Kevin McKernan (you know, that guy with more than 20,000 citations) suggests that "20-30% of COVID deaths have aspergillosis. COVID isn't the issue, immune suppression is"
As often the case, this is semantic imprecision. If everyone but the really slow deer outrun the lion, you can say "slowness kills the deer" but literally the lion kills the deer. Of course older people have weaker immune systems than children. The virus is still what kills them.
Regarding not having a control group in the "VAIDS" study: the authors explained that it would be "unethical" to have a control group (crazy, I know)
> Limitations include the inability to include an unvaccinated control group due to the ATAGI recommendation for all children aged 5 to 11 years to receive the BNT162b2 vaccine. It was unethical to randomise children into an unvaccinated, placebo or delayed vaccination group, given that ATAGI recommended the BNT162b2 vaccine for the age group of interest and that Melbourne was experiencing a surge in COVID-19 cases in the community during the study period.
On a different topic, it seems that there is evidence that those who have accepted the #ClotShot seem to create the Spike Protein for 69-187 days, but the upper limit is because they stopped measuring at 187 days. If you check 1B people you might find the upper range is larger.
You have pointed out that what seems to be happening is DAD in many of the victims.
This means lots of dead cell detritus in the lungs and it would seem that bacteria would have a party in that case. So, why is bacterial pneumonia not an issue here?
I haven't gotten to writing an assessment on the immune study. It does seem like an initial exploratory study that would require an actual control. I commented that there may also be some sort of ebb and flow in our immune system where our responses may be biased by recent prior experiences, and so just as important as "weak immune system = death" is "can the immune system 'recover' or be modified by its experience". The thing to consider is that children have gotten routine illnesses, but a rather poor immune system would seem to be suggestive of an inability to recover and hence either worse outcomes or death. At least that's my assumption.
Absolutely requires a control. For all we know it is normal for kids to show log 1 swings in cytokines by season, this would still keep them well above adults in terms of innate immunity because the bigger difference needs to be looked at in immune cells in tissues anyway
Even worse - what if all the study is showing us is a quality control problem on the reagents used to stimulate cytokines. Off hand I would guess that actually they collected everything gradually and tested at the same time, but still the mere possibility of this kind of thing shows why the reader wants a control
Also, with respect to stimulation the supplementary material suggests that the samples were stimulated around 2 hours post-collection if that adds some additional context.
That's sort of my line of thought as well. Well, maybe not a QC issue, but given that the mRNA vaccines are designