A Possible Relationship between ER Stress, COVID Infection, and Vaccine Adverse Reactions

A Proposed "Pseudo-infection" Hypothesis

Note: This post is not exhaustive, and is intended to be informative and present a possible hypothesis. The information here should not be used as medical advice and is intended to inform and provide perspective to the scenario presented below.

When I first started looking into Fluvoxamine the first papers I came across were ones discussing its Sigma-1 agonistic activity. Not knowing much about Sigma-1 receptors, and how targeting this receptor may help with fighting COVID, quick research brought up additional papers detailing that the Sigma-1 receptor is found on the endoplasmic reticulum. More importantly, attention was brought to the idea of the unfolded protein response (UPR). I wasn’t aware that our cells have a feedback pathway for something as ubiquitous as protein synthesis and folding, yet it makes sense to have a built-in fail-safe for something so commonly found in all eukaryotic cells.

But that got me to start thinking about the COVID vaccines. These vaccines are not like vaccines of old where either the virus itself or an antigen from the virus is presented to us in a neat, little package for our immune systems to deal with as they please. Instead, these vaccines are more like those mail-order meals like Blue Apron, which deliver you the ingredients with the expectation that you make the dish yourself.

For many of us the approach to these COVID vaccines has been one of looking at the end product. How does the dish taste, and is there something concerning, possibly toxic about it that I am unaware of? Am I possibly allergic to it, and eating it may cause a large autoimmune response to occur? That’s been the main way we have examined these vaccines, looking at it from the role of the end product, the spike protein, and the possible adverse reactions from the spike protein itself.

But such a myopic view may miss out on many of the processes leading up to the spike protein itself. Sure, you may be able to create that meal that you ordered, but what if it required you to scald all of our pots and pans, or to clog your sink from tons of gunk being shoved into the garbage disposal? Or if you barely made it out from the ensuing fire because high heat and grease don’t mix well together? Sure, you’ve been able to make your chicken Parmesan, but at what cost?

My examination into Fluvoxamine, and subsequently of the unfolded protein response has brought me to the scenario above, one that has possibly been overlooked with these COVID vaccines. Because the intent of these vaccines is to use our own machinery to produce the spike protein, shouldn’t we be concerned about the cascade of events required to produce the spike protein, and how the response could lead to adverse reactions?

And so it is from this that I propose an additional hypothesis to the adverse reactions we are seeing with these vaccines. Here, I posit that many of the adverse reactions from the vaccines are not just a results of spike protein cytotoxicity, but of the hijacking of our host cells and forcing them to produce the spike protein itself that is causing damage. Therefore, it is my belief that ER Stress, brought on by the forced production of these spike proteins, and thus leading to an activation of inflammatory pathways, may also play a role in the adverse reactions we are seeing with these vaccines.

I will back up such a hypothesis with as much evidence as possible, although note that there will be gaps that would hopefully be filled in as additional information comes about. Nonetheless, we will work with what’s available and try to get as close to the truth as possible.

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Drawing Parallels

I never gave much thought to what it means when something runs or is parallel to something else. However, I find myself using the phrase of “drawing parallels” a lot more often than before.

When drawing parallels between two ideas or objects, we do so with the intent of comparing the things we are investigating. Essentially, how much can the events of one thing parallel what one would expect in something else.

I’ve been quite shocked to see how many parallels can be drawn between COVID vaccines and the infection itself. Prior to COVID I would normally get an annual flu shot. The symptoms were always typical redness in injection sight, slight fever and maybe some muscle aches around the site of injection. Many of these symptoms are indicative of an immune response, and it’s one that people tend to conflate with an actual flu infection, believing that the fever from a vaccine may parallel one seen when infected with the flu. Although, they are indicative of an immune response occurring, it may not be proper to say that are fully comparable. However, I have never gotten a flu vaccine where the symptoms actually paralleled a flu infection such as coughs, sore throat, and runny nose. If such a thing occurred I would be absolute concerned why my vaccine is causing me to have similar symptoms as if I was sick.

