Are the COVID Vaccines Unusually Ineffective?

[jim mcnamara]

Vaccination is a point well taken here. Much lower death rate. However, vaccination does not work after a patient has contracted Covid.

US 1918 H1N1 versus SARS-Cov2 --
In discussing this very point - deaths in the pandemic - with an internist who thinks some of the death rate limiting is due to the level of increasing positive medical intervention during the pandemic in the US. She indicated that "phases" of Covid disease progressed and led to deaths very early on. Her hospital had to rent a refrigeration unit because the morgue was overflowing. As treatment modalities improved, patient survival improved. Monoclonal antibody treatment is an example of this kind of change.

She mentioned that NYC Optum data showed for 2nd week of April 2020, very roughly, 10% fatality on any admission of a Covid patient. The last data she saw showed <2% death rate. This only applies to unvaccinated patients.

I do not have access to the data, so I cannot provide any links.

Edit: Optum is a medical group, forgot to mention that.

 

[pinball1970]

Vaccination is a point well taken here. Much lower death rate. However, vaccination does not work after a patient has contracted Covid.

US 1918 H1N1 versus SARS-Cov2 --
In discussing this very point - deaths in the pandemic - with an internist who thinks some of the death rate limiting is due to the level of increasing positive medical intervention during the pandemic in the US. She indicated that "phases" of Covid disease progressed and led to deaths very early on. Her hospital had to rent a refrigeration unit because the morgue was overflowing. As treatment modalities improved, patient survival improved. Monoclonal antibody treatment is an example of this kind of change.

She mentioned that NYC Optum data showed for 2nd week of April 2020, very roughly, 10% fatality on any admission of a Covid patient. The last data she saw showed <2% death rate. This only applies to unvaccinated patients.

I do not have access to the data, so I cannot provide any links.

Edit: Optum is a medical group, forgot to mention that.

Yes I should have noted that over time your chances of getting out of hospital once you were in improved over time between March 2020 and Jan 2021 in the UK. Same elsewhere as care changed.

 

[artis]

There is one major difference though that often gets forgotten. Aslo the reason I think the 1918 Flu was worse than current Covid, back in 1918 there simply were not enough old and sick people around going about meeting others as if their 18 teen and healthy. Back in those days the world especially outside US or western Europe was pretty much a real survival game.

If the knowledge I have from my own relatives and the statistics of my country is of any measure and I do believe they are, then pretty much everyone who has died from Covid either had a serious preexisting condition or was very old, or both. I know of no one personally that would have had a serious case of Covid let alone died under the age of 60. I knew one woman though my former teacher , she had a huge weight problem, she was 49. She contracted Covid recently so the delta variant , had not yet vaccinated and missed the signs at the beginning when she already needed to start treating her symptoms.
Died in ICU after few days from heart failure. She was overweight and had previous heart problems.

I have nothing against old people or sick people but we do have a ever increasing population size in that group which is also largely the group that fills the Covid death statistic.
So I'm kind of willing to bet if we had the population fitness of 1918 and current medical methods/drugs Covid would be far less of a problem. But I will not go there as that would be speculation outside of reasonable prediction abilities.

One thing I can say is that Covid is a weird virus, for those that do develop pneumonia from it the actual suffering comes mostly not from the pneumonia but from the effects of the spike protein.
Given the studies we now have on how it affects CNS and even crosses the blood brain barrier it's a really nasty gift.
I recovered from my Covid pneumonia within a few weeks but the CNS effects continued for couple of months. I guess this is also what causes the so called "long Covid". My blood tests were even fine so physically your fine but mentally you feel like sh**.

 

[artis]

Yes I should have noted that over time your chances of getting out of hospital once you were in improved over time between March 2020 and Jan 2021 in the UK. Same elsewhere as care changed.

And given overall vaccination and new drugs targeting infection I'd say these chances have increased even more now. I'd say you have to be with serious prior illness or in very bad shape to die from Covid now, given you started treatment early and did not do the "ehh I'm fine, I'll ride this one out" routine.

 

[jim mcnamara]

@artis - You need to learn about U-shaped and W-shaped mortality curves. Read the link below
And. Please stop speculating. Post a link to a decent paper please. In other words Biology is often weirder than you would ever dream up on your own. Example: Enzootic pigs are big deal in this whole affair as well.
And H1N1 is still extant after all these years. It is a Type A flu.

The average for deaths in 1918-19 was low, not a U shaped curve. On a population basis, humans in most of the world had not been exposed to the H1N1 virus family since 1887. So relatively younger people died off in droves back then. Data does not back your point about age class distributions back then. There was a mini-epidemic in 1915 of what is thought to be an H1N1 ancestor. See link.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3291398/
Long paper but considered definitive on many aspects of 1918.
Scroll or forward find to heading:
Why Did the 1918 Virus Kill So Many Healthy Young Adults

 

[artis]

Post a link to a decent paper please.

With regards to which statement?

As for the deaths I was only talking about the total deaths not the curves of them. Truth be told Covid is not over yet so only time will tell.
As for age distribution of Covid deaths, I looked at this study
https://www.nature.com/articles/s41598-020-73777-8/figures/2

But I think this statistic is well known and rather similar all around the world by now with few variations from country to country.

PS. @jim mcnamara that paper you linked is interesting , will have a read, with regards to the U or W shaped curves I see how that plays out for the 1918 pandemic but what I said in my post was with regards to Covid and for Covid I'm not sure how to call the mortality curve but it's very low for young kids and young adults and then slowly ramps up until it climbs steeply at around the age of 60 from the graphs I see, so there's that which is why I made the comparison of a healthier younger population having less problems with Covid and our current demographic situation.
But that was just a comment feel free to disregard it, I'm not stating anything.

 

[pinball1970]

With regards to which statement?

As for the deaths I was only talking about the total deaths not the curves of them. Truth be told Covid is not over yet so only time will tell.
As for age distribution of Covid deaths, I looked at this study
https://www.nature.com/articles/s41598-020-73777-8/figures/2

But I think this statistic is well known and rather similar all around the world by now with few variations from country to country.

PS. @jim mcnamara that paper you linked is interesting , will have a read, with regards to the U or W shaped curves I see how that plays out for the 1918 pandemic but what I said in my post was with regards to Covid and for Covid I'm not sure how to call the mortality curve but it's very low for young kids and young adults and then slowly ramps up until it climbs steeply at around the age of 60 from the graphs I see, so there's that which is why I made the comparison of a healthier younger population having less problems with Covid and our current demographic situation.
But that was just a comment feel free to disregard it, I'm not stating anything.

https://www.paho.org/en/news/5-5-20...eople-soar-due-covid-19-paho-director-reports

https://www.cidrap.umn.edu/news-per...-reveal-deadliness-covid-19-even-young-adults

 

[artis]

@pinball1970 That data from the graph I posted was collected I think before the delta variant became the dominant variant so it is entirely possible these graphs will now change with time.

 

[pinball1970]

With regards to which statement?

As for the deaths I was only talking about the total deaths not the curves of them. Truth be told Covid is not over yet so only time will tell.
As for age distribution of Covid deaths, I looked at this study
https://www.nature.com/articles/s41598-020-73777-8/figures/2

But I think this statistic is well known and rather similar all around the world by now with few variations from country to country.

PS. @jim mcnamara that paper you linked is interesting , will have a read, with regards to the U or W shaped curves I see how that plays out for the 1918 pandemic but what I said in my post was with regards to Covid and for Covid I'm not sure how to call the mortality curve but it's very low for young kids and young adults and then slowly ramps up until it climbs steeply at around the age of 60 from the graphs I see, so there's that which is why I made the comparison of a healthier younger population having less problems with Covid and our current demographic situation.
But that was just a comment feel free to disregard it, I'm not stating anything.

Of course an 89 year old has a worse chance of survival than a 30 year old.
I am never sure what point you want to make from this though.
Everyone over 80 we can write off? Over 70? Had their life?
Plus the chances of dying or leaving hospital after Covid with long standing sometimes life changing issues are NOT zero for a young person.

 

[pinball1970]

@pinball1970 That data from the graph I posted was collected I think before the delta variant became the dominant variant so it is entirely possible these graphs will now change with time.

