Are the COVID Vaccines Unusually Ineffective?

[artis]

Is there any indication that Covid vaccine makes Parkinson's symptoms progress more rapidly?

Well there are complaints of neurological side effects from people but the jury is still out on what could cause them.

As for real Covid, it seems there is a continual influx of evidence that points to the spike protein being a neurotoxin of wide capabilities.
I cannot find all the studies in this regard which I have overlooked as I don't save them, but even a quick search reveals plenty.
Here University of Washington talked about this back at December last year
https://newsroom.uw.edu/resource/covid-19-spike-proteins-may-cause-neurological-issues

https://inflammregen.biomedcentral.com/articles/10.1186/s41232-021-00165-8

Several studies have been reported in which pseudovirus or SARS-CoV-2 was added to brain organoids prepared from iPSCs to examine whether infection was established. When SARS-CoV-2 is added to neural progenitor cells and brain organoids prepared from human iPSCs in vitro, infection is established, and viral proliferation and neuronal cell death are induced. In this system, antibodies against ACE2 or CSF (containing IgG antibodies specific to S protein) from COVID-19 patients prevent neural infection with SARS-CoV-2 [32], indicating that ACE2 acts as a receptor for SARS-CoV-2 in neural cells.

The study also compares different known viruses like MERS and others and their ability to induce neurological damage, it seems from what they say that out of these examples Covid is among the worst for neurology because of the types of cells that it can infect, namely the S protein can attach to the ACE2 receptor expressing cells and among those are neural cells.

HCoV-229E, HCoV-NL63, HCoV-HKU1, and HCoV-OC43 are the causative viruses of the so-called winter cold. There are fewer studies on neural disorders caused by these viruses than by SARS-CoV-1 or SARS-CoV-2. This is because, when the existence of these viruses was confirmed, they had already become established as the causative virus of the winter cold in human beings, and they were not paid much attention as research subjects.

Nevertheless, among these four viruses, HCoV-229E [15] and HCoV-OC43 have been reported to cause neural disorders. HCoV-229E and HCoV-OC43 use aminopeptidase N [16] and 9-O-acetylated sialic acids [17] as receptors for adsorption. It has been reported that HCoV-OC43 may cause multiple sclerosis [15] and encephalitis [18, 19], and experiments have been conducted to infect neural cells in vitro [20]. In addition, axonal transport is cited as a possible route of infection of the nervous system for HCoV-OC43 [21].

MERS-CoV is a dromedary-hosted virus that was identified in Saudi Arabia in 2012. Even now, there are sporadic cases of MERS. MERS is a very serious and fatal disease with a case fatality rate of 35% [13, 22]. However, it has also been reported that 0.15% of Saudi Arabians have anti-MERS-CoV antibodies [23]; taking these potentially infected people into account, the case fatality rate can be estimated to be approximately 2%.

Dipeptidyl peptidase-4 (DPP4) has been identified as a receptor for MERS-CoV infection [24]; however, few reports have verified whether DPP4 is expressed in neural cells. Although neural disorders due to MERS-CoV infection have been reported [25, 26], the low number of reports may be because DPP4 expression is not detectable in the nervous system. Thus, MARS-related neural disorders may be limited to those caused by systemic inflammation and angiopathy.

SARS-CoV-1 was identified in 2003 and causes SARS [14], which is a serious disease with a case fatality rate of up to 10–20%. There is a case report that SARS causes neural disorders [27], and there is also a report that SARS-CoV-1 caused neural cell death in an experiment using mice [28]. The receptor for SARS-CoV-1 is angiotensin-converting enzyme 2 (ACE2), which is the same as that for SARS-CoV-2 [29]. As described later, there are some reports showing that ACE2 is expressed in neural cells, and SARS-CoV-1 may thus directly infect neural cells and cause neural disorders.

An interesting study all in all.

Here is a study from nature
https://www.nature.com/articles/s41531-020-00123-0

Because SARS-CoV-2 proteins can interact with host proteins involved in pathways that are altered during aging, including potential mitochondrial dysfunction, loss of proteostasis, autophagy dysfunction, inflammation, and endoplasmic reticulum stress, it is possible that SARS-CoV-2 infection may prompt protein misfolding and aggregation (Fig. 1)103,104,105. Of particular relevance for PD, recent studies have suggested that the aggregation-prone protein, alpha-synuclein, plays a role in the innate immune response to viral infections

But then again the study seems to say that there isn't a clear sign, maybe newer studies show different outcomes I'm not sure, this one is from August of 2020

Currently there is no robust evidence that having PD imparts an increased risk for susceptibility to COVID-19 or that COVID-19 confers a greater risk of PD, although, as noted above, there are reported cases of worsening of PD symptoms in infected patients, particularly in older frail patients on advanced therapies and one case report of development of an acute hypokinetic syndrome with hyposmia post COVID-19.

 

[nsaspook]

So what’s happening to Europe right now? In the Northern Hemisphere, where the increases are unfolding, we believe that this is the expected increase due to winter but it’s more intense in places where, paradoxically, they have done a better job during the pandemic with vaccination campaigns and have lower levels of natural immunity (due to previous infection). It’s hard to explain the North-South gradient otherwise. And then in Europe, there’s a very sharp East-West gradient where countries like Bulgaria, Romania, Belarus, the Baltic states, the Russian Federation – here, transmission is decreasing, and yet these are the places with the lowest vaccination rates that have dramatically high levels of past infection. So trying to put all the pieces together, what we think we’re observing is the combination of winter seasonality, the levels of past infection, and waning immunity from vaccine-derived immunity. This may suggest that when you take all the studies on waning vaccine-derived immunity into account, the winter surges in the rest of the Northern Hemisphere may be larger than we currently predict and then what most people expect because there is this cohort of people that were vaccinated more than six months ago, particularly the most vulnerable. This is something we’ve been watching quite closely, and there’s a real potential risk of a worse winter than perhaps we have been expecting.

In the US
https://forum.allaboutcircuits.com/attachments/1637687704773-png.253326/

https://www.nytimes.com/interactive/2021/us/covid-cases.html

Get your booster.

 

[Ygggdrasil]

As for real Covid, it seems there is a continual influx of evidence that points to the spike protein being a neurotoxin of wide capabilities.

These articles certainly address the neurological effects of the SARS-CoV-2 virus (for which there is an influx of evidence), but I don't think any of them provide evidence that the spike protein is neurotoxic.

The University of Washington press release that you cite refers to this paper published in the journal Nature Neuroscience:

The S1 protein of SARS-CoV-2 crosses the blood–brain barrier in mice
https://www.nature.com/articles/s41593-020-00771-8

The paper shows that the S1 protein from SARS-CoV-2 can enter the brain of mice (suggesting that the virus could use similar means to enter the brain), but the article does not report any observed ill effects of spike protein entering the brain.

The papers you cite from the journals Inflammation and Regeneration and Npj Parkinsons's Disease both deal with the effects of intact SARS-CoV-2, so it is difficult to conclude from these articles whether the isolated spike protein would damage the brain.

Researchers are investigating how SARS-CoV-2 causes neurological symptoms, and there are various (non-exclusive) possibilities that can explain the neurological COVID-19 symptoms without the spike protein being neurotoxic. For example, studies suggesting that SARS-CoV-2 can infect astrocytes in the brain, that SARS-CoV-2 can affect blood flow to the brain through infection of pericytes, and that COVID-19 can induce autoantibodies that attack the brain. These hypotheses are described in more detail in this news article from Nature: https://www.nature.com/articles/d41586-021-01693-6

Finally, COVID-19 vaccines that are based on getting the body to produce spike protein have been given to more than 4 billion people worldwide, but despite many programs tracking adverse outcomes from the vaccinations (discovering things such as vaccine-induced blood clotting events that occur at a rate of on the order of 1 per million), there are no reports that the vaccines are associated with major neurological side effects suggestive of neurotoxicity from the spike protein.

 

[artis]

Now since this is one study and it is related to both the vaccine as well as Covid previous infection I decided not to make a new thread but to post it here and ask for other's commentary.
Here is the study
https://journals.asm.org/doi/10.1128/mBio.01987-21

What caught my eye is this , later on in the study, under the subtitle "

Contribution of ADE of SARS-CoV-2 infection to cytokine expression in macrophages​

The emergence of several SARS-CoV-2 variants prompted us to assess the risk for reinfection with SARS-CoV-2, because these variants’ antigenicity has been reported to differ from that of early strains (23, 24). ADE of infection was identified for variants in this study (Fig. 3B). In our cohort samples, ADE of infection was observed only in plasma diluted more than 1:400, and strong neutralizing activity was found with lower dilutions (Fig. 2). These results indicate that neutralization may occur with plasma containing sufficient neutralizing antibodies but that ADE-inducing antibodies may function at lower concentrations than neutralizing antibodies. Given that recent studies have shown that neutralizing antibodies against SARS-CoV-2 S protein can exist for up to 8 months (25, 26), ADE-inducing antibodies may not elicit ADE of infection for several months.