It’s why I’ve become deeply concerned with many of the adverse reactions that have been experienced by people with COVID vaccines. It’s not just an overwhelming unwell feeling (so many people I know talk about feeling like shit for a week after getting their vaccines) but that people have reported neurological symptoms such as severe headaches and fatigue, which are strangely also found in some instances of long COVID. Most worrying are the incidences of myocarditis, a rare event nonetheless but a shocking one to be seen in both circumstances of COVID infection and vaccination. Now, many people may use this point to make an argument that rates of myocarditis are greater in COVID infection than vaccination, and thus these vaccines are more beneficial than harmful. My concern here is not the prevalence of myocarditis, but that its appearance in both scenarios points to possible parallels, such that something within the vaccine may be causing the presentation of myocarditis similar to a COVID infection.

Because of this I find it more appropriate to assess the causative agents within the COVID vaccines in a manner that parallels the agents found in SARS-COV2.

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A Look at the Culprits

With vaccines there are 3 main candidates to look at; the lipid nanoparticles, the mRNA, and the spike protein. There is so much that we don’t know about the lipid nanoparticles, and taking into account many of the other adverse reactions seen with COVID vaccines the roles of LNPs should not be dismissed. Again, for the sake of drawing parallels I will leave the asessment of LNPs for possibly another post.

That leaves us with either the spike protein or the mRNA. Many people are already looking into the spike protein as the causative agent, and unfortunately there’s still so much that we don’t know about the role of the vaccine’s spike protein. What we do know for a fact is that the spike protein of SARS-COV2 is indeed cytotoxic. I have mentioned the study that found many of SARS-COV2’s proteins, including the spike protein can activate the signaling cascade for ER Stress (Echavarría-Consuegra et. al.). In fact, there is actual evidence from SARS-COV that the spike protein can be cytotoxic as well, and in fact many coronavirus spike proteins have been implicated in causing cytotoxic damage.

All this to say that the spike protein of the vaccine is absolutely worth investigating, and the idea that pushback has been brought not just to the cytotoxic nature of the vaccine’s spike but to even the virus’ spike is absolutely absurd. However, because many people have already drawn attention to the spike protein, and that it falls outside of the purview of this post, we will exclude it for now even though it is something that should still be considered.

So that leaves us with the mRNA. The mRNA encoded within the vaccine has not been discussed much. Its sole responsibility is to produce the spike protein so not a lot of attention has been brought to the mRNA. However, emerging evidence, and for the sake of this hypothesis, we can see that the mRNA is not just a side character but presents with its own concerning features.

The mRNA used to translate the spike protein contains a unique base called pseudouridine (usually shortened with the greek letter Ψ) in place of uridine. There are two reasons for doing so: 1) mRNA containing the regular uridine is likely to be recognized by nucleases which would digest the mRNA and 2) viral mRNA itself may elicit an immune response to target the mRNA. The swap for a Ψ is mainly done to reduce the risk of the two concerns above. It is worth noting that a COVID vaccine was developed utilizing regular uridine and the results were not as good as was expected (Kremsner et. al.).

The perspective of these Ψ-containing mRNAs has been all but great; they have done their job by creating spike proteins and not dying in the process. No harm there right? Well, what if they persist longer than expected? A recent study by Röltgen et. al. has made its way around Substack. In one part of this study researchers found that both the spike protein and vaccine mRNA were still detectable several weeks after vaccination, and in some instances up to two months afterward. The same did not occur in patients who died from COVID, raising questions as to the survivability of the mRNA and spike. Now, the sample sizes were small in both groups and the sourcing of the germinal centers were different (vaccine mRNA were sourced from nearby mammary glands while post-mortem sourcing came from the peribronchus of COVID deceased individuals). What’s important about this finding is that it raises questions, and a possible backfiring of the longevity of these mRNAs. It appears, by virtue of adding Ψ residues to prevent being targeted by nucleases, that the mRNA may not be degraded for long periods. If that were the case, one has to wonder how long protein production may be occurring, and if the constant production of spike protein may be contributing to the adverse reactions being seen.

For the sake of this hypothesis we are concerned about the protein production itself, and the recent results from this study may indicate that host cells may be hijacked for the production of spike proteins for long periods of time. As of now there’s no evidence to support this, but it may provide a perspective from which we can come up with an assumption that spike protein is continuously produced for several weeks, thus requiring the machinery to do so and thus may be exerting continuous ER stress along with the inflammation that accompanies it.

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Mimicking Viral Infection

So let’s first propose a scenario.

Let’s say you’re house is like a cell. A foreign object stops by at your doorstep and wants entry. It makes its way into your house, making itself comfortable. However, you’re a little suspicious and unsure if you should call the police, so you wait a while and give it time. Now, this uninvited guest wants to make use of your kitchen and all your groceries to make food. It has a recipe but no cookware or ingredients so it decides to steal yours to make a meal. And it keeps making a meal, using up all of our resources and destroying your kitchen, and by extension your house. By the time you try to react it’s too late; the perp has left (or attempts to leave) with all the goodies it made leaving your house in total disarray and ruin.

So what scenario does this sound like? Exactly, the vacc- er, a viral infection! Sorry, I tend to get them mixed up!

It’s interesting that the mRNA vaccines, although not intentionally nefarious, can parallel the behaviors of viruses. Viruses cannot replicate alone and require the hijacking of their host’s machinery to replicate their genome and produce proteins. By doing so, viruses are able capable of causing ER stress by the rampant production of proteins.

Here’s an excerpt from He, B. highlighting this point:

Recent evidence has suggested the importance of ER stress response in virus infection.5, 6, 7, 8 As a processing plant for folding and post-translational modification of proteins, the ER is an essential organelle for viral replication and maturation. In the course of productive infection, a large amount of viral proteins are synthesized in infected cells, where unfolded or misfolded proteins activate the ER stress response. ER stress caused by viruses has been observed to modulate various signaling pathways leading to cell survival or cell death.9, 10, 11 Obviously, differential regulation of ER stress dictates the viral pathogenesis or replication. It has been suggested that in mammalian cells the ER chaperone immunoglobulin heavy-chain binding protein (BiP), also known as glucose-regulated protein 78 (GRP78), works as a master control interacting with three mediators: PKR-like ER kinase (PERK), activating transcription factor 6 (ATF6) and the ER transmembrane protein kinase/endoribonuclease (IRE1).12, 13, 14 In response to ER stress, these components function to reduce the levels of new proteins translocated into the ER lumen, to enhance the protein-folding capacity and secretion potential of the ER, and to facilitate transport and degradation of ER-localized proteins (Figures 1 and 2).

Coronaviruses are an example of a family of viruses that are capable of eliciting an ER Stress and possibly causing cellular apoptosis (Fung, T. & Liu, D.) So we can see why it may be accurate to compare viral infections to the behaviors of these mRNA vaccines, as they both require the use of host machinery in order to create more proteins, although these actions may prove detrimental to the cell and the host as a whole.

One thing that does make viruses different is their ability to alter the ER Stress induced by a cell. The ER Stress signaling cascade is not inherently evil; it could be a signal for the cell to try to maintain homeostasis that may be disturbed by the actions of a viral infection. Because of this many viruses have evolved with abilities to manipulate the ER Stress response for their own benefit (Li, et. al.).

So the issue with these mRNA vaccines is whether the hijacking of the ER to produce spikes elicits an ER stress signal to quell the rampant spike protein production, or if the nature of forcing constant spike protein production, followed by the release of pro-inflammatory cytokines and interleukins plays a role in the clinical manifestations of myocarditis and other adverse reactions? We do know that many spike proteins are produced by the vaccines, and it’s highly unlikely that each host cell produces one measly spike protein alone. It’s also unlikely that the mRNA from the vaccines alone are capable of halting the final apoptosis signal after the ER Stress goes on for too long, but it is also likely that large-scale, ER Stress-induced apoptosis contributes to the local cellular environment, with the release of all of those pro-inflammatory markers affecting nearby cells including immune cells.

Therefore, it’s hard to discern if the effects of ER Stress are intended to be protective or if they may backfire and elicit a deleterious response through prolonged ER Stress.

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Implicating ER Stress in Other Diseases

Because we have no way of testing (at least I can’t) whether the mRNA from vaccines is causing ER stress, we may be able to examine whether ER stress is associated with many of the adverse reactions seen with vaccination. In doing so, we may confer some association, such that if ER Stress may contribute to myocarditis, and mRNA invasion into myocardiocytes may cause ER Stress, then we may consider that ER stress caused by vaccine mRNA may lead to dangerous outcomes such as myocarditis. It’s a bit of a leap, but it provides us some measure to compare. This is an untested hypothesis, and so we may provide ourselves with a bit of leeway.