All you need to know is Covid is very dangerous to all age groups just not equally or in the same way.
Re Vaccines
All that is needed to be pinned down is how young the age group they need to go to,how often and what combo (RNA, adenovirus)

 

[Rive]

only mutations that increase the organisms' fitness will become common in the population.

Regarding this, I've come across a really tempting misunderstanding a while ago. Some folks were speculating, that the virus would have only a few possible configuration while converging to some kind of 'optimal' variation, and so once the 'possible' configurations depleted, it would just vanish.

I'm just thinking to myself , it can't be that a virus can just keep on making a better more resistant version of itself every next step can it ?

While it's not entirely impossible to have some kind of 'optimal' variation with a theoretically maximal R0 (! only R0 here) value, the actual effective R depends on the ratio of the already immune people in the population. So when you have the 'optimal' R0 but 70% already immune (by any means), then any 'less optimal' but partially immunity bypassing variant would easily overgrow the 'optimal', regardless of its less potent R0.

In short, that 'fitness' is tricky and really heavily depends on the vaccination/immunity rate. Any 'higher R0' has only a limited and really short lived meaning - don't fall for it.

 

[artis]

Everyone over 80 we can write off? Over 70? Had their life?

No, not at all, that is why I said I don't mean that in a personal way just a statement of statistics.
I am following my local government twitter account and there they report the daily death count and age groups. I don't write the statistics down but I do keep seeing folks in that category with usual age 60+, the next less often one is 40+, very rarely I see anyone under 40 in that group.
Keep in mind my country is about 58% doubly vaccinated overall, so the doors are still open for various outcomes.
One can see in the places where elderly have been almost entirely vaccinated death counts fall, like UK for example I think.
But I guess it's a combination of everything, better tailored drugs, vaccines, safety measures etc that accounts for the global fall of deaths. So we have adapted somewhat is what I see.

 

[jim mcnamara]

I think we are getting into problems with R₀ usage. I have abused it myself mostly because I would have to explain why R₀ obtains only at the start of an epidemic -- if you want to follow the base epidemiology usage. After the susceptible population either dies or becomes immune or vaccinated or whatever, then R₀ no longer has its original meaning and is usually not used. Media reporting excepted, of course.

If you have a R value it will vary depending on how many people a given person interacts with, positivity rates in the population, along with climatic changes, seasonal changes, primary reproduction of the pathogen at the outset of infection (like how many days until the victim can infect new hosts), secondary attack rate (rate of new infections breaking into people in a closed environment -- like worker returning to a house and family) and duration of the outbreak.

Ex: Rancher in Montana versus street vendor in Times Square. There will be a different R values for these populations. This is one reason why it took a longer time for some rural states to reach "critical mass" for Covid to enter logarithmic growth phase in local population there.

Measles has an incredibly high R value - often as high as 10. Epidemics continue as long as the observed R for the population remains above 1.0 Covid in the US as a whole has an R value between 1.0 and ~2.0.

For what it is worth some researchers use
R_t for time changes like April->May
R_s for seasonal -- ex: flu virus does not "like" long days & high solar irradiance (UV)
R_e behavioral and population density like masking/no masking

So you could get an R value for all sorts of conditions if you can work out how to identify them. That means epidemiologists work very hard to develop useful-to-policy-makers-and-general-public R values that can be turned into public health suggestions and policies.

 

[morrobay]

I found this painful to read. The purpose of a vaccine in the very short term (months) is related to anti-bodies. If you are expecting to have benefits longer than a year, antibodies can't be the driver; vaccines need to induce T and B cell immunity as well. Focusing only on antibodies is a horribly inaccurate model.

Adding T and B cells to the mental model is not that hard. I can't understand why people constantly miss this on a science site.

Yes outside of healthy foods and herbs, excercise , healthy weight... I don't know of any natural ways to increase/add T and B cells to the biological model. Following : ' Most of the CD8+T cell responses were specific to viral internal proteins rather than the spike protein'. https://www.cebm.net/covid-19/what-...n-why-immunity-is-about-more-than-antibodies/

 

[Chestermiller]

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

 

[Laroxe]

Regarding this, I've come across a really tempting misunderstanding a while ago. Some folks were speculating, that the virus would have only a few possible configuration while converging to some kind of 'optimal' variation, and so once the 'possible' configurations depleted, it would just vanish.While it's not entirely impossible to have some kind of 'optimal' variation with a theoretically maximal R0 (! only R0 here) value, the actual effective R depends on the ratio of the already immune people in the population. So when you have the 'optimal' R0 but 70% already immune (by any means), then any 'less optimal' but partially immunity bypassing variant would easily overgrow the 'optimal', regardless of its less potent R0.

In short, that 'fitness' is tricky and really heavily depends on the vaccination/immunity rate. Any 'higher R0' has only a limited and really short lived meaning - don't fall for it.

Well like most things the virus will continue to evolve as indeed will its prey. An optimal variation will be in the context of the time and place but if we want to put this in evolutionary terms, its optimal for the virus, the R number and vaccination rate are human concerns though they describe drivers of selection. If you think about fitness for a virus it really is an issue of maintaining its ability to spread and for longer periods. The fact that Covid-19 induces an obvious symptomatic disease that can kill, is not at all in its own interest, people who are ill isolate themselves and limit spread and of course provoked vaccine development and deployment. It is possible that the delta variant was a response to these strategies, but its success can't last, if you look at the other 4 human adapted coronavirus's they have been hugely successful and still are.

 

[artis]

If you think about fitness for a virus it really is an issue of maintaining its ability to spread and for longer periods. The fact that Covid-19 induces an obvious symptomatic disease that can kill, is not at all in its own interest, people who are ill isolate themselves and limit spread and of course provoked vaccine development and deployment.

Well for a virus like Covid , I'd say it has a smart strategy, kill off the weak while maintain spread on the backs of those that are unlikely to die and are also most likely to spread.
So spread through young and healthy and kill old, weak and compromised , given it;s very high transmission rate I'd say if we wouldn't use combating measures I would bet it could go around and around for years until pretty much every weaker individual is gone. It will be interesting to see whether Covid will be able to come up with an even better mutation to increase it's transmission or lethality, I myself would bet that it has already reached it's peak fitness given the delta has now been the dominant variant for quite some time and currently there seem to be no other "better" ones on the horizon.
What I find interesting is that on the random mutation game as I like to call it , having one or more beneficial mutations doesn't increase your chances of coming up with a better or another beneficial mutation, sort of like a gambler doesn't necessarily become better after one or two wins.
In this regard the Spanish flu was much more self limiting as it murdered it's most potent transmission source, namely those that are in their best years of life. 20-40, although pardon if this seems to upset someone, I'm just quoting statistics, on a personal level the "best years of life" might differ from person to person

 

[Laroxe]

Well for a virus like Covid , I'd say it has a smart strategy, kill off the weak while maintain spread on the backs of those that are unlikely to die and are also most likely to spread.
So spread through young and healthy and kill old, weak and compromised , given it;s very high transmission rate I'd say if we wouldn't use combating measures I would bet it could go around and around for years until pretty much every weaker individual is gone. It will be interesting to see whether Covid will be able to come up with an even better mutation to increase it's transmission or lethality, I myself would bet that it has already reached it's peak fitness given the delta has now been the dominant variant for quite some time and currently there seem to be no other "better" ones on the horizon.
What I find interesting is that on the random mutation game as I like to call it , having one or more beneficial mutations doesn't increase your chances of coming up with a better or another beneficial mutation, sort of like a gambler doesn't necessarily become better after one or two wins.
In this regard the Spanish flu was much more self limiting as it murdered it's most potent transmission source, namely those that are in their best years of life. 20-40, although pardon if this seems to upset someone, I'm just quoting statistics, on a personal level the "best years of life" might differ from person to person

