shown with other respiratory type viruses (SARS-CoV, MERS-CoV, RSV and measles) that antibodies produced can intensify disease ferocity via antibody dependant enhancement (this means the infection can get worse or the intensity of the immune response can be overwhelming).
The Pfizer and AstraZeneca vaccines are ‘nanotechnologies’ and these have not been proven before in clinical environments. In fact, this technology (called an mRNA vaccine) has been researched and tested for 30 years but never been approved.
Every virus is contrasting so there isn’t one perfect solution for all infections. Even within this single SARS-CoV 2 virus some hugely infected people are asymptomatic while others become critical. The enormous inconsistency may infer that a vaccine will not deliver consistent or prolonged immunity in all?
The Questions ...
One of the major questions is what type of immune response in needed to guard against the virus?
At this point in time, we don’t know definitively. This should be somewhat of a concern given that we now have two (in Australia) vaccines available designed to produce a response without knowing if it the specific response we need.
In the entire history of vaccines, there has only ever been one that has eradicated a disease: the smallpox vaccine. Some have come close, but eradication is evasive: polio, measles and mumps ...
Respiratory viruses, as the SARS-CoV 2 is, are particularly hard to vaccinate for, despite heavy efforts to manufacture a vaccine. This is partly because the airways and lungs are not an enclosed environment and can’t be protected as can cervical cancer, for example. With respiratory viruses you can be continuously exposed to the infection, in theory.
Most vaccines are delivered by intramuscular injection, and as such, they produce an antibody response that is better developed in the blood (called IgM or IgG responses). The type of protection we need on the mucosal surfaces of the lungs is an IgA response, which is minimal with intramuscular vaccines. At this point in time, there are other vaccines in trials that are looking at improving the IgA response, but this is not the mechanism of the vaccines that are on offer in Australia.
SARS-CoV 2 is different for a respiratory virus because it hitches to a receptor called the angiotensin converting enzyme 2 (ACE2). This receptor is found in almost all organs but particularly on the surfaces of the lungs and the digestive system, along with the brain. Hence, this particular virus damages at sites distal to its entry point. This is why it can have such destructive and broad effects. Predominantly, it hangs around in respiratory, circulatory, nervous and urogenital systems and why it’s responsible for many varied symptoms. Much of the pathology here, outside of the airway, is defended by IgG antibody responses, and this is the target of the vaccines we now have. This is vital to note, because the vaccine is not designed to promote an IgA response, and therefore, it’s not designed to prevent infection or its transmission in the airways.
This is one of the issues that hasn’t been addressed by governments or chief health officers. If the vaccine isn’t designed to prevent positive tests, do we shut down a city or state again when someone tests positive, as they will?
So, what is different about the Pfizer and AstraZeneca vaccines compared to traditional vaccines?
Both rely on nanoparticle technology. These nanoparticles are of the same proportions as the virus. As such, it confers an ability to enter cells as the virus would. Nanoparticles encapsulate the nuclear material (mRNA for Pfizer and DNA for AstraZeneca) and adjuvants for use of the immune system once inside the target cells.
Once inside the nucleus of the cell, the lab formulated genetic material from the virus is incorporated with our genetic material to produce an inert viral protein that our cells recognise as foreign and subsequently mounts an immune response.
Different nanoparticles are available. In the case of Pfizer, they use lipid (fats) nanoparticles (LNPs) and for AstraZeneca, they use another virus (which comes from chimps. It can enter human cells but seems to be inert once inside).
Older types of vaccines would have used actual live or dead virus.
What about the issue of adjuvants?
Adjuvants are immunostimulatory molecules that are designed to annoy the inflammatory and immune systems to hopefully produce a heightened response to vaccine stimulation. The issue here is that many adjuvants have earlier not passed muster due to toxicity pitfalls. In the past, and at times today, the adjuvants in vaccines include molecules like mercury and aluminium. These have no business being in the human body.
Where the Australia’s available vaccines should potentially improve their efficacy is that when encapsulated in nanoparticles, both viral nucleic material and adjuvants should reach their target destination cells. This serves multiple purposes that other types of vaccines don’t.
Firstly, it means that adjuvants aren’t as likely wander off and affect other cells. If you are targeting lung cells, you don’t want the adjuvants backstroking towards the brain, for example.
Secondly, it may mean that the amount of adjuvant is less because you don’t have to account for the loose amount that wanders off, reducing its effectiveness.
Thirdly, the adjuvant is less likely to degrade along its journey, also reducing its effectiveness.
Fourthly, if the antigen (here, nucleic material) and the adjuvant arrive at the target cells at different times, it can set up an autoimmune response where we react against our cells (self-antigens) if these other cells, rather than the target cells, have taken up the adjuvant.
This type of nanoparticle delivery process is already utilised with common supplements or formulas you may have taken. For example, liposomal vitamin C or Mutaflor (an Iron formula), in which the iron molecule is attached to a sugar molecule for ease of absorption.
Another possible positive for this nanoparticle process is that the smaller molecules can also move through the spaces between cells, where other larger, non-nanoparticle vaccines cannot. Material in these spaces is picked up by the lymphatic system rather than the circulatory system. The lymphatic system is vital to our immune response whereby certain cells in the lymphatic system called antigen presenting cells take the antigen (inert viral material) to the lymph nodes to meet other immune cells which go on to stimulate much longer lasting immune responses (sometimes years, although we’re not sure this is the case yet with SARS-CoV 2?).
Although this may be seen as a positive, what is not talked about is that if viral material can be delivered to the lymphatic system, then so can the adjuvants. If we react to the adjuvants then this is a problem, because as many of you will know, once something is in the lymphatic system (like cancer), it can end up creating a problem anywhere.
So, while nanoparticle technology would seem to be a safer, more efficient way of delivering a vaccine, there are issues as noted in the previous paragraph.
So, what are they adjuvants in the Pfizer and AstraZeneca vaccines?
Only 29 of the 202 companies that applied to produce a vaccine made it through the initial standards to start trials. Of these companies, very few have released their initial data on safety and ability to produce an immune response.
To get the viral material into the cellular mechanism, amongst others, Pfizer has used lipid nanoparticles cholesterol, phosphatidylcholine and polyethylene glycol-lipid. They did not list all the LNPs they used. There is no indication from Pfizer that they did or did not use adjuvants. However, they do mention that the viral material can act as an adjuvant and there is increasing use of certain LNPs themselves as adjuvants. This would seem to be better than, say, mercury.
Early trials did not list any severe reactions, but common adverse events included headache, fever and pain. Note here that Pfizer was judging its response on IgG mediated assays, which, as already mentioned, is not aimed at preventing infection or transmission of coronavirus.
The AstraZeneca vaccine doesn’t mention whether it used an adjuvant. It only tested for an IgG response and its adverse events were listed as pain, fatigue and headache.
Of the 29 listed trial participants, only 4 companies directly mention the use of adjuvants. The rest? Do they or don’t they?
Part of the problem with both vaccines is that limited information is available. Many researchers and scientists outside of the company bubble are guessing at the possible mechanisms of function.
Adjuvants should be fully and specifically listed. According to an article in Frontiers in Immunology titled Adjuvants for Coronavirus it is written:
Aluminium salt-based adjuvants (alum) were the first adjuvants used in licensed human vaccines. They are still the most widely used because of their wide-spectrum ability to strengthen immune responses and their excellent track record of safety. In limited coronavirus vaccine studies, it has been suggested that neutralizing antibody against the spike protein might be mechanistically correlated with immune protection. When alum was formulated with S protein or receptor- binding domain (RBD), it significantly enhanced humoral immune responses. This was demonstrated by higher titres of serum IgG1, increased high affinity viral neutralising antibodies, and the generation of long-lasting memory B cells in mice.
The Pfizer vaccine uses the S protein / RBD mechanism for its action, but it doesn’t it doesn’t say whether it does or doesn’t use aluminium as a adjuvant?
Mentioned above in the Pfizer vaccine ingredient list is the lipid nanoparticle polyethylene glycol. Whilst it is not a heavy metal adjuvant like mercury or aluminium, please read the following article elsewhere in this newsletter:
Immediate Hypersensitivity to Polyethylene Glycols and Polysorbates: More Common Than We Have Recognized.
This article highlight just a few of the questions that should be asked about when making this important decision. Unfortunately, it’s not the kind of information you are likely to get via many of the media outlets we utilise. It’s important to be informed.