ER Stress is Implicated in Cardiovascular Disease

As previously mentioned ER stress has been associated with a plethora of disease pathologies. The heart is no exception, and there is plenty of evidence of ER Stress contributing to cardiovascular diseases including heart attacks, heart failure, and myocarditis (Hong, et. al.).

In short, myocarditis refers to inflammation of the myocardium/myocardiocytes of the heart (note that any -itis suffix is indicative of inflammation). Myocarditis tends to be attributed to viral infection, although immune dysfunction can contribute to myocarditis as well. In general, activities that may inflame the tissue surrounding the heart is concerning regardless of the source.

Myocarditis is not a rare condition with coronavirus infections, with some previous MERS-COV and SARS-COV infected individuals having experienced myocarditis (Siripanthong et. al.). In many instances of viral-induced myocarditis ER Stress has been responsible for aggravating the severity of heart damage (Zha, et. al.), and so there are concerns about whether it is the actual act of viral infection that contributes to the myocarditis, or if ER Stress caused by viral infection may exacerbate the damage and lead to severe heart damage and death.

Another responsible player are cardiac macrophages who may aggregate during a viral infection and cause a large inflammatory response, and one that may eventually lead to inflammation and damage of the heart. In short, cardiac macrophages are one of the first lines of innate immune defense and will aggregate within the heart during the first signs of viral infection. ER Stress activation in macrophages is likely to play a role in the production of pro-inflammatory cytokines. What’s interesting is that cardiac macrophages may not need to be infected to elicit ER stress and cause inflammatory damage, but may be affected by molecules released by virally infected cardiomyocytes.

In a study by Zhang et. al. researchers examined the dynamics between cardiomyocytes infected by coxsackievirus B3 (CVB3), a virus known to induce myocarditis, and the effect on local macrophages. It’s a long study, but to summarize the researchers found that macrophages were not directly targeted by CVB3 to induce ER Stress, but were tangentially affected by CVB3 infected cardiomyocytes. Apparently, various molecules may be released by infected cardiomyocytes into the surrounding medium and may signal to cardiac macrophages. Doing so induces ER Stress in cardiac macrophages, causing them to release their own inflammatory cytokines leading to further exacerbated myocarditis and possibly death of the host.

In essence, a damaged heart may damage itself further through the ER Stress response of localized cells and the cascading inflammatory response, likely causing severe or even deadly myocarditis in the process. Adding onto that, mouse models have shown that after myocardial infarction (heart attack), death may result several days afterward due to ER Stress caused by tissue remodeling and further cell death (Luo et. al.). Once again, the acute cardiac cell death causes ER Stress to occur, with UPR and inflammatory markers persisting for several weeks after a heart attack and likely causes the death of mice several days after the acute incident. Treatment of these mice with 4-PBA attenuated the ER Stress response and provided a protected effect in existing cardiomyocytes, such that less than ¼ of the post-MI treated mice died from subsequent hypoxia or cardiac necrosis compared to more than ½ of the untreated mice. Now, this study occurred in mice who had heart attacks and not myocarditis, but we can still gain some insights from this study.

What this means, taken altogether, is that cardiac damage does not depend on just the acute infection or damage, but is likely caused by the subsequent fallout of persistent inflammation, continuous cell death, and improper healing mechanisms. What the Zhang et. al. studies indicates is that ER Stress not only alters the infected cells, but affects the local environment as well, meaning that uptake of either virions or even possible lipid nanoparticles containing mRNA may cause rampant protein production, leading to the cell’s UPR and eventual death, which may then release molecules that then cause their own inflammation in nearby cardiac cells and macrophages. In essence, a minor infection may cause a cascade of events that can eventually trigger severe heart damage and death. Although the Luo et. al. study did not examine myocarditis, it does suggest that persistent ER Stress may play a role in death days after the incident. It may explain why incidences of myocarditis death in vaccinated individuals is not immediate, and instead acute damage a day or two after vaccination may lead to persistent stress that eventually leads to cardiac death a week after vaccination. Although we are speculating, if this is the likely cause of myocarditis-related death then we can see why this is likely missed or even not considered as a possible cause of death attributable to vaccination. Just to emphasize this point is a recent article released in JAMA suggesting that vaccine-induced myocarditis may be multiple magnitudes higher than in infection (Oster et. al.) Also, considering that myocarditis increases in frequency with each subsequent vaccination, it is more than likely that damage to the heart, even when properly healing, may once again become damaged by the introduction of another exogenous substance shortly after the initial introduction (1st injection). In some ways, it’s as if constant vaccination procedures may be akin to constant viral infection, such that continuous exposure provides for continuous opportunities to allow for inflammation and cell death.

