Part two: Geert Vanden Bosschens vaccine warning letter:
Well, similar to the rules applying to classical antimicrobial antibiotics, it is paramount that our self-made ‘antiviral antibiotics’ are made available in sufficient concentration and are tailored at the specific features of our enemy. This is why in case of bacterial disease it is critical to not only chose the right type of antibiotic (based on the results from an antibiogram) but to also take the antibiotic for long enough (according to the prescription). Failure to comply with these requirements is at risk of granting microbes a chance to survive and hence, may cause the disease to flare up. A very similar mechanism may also apply to viruses, especially to viruses that can easily and rapidly mutate (which is, for example, the case with Coronaviruses); when the pressure exerted by the army’s (read: population’s) immune defense starts to threaten viral replication and transmission, the virus will take on another coat so that it can no longer be easily recognized and, therefore, attacked by the host immune system. The virus is now able to escape immunity (so-called: ‘immune escape’). However, the virus can only rely on this strategy provided it still has room enough to replicate. Viruses, in contrast to the majority of bacteria, must rely on living host cells to replicate. This is why the occurrence of ‘escape mutants’ isn’t too worrisome as long as the likelihood for these variants to rapidly find another host is quite remote. However, that’s not particularly the case during a viral pandemic! During a pandemic, the virus is spreading all over the globe with many subjects shedding and transmitting the virus (even including asymptomatic ‘carriers’). The higher the viral load, the higher the likelihood for the virus to bump into subjects who haven’t been infected yet or who were infected but didn’t develop symptoms. Unless they are sufficiently protected by their innate immune defense (through natural Abs), they will catch Covid-19 disease as they cannot rely on other, i.e., acquired Abs. It has been extensively reported, indeed, that the increase in S (spike)-specific Abs in asymptomatically infected people is rather limited and only short-lived. Furthermore, these Abs have not achieved full maturity. The combination of viral infection on a background of suboptimal Ab maturity and concentration enables the virus to select mutations allowing it to escape the immune pressure. The selection of those mutations preferably occurs in the S protein as this is the viral protein that is responsible for viral infectiousness. As the selected mutations endow the virus with increased infectious capacity, it now becomes much easier for the virus to cause severe disease in infected subjects. The more people develop symptomatic disease, the better the virus can secure its propagation and perpetuation (people who get severe disease will shed more virus and for a longer period of time than asymptomatically infected subjects do). Unfortunately enough, the short-lived rise in S-specific Abs does, however, suffice to bypass people’s innate/natural Ab. Those are put out of business as their affinity for S is lower than the affinity of S-specific Abs. This is to say that with an increasing rate of infection in the population, the number of subjects who get infected while experiencing a momentary increase in S-specific Abs will steadily increase. Consequently, the number of subjects who get infected while experiencing a momentary decrease in their innate immunity will increase. As a result, a steadily increasing number of subjects will become more susceptible to getting severe disease instead of showing only mild symptoms (i.e., limited to the upper respiratory tract) or no symptoms at all. During a pandemic, especially youngsters will be affected by this evolution as their natural Abs are not yet largely suppressed by a panoply of ‘acquired’, antigen-specific Abs. Natural Abs, and natural immunity in general, play a critical role in protecting us from pathogens as they constitute our first line of immune defense. In contrast to acquired immunity, innate immune responses protect against a large spectrum of pathogens (so don’t compromise or sacrifice your innate immune defense!). Because natural Abs and innate immune cells recognize a diversified spectrum of foreign (i.e., non-self) agents (only some of which have pathogenic potential), it’s important, indeed, to keep it sufficiently exposed to environmental challenges. By keeping the innate immune system (which, unfortunately, has no memory!) TRAINED, we can much more easily resist germs which have real pathogenic potential. It has, for example, been reported and scientifically proven that exposure to other, quite harmless Coronaviruses causing a ‘common cold ’ can provide protection, although short-lived, against Covid-19 and its loyal henchmen (i.e., the more infectious variants).
Suppression of innate immunity, especially in the younger age groups, can, therefore, become very problematic. There can be no doubt that lack of exposure due to stringent containment measures implemented as of the beginning of the pandemic has not been beneficial to keeping people’s innate immune system well trained. As if this was not already heavily compromising innate immune defense in this population segment, there comes yet another force into play that will dramatically enhance morbidity and mortality rates in the younger age groups: MASS VACCINATION of the ELDERLY. The more extensively the latter age group will be vaccinated and hence, protected, the more the virus is forced to continue causing disease in younger age groups. This is only going to be possible provided it escapes to the S-specific Abs that are momentarily raised in previously asymptomatically infected subjects. If the virus manages to do so, it can benefit from the (momentarily) suppressed innate immunity, thereby causing disease in an increasing number of these subjects and ensuring its own propagation. Selecting targeted mutations in the S protein is, therefore, the way to go in order for the virus to enhance its infectiousness in candidates that are prone to getting the disease because of a transient weakness of their innate immune defense.
But in the meantime, we’re also facing a huge problem in vaccinated people as they’re now more and more confronted with infectious variants displaying a type of S protein that is increasingly different from the S edition comprised within the vaccine (the latter edition originates from the original, much less infectious strain at the beginning of the pandemic). The more variants become infectious (i.e., as a result of blocking access of the virus to the vaccinated segment of the population), the less vaccinal Abs will protect. Already now, lack of protection is leading to viral shedding and transmission in vaccine recipients who are exposed to these more infectious strains (which, by the way, increasingly dominate the field). This is how we are currently turning vaccinees into asymptomatic carriers shedding infectious variants.
At some point, in a likely very near future, it’s going to become more profitable (in term of ‘return on selection investment’) for the virus to just add another few mutations (maybe just one or two) to the S protein of viral variants (already endowed with multiple mutations enhancing infectiousness) in an attempt to further strengthen its binding to the receptor (ACE-2) expressed on the surface of permissive epithelial cells. This will now allow the new variant to outcompete vaccinal Abs for binding to the ACE receptor. This is to say that at this stage, it would only take very few additional targeted mutations within the viral receptor-binding domain to fully resist S-specific anti-Covid-19 Abs, regardless whether the latter are elicited by the vaccine or by natural infection. At that stage, the virus will, indeed, have managed to gain access to a huge reservoir of subjects who have now become highly susceptible to disease as their S-specific Abs have now become useless in terms of protection but still manage to provide for long-lived suppression of their innate immunity (i.e., natural infection, and especially vaccination, elicit relatively long-lived specific Ab titers). The susceptible reservoir comprises both, vaccinated people and those who’re left with sufficient S-specific Abs due to previous Covid-19 disease). So, MISSION ACCOMPLISHED for Covid-19 but a DISASTROUS SITUATION for all vaccinated subjects and Covid-19 seropositive people as they’ve now lost both, their acquired and innate immune defense against Covid-19 (while highly infectious strains are circulating!). That’s ‘one small step for the virus, one giant catastrophe for mankind’, which is to say that we’ll have whipped up the virus in the younger population up to a level that it now takes little effort for Covid-19 to transform into a highly infectious virus that completely ignores both the innate arm of our immune system as well as the adaptive/acquired one (regardless of whether the acquired Abs resulted from vaccination or natural infection). The effort for the virus is now becoming even more negligible given that many vaccine recipients are now exposed to highly infectious viral variants while having received only a single shot of the vaccine. Hence, they are endowed with Abs that have not yet acquired optimal functionality. There is no need to explain that this is just going to further enhance immune escape. Basically, we’ll very soon be confronted with a super-infectious virus that completely resists our most precious defense mechanism: The human immune system.