My thinking is based on what we know about other coronaviruses that jumped species, though a lot of this is guesswork. It may very well be that every one of these crossover events may have started with an infection that caused serious problems. We know that the Coronavirus OC43 crossed species in the 1890's and its appearance coincided with a pandemic that killed around a million people, this was labelled as Russian flu but they had no way of identifying different viral diseases or even virus's generally. The same virus remains in circulation as the cause of the common cold along with its 3 close relatives from earlier events.
Remember for a virus to kill its host is effectively suicide and people with obvious illness alter their behaviour and the behaviour of people around them in ways which limit spread. Generally, people are exposed to these viruses when they are young, traditionally a period of high risk but for whatever reason they cause few problems but leave the individual with some level of immunity. Most people were not even aware of their existence until Covid-19 appeared.
Flu is not really a very good model because of its particular predisposition to recombine with other flu viruses, this causes massive changes in their genome, significantly altering their immune signatures. However there are some lessons to be learned, like the coronavirus, that pandemic occurred in waves which were of different severity, the first wave occurred primarily in young people and was usually mild. It seemed to spread most readily in the army camps and in army camps with attached field hospitals treating mustard gas victims who were immune compromised and had lung damage. This may have provided the ideal conditions for further viral adaptations as the second wave of disease was more severe and the 3rd worse still. After that the virus started to loose its virulence but the virus family, H1N1 is still in circulation. Its considered some earlier strains of flu may have been sufficiently similar to provide the people exposed with some level of cross immunity, this exposure would have probably been some 30 - 40 years prior to the pandemic but it might help explain its pattern of mortality. The rapid reactivity of young peoples immune response also worked against them with the occurance of the so called cytokine storm, an immune over reaction. Interestingly the virus is now commonly thought to have originated in the USA in military camps and the animals involved in the virus reassortment is still unclear, these are the same issues causing controversy with SARS CoV-2. Remember that a great deal of information about the 1918 pandemic is speculative.
https://www.sciencedirect.com/science/article/pii/S1755436514000346
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6187080/

 

[atyy]

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

https://movementdisorders.onlinelibrary.wiley.com/doi/10.1002/mds.28851
A total of 181 patients with PD met the inclusion criteria; 107 men and 74 women were included. Mean age was 65 years old (range, 31–99). A total of 178 patients received two doses of the SARS-CoV-2 vaccine (177 Pfizer/BioNTech and 1 Sinopharm), and three patients received only one dose of the Pfizer/BioNTech vaccine. A total of 11 patients (6%) had COVID-19 during the pandemic. The effect of the infection on parkinsonian symptoms was not evaluated for this report. Only two patients (1.1%) reported some degree of deterioration following one of the doses of the vaccine. The first patient presented with increased rigidity and gait impairment soon after the first dose that lasted a few days. The second patient presented with increased resting tremor that lasted for 2 weeks also after the first dose. In both cases, symptoms improved spontaneously without any modification of their antiparkinsonian medications.

https://movementdisorders.onlinelibrary.wiley.com/doi/10.1002/mds.28772
In June 2021, the day after her second vaccine dose, she developed fever (38°C), confusion, delusions, and continuous severe dyskinesia for 3 days. Laboratory tests revealed an increased D-dimer level (3228 ng/mL). She was treated with paracetamol, and her levodopa was reduced to 350 mg daily. After 2 weeks, she was afebrile, but mild confusion and dyskinesia that are more severe than her baseline persist.

https://link.springer.com/article/10.1007/s10072-021-05753-7
Conversely, we herein describe a PD patient who benefited from the administration of the mRNA-1273 vaccine. ... The first and second doses of the mRNA-1273 vaccine were respectively administered on May 28 and June 26. Right after the first shot, the patient reported global improvement of his motor and non-motor off symptoms, with greater efficacy on the most affected side (NoMoFA score = 4, 43% improvement; MDS-UPDRS part IV = 7, 30% improvement), and a sustained benefit for almost one week after the second shot.

 

[TeethWhitener]

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

The vaccine doesn't seem to adversely affect Parkinson's patients disproportionately.
https://www.parkinson.org/blog/awareness/COVID-Vaccine-Live-DrOkun
However, persons with Parkinson's who contract COVID-19 are at increased risk of hospitalization and death:
https://www.parkinson.org/understanding-parkinsons/covid-19
There is also speculation that contracting COVID-19 puts patients at higher risk for developing Parkinson's-like symptoms:
https://www.webmd.com/lung/news/20201106/covid-19-linked-to-increased-risk-for-parkinsons

 

[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.