On a last point, I’ll turn to this point made within the discussion of the Oster et. al. paper:

However, the onset of myocarditis symptoms after exposure to a potential immunological trigger was shorter for COVID-19 vaccine–associated cases of myocarditis than is typical for myocarditis cases diagnosed after a viral illness.24-26 Cases of myocarditis reported after COVID-19 vaccination were typically diagnosed within days of vaccination, whereas cases of typical viral myocarditis can often have indolent courses with symptoms sometimes present for weeks to months after a trigger if the cause is ever identified.1 The major presenting symptoms appeared to resolve faster in cases of myocarditis after COVID-19 vaccination than in typical viral cases of myocarditis. Even though almost all individuals with cases of myocarditis were hospitalized and clinically monitored, they typically experienced symptomatic recovery after receiving only pain management. In contrast, typical viral cases of myocarditis can have a more variable clinical course. For example, up to 6% of typical viral myocarditis cases in adolescents require a heart transplant or result in mortality.27

What could explain the shorter time frames for both incidences of myocarditis and recovery? It could possibly be a front load effect, such that viruses need time to replicate and propagate while these vaccines provide all of the mRNA and protein production capabilities upfront immediately after injection. Also, because the mRNA does not have the ability to self-replicate, we may assume that prolonged viral infection would eventually reach greater levels of viral load and damage, possibly explaining the prolonged damage seen in viral infection. Variation in viral load production may explain the variability seen in myocarditis symptoms as well. Therefore, comparative analysis of myocarditis in both vaccinated and virally infected individuals should take into account the dosage and time delay seen in viral infection compared to the acute nature of these vaccines.

ER Stress is Implicated in Neurodegeneration

Just like with cardiovascular diseases, ER Stress is associated with many of the most common neurodegenerative diseases.

Here’s a summary from Rao, R. & Bredesen, D.:

Misfolded proteins, and the associated ER stress, are emerging as virtually constant features of neurodegenerative diseases. That UPR- and ER-stress-induced cell death could be involved in the pathogenesis of several neurodegenerative disorders (as opposed to being causally unrelated correlates) comes from several recent reports. The accumulation of misfolded proteins resulting in alterations in the structure of organelles, including the ER, has been observed in transgenic models of HD, AD and ALS, as well as in huntingtin-null mice [83–99]. Examples of such misfolded proteins, and related complexes, include the neurotoxic oligomers of the Aβ-peptide in AD [100–102]; cytoplasmic inclusions (Lewy bodies) that stain for α-synuclein, parkin and an unfolded form of the PAEL (parkin-associated endothelin receptor-like) protein [2,102–105] in PD; intracellular inclusions in degenerating neurons and glia that stain for mutant CuZnSOD [83,106,107] in murine models of ALS; and the expanded polyglutamine (poly Q) aggregates that trigger ER-stress-induced cell death in HDand other polyglutamine expansion diseases [104,105,108, 109•,110,111]. Since these neurodegenerative diseases may be caused by specific mutant proteins that accumulate as misfolded proteins and escape degradation, it is likely that ER stress plays an important pathogenetic role in these diseases.

Unfortunately, unlike comparisons to myocarditis the neurological effects of vaccinations are harder to pin down. More importantly, what’s strange is the numerous accounts of various neurological symptoms post vaccination including seizures, encephalomyelitis, extreme fatigue, severe headaches, facial paralysis, tinnitus and brain fog just to name a few. Many of these symptoms are not seen in viral SARS-COV2 infection, and so the extent to which comparisons can be drawn between vaccines and infection will be difficult.

Even now, the role of CNS invasion in SARS-COV2 infection is spotty. Some have argued a possible penetration of the blood-brain barrier by SARS-COV2 with help from the spike protein, although not many studies have come from this hypothesis. Another, more viable hypothesis is neuroinvasion through the nasal passage, with virions gaining entry into the CNS possibly through the olfactory bulb. This would be consistent with the route of viral entry, and considering that the barrier within the nose is thinner and more permeable, and that CNS invasion has been seen in other respiratory viruses, it would make more sense as a plausible viral entry mechanism. However, that wouldn’t explain the number of neurological symptoms people experience post-vaccination as the vaccines are not administered intranasally.

The CNS, by virtue of the blood-brain barrier, creates problems as to what extent the mRNA vaccines may cause neuroinvasion. Nonetheless, the vast number of neurological impairments suggest some possible targeting of the nervous system.

What is well known is the role of Sigma-1 Receptors in the health of the nervous system. Sigma-1 Receptors are found throughout many cells in the body, and especially within many cells of the nervous system. It serves to help support the homeostasis of a cell and helps support the calming effects of ER Stress by managing the effects of the unfolded protein response. Both neuroinflammation and misfolded proteins contribute to such neurodegenerative diseases as Alzheimer’s, prion disease, and Parkinson’s. The age-related nature of many neurodegenerative diseases are likely to have been derived from epigenetic changes that accompany age (Prasant et. al.). Sigma-1 expression apparently increases with age as a possible compensatory mechanism for the downregulation and reduced expression of other membrane receptors. An exception to this is in cases of Alzheimer’s where Sigma-1 expression appears to be attenuated. Loss of Sigma-1 expression would mean a loss of corrective action against misfolded protein accumulation and contributes to increased neurodegeneration (Jin et. al.).

There have been a few anecdotal remarks about Alzheimer’s Dementia emerging post-vaccination, yet many of these claims have yet to be substantiated. However, what may be occurring, if the change in Sigma-1 expression is to be believed, is that those who are more susceptible to AD due to reduced expression of S1R may be more susceptible to the ER Stress brought on by vaccination. Essentially, it may be worth investigating to determine if such instances of AD are caused by vaccination, or if these people may be more susceptible due to loss of S1R expression and would inevitably experience AD regardless. As such, the symptoms of AD may be indicative of early onset dementia brought on by neuroinflammation and ER Stress that pushes the accumulation of misfolded proteins over the edge.

Another way of interpreting these circumstances is that these people will inevitably present with AD, and under normal circumstances the accumulation of misfolded proteins is slow and clinical deteriorating would present as mild for several years. However, introduction of a stressor, in this case the vaccine, will cause large levels of neuroinflammation and accumulation of misfolded proteins over a short period of time, essentially pushing the clinical presentation of AD forward several years from when it may likely present itself. If AD brought on by vaccination is to be believed, researchers should check for the expression of S1R relative to the standard population, and it may also be worth examining family history and genetic factors that would also indicate a family history of AD as well.

S1R is one of the only available windows into the world of ER Stress, neurodegeneration, and the possible association to these mRNA vaccines. Because of this, Fluvoxamine and other S1R agonists provide the best windows into therapeutics against COVID infection. We’ve already covered this extensively, but it’s important to emphasize that Fluvoxamine is being considered not only for COVID but for many neurodegenerative diseases including Alzheimer’s Dementia. It would make sense then, that if there are possible concerns of AD incidences after vaccination that something such as Fluvoxamine may provide therapeutic benefits as well.

In fact, Fluvoxamine is likely to serve as a good candidate for long COVID. Long COVID is very difficult to pin down, mostly because it’s hard to provide concrete evidence of prior viral infection under many circumstances, especially at the beginning of the pandemic when PCR tests were not widely available. Long COVID can come with many presentations similar to COVID infection, such as chronic fatigue, persistent coughs, headaches, brain fog and respiratory problems. People who may be experiencing long COVID also don’t have any evidence of persistent viral infection, indicating that long-term damage may be attributable to the symptoms. One of these possibilities is persistent neuroinflammation. There is one hypothesis that persistent coughs may be attributed to neural hypersensitivity after infection, and that coughs are due to neural signaling alterations (Song et. al.). One treatment option may be Dextromethorphan, an over the counter cough suppressant. One possible mechanism of Dextromethorphan could be its targeting of the nerves and inhibition of signals required to evoke a cough response. NSAIDS and corticosteroids have also been taken into consideration as treatment options, once again highlighting the idea of persistent inflammation as a possible explanation for long COVID.

It’s the idea that inflammation, and more specifically neuroinflammation, may play a role in long COVID that makes Fluvoxamine a good candidate for a therapeutic due to its anti-inflammatory properties. Interestingly, long COVID-like symptoms from vaccines are now gaining more attention as well, as indicated by this Science article that was published last month. Not only would this mean that Fluvoxamine may be used to treat long COVID-like symptoms in those who have been vaccinated, but that both the vaccines as well as the COVID infection may share some parallels in order for similar symptoms to occur.

As an aside, here’s a nearly year old video from Dr. Mobeen discussing Fluvoxamine’s use in long hauler COVID, which could be found here.

There’s a lot more to discover when it comes to neurological symptoms and their relationships to both COVID infection and possibly to vaccines. As of now the information is far too spurious and lies on conjecture more than anything. Regardless, the role of the S1R receptor should be looked at extensively along with the ideas of neuroinflammation as a whole. This means that anti-inflammatories that directly act as S1R agonists such as Fluvoxamine should be looked into extensively as well, for not only may they help reduce symptoms of long COVID and even help reduce the severity of COVID illness, but they may also tie up connections between neurological symptoms and vaccination.

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A Change in Hypothesis

All of this may seem like the ramblings of some sort of madman, in which case I would not deny it. However, there’s still something to be said about these vaccines and many of the adverse reactions people have experienced. COVID itself is real, and so too are the adverse reactions. Even stranger is the fact that many symptoms from COVID infection can be seen in those who have been vaccinated, including long COVID-like symptoms. It brings attention to how something that should otherwise be considered innocuous may mimic symptoms seen from an actual viral infection.

Going into this I proposed that my hypothesis would be to examine ER Stress as a likely factor for all of the symptoms people are experiencing, and that people may be missing out on this part of the process when they only look at the end product of spike proteins. However, through my ramblings I realized that my perspective itself is parochial. We know full well that the spike protein is cytotoxic, we also know that the process of making proteins elicits ER Stress that may cause its own host of problems, but we also know that the so-called behavior of these vaccines are ones that are completely new to us. We have never been provided a vaccine that requires entryway into our own cells, requires the use of our own cell’s machinery to produce proteins, who may cause our own cells to be targeted for death and destruction, only to have these possibly cytotoxic products be released into the environment to cause even more havoc.

Although my comment was made in jest about such an idea, I am finding it more appropriate to not refer to these vaccines due to their role in ER Stress or production of spike proteins, but to consider the entire process as a whole as a form of viral mimicry or more aptly from the perspective of a pseudoinfection.

At this point I should heavily emphasize that this absolutely does not mean that these vaccines are viruses, or that people are being “infected” with vaccines. But what I am stating is that the entire process, from the entryway to the production and release of spike protein, parallels that of what one would expect in a viral infection. Because of that a more fitting hypothesis would be one that emphasizes viral mimicry/pseudoinfection as a method of examining the whole vaccination process and not just on the merits of its cytotoxic product.

From a medical and scientific perspective, it may be more fitting to not refer to these as vaccines but more as non-replicating pseudoviral particles (NRPP), and may need to be looked at similarly to viral exposure. Examining the way in which these NRPP scour our bodies, find which cells to “infect” and enter are just as important as the end product of releasing completed spike proteins. Viral myocarditis is the leading cause of sudden cardiac arrest in children, and so comparisons may be appropriately drawn between viral myocarditis and “pseudoviral” myocarditis (OK, I may be abusing the term now), and the same can be done with long COVID-like symptoms in vaccinated individuals as well.

I hope people do not misinterpret what I mean to push forward a crusade against these vaccines. Instead, we need a way to examine these vaccines in a scientifically driven manner, including all of the possible adverse reactions. Doing so requires robust experimentation, and it requires an open mind to try to look at the manner in an open discourse fashion.

This post was intended to be far more robust and exhaustive in nature, but I found it particularly exhaustive mentally and my ideas may already be confusing and redundant as is.

If anyone has any questions, or if anyone would like to provide feedback please comment! I would like to hear many people’s thoughts on the manner or if there are some things they would like to be clarified.

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