Then there is this later on

To investigate whether ADE of infection contributes to hypercytokinemia, we examined inflammatory cytokine release from macrophages incubated with ADE-inducing plasma. However, we found that inflammatory cytokine levels were not increased in macrophages incubated with ADE-inducing plasma. These results suggest that ADE-inducing antibodies do not function as inducers of inflammation but may function as antivirals, trapping the viruses in the macrophages; of note, no SARS-CoV-2 replication was observed in macrophages in our experiments (data not shown), which is consistent with previous studies

can someone please also take a look at the study, how should I interpret their results?

 

[Laroxe]

I would suggest that really you don't need to spend too much time on interpreting these results, it really just supports the current views.
ADE has only recently become an issue in the study of viral diseases and was highlighted in the pathology of dengue fever and has since been recognised in a number of other infections. It is usually associated with organisms that are known to have a number of serotypes, that is, a grouping of virus's of the same species that have marked antigenic differences. This typically means that infection with one serotype offers little or no protection against infection with different serotypes. It was found that antibodies to one serotype, which appeared to be cross reactive to the others, could in fact lead to a more severe disease.
When we read this sort of work it's important to consider some terminology used, this is a useful description of common terms used.

https://www.virology.ws/2021/02/25/understanding-virus-isolates-variants-strains-and-more/

Unfortunately, many of these terms are used interchangeably and to describe different meanings, its useful perhaps to stick with the idea of a virus strain as describing a functionally or immunogenetically different version of the virus. These differences have to be very significant, variants due to mutations occur very frequently, but so far it's suggested that there is only one strain of SARS-CoV-2. Infection generates immunity, with some variation, to all the variants.
Researchers have been aware of ADE since the very beginning of the pandemic and have been actively monitoring disease data for any indication of it occurring. This provides a useful overview and some history of its occurrence in other diseases

https://www.chop.edu/centers-progra...y/antibody-dependent-enhancement-and-vaccines#

Perhaps the most telling, is the fact that despite the number of infections and vaccinations there has been no indication of an association with more severe disease.

This paper suggests a mechanism by which ADE could occur and how this might contribute to the problems with aberrant cytokine production, though it states that this simply doesn't occur. I don't even understand why the researchers continue to talk about ADE in Covid-19 when they identify part of the immune response which is most likely adaptive, that is implicated in ADE in other viral diseases. It supports the current position that ADE does not occur in SARS-CoV-2 infections.

 

[valenumr]

I don't think it's reasonable to compare (at this time) the effectiveness of, say, the measles vaccine and the Covid vaccine, without accounting for the fact that Covid is running rampant, so there is a significant risk of exposure. It is very unlikely a person in most of the world would even be exposed to measles, on the other hand.

 

[Astronuc]

ADE

I had to look up the term.

Antibody-dependent Enhancement (ADE) and Vaccines​

https://www.chop.edu/centers-progra...y/antibody-dependent-enhancement-and-vaccines

 

[Laroxe]

I had to look up the term.

Antibody-dependent Enhancement (ADE) and Vaccines​

https://www.chop.edu/centers-progra...y/antibody-dependent-enhancement-and-vaccines

Sorry, it was part of earlier discussions, so I just went with it, but your right it can get confusing, I was being lazy. I know that's a poor excuse, but I am looking for a better one. :)

 

[Astronuc]

Sorry, it was part of earlier discussions, so I just went with it, but your right it can get confusing, I was being lazy. I know that's a poor excuse, but I am looking for a better one. :)

No worries. I had looked it up before, but I don't remember when or where. I find myself needing to explain acronyms in reports at work, so I try to do when posting. I also have to look up acronyms at work, and sometimes, the same acronym is used for different meanings.

 

[pinball1970]

No worries. I had looked it up before, but I don't remember when or where. I find myself needing to explain acronyms in reports at work, so I try to do when posting. I also have to look up acronyms at work, and sometimes, the same acronym is used for different meanings.

Pretty sure it was either @atyy or @Ygggdrasil mentioned this a while ago on another thread.
No evidence of ADE with the current vaccines but this was a few months ago. Hopefully that is still the case.

 

[artis]

The reason I quoted that study was because they said that it was when antibodies decreased when they seem to had ADE so if translated to vaccinated people it would be after their vaccine antibodies drop, but it seems so far we haven't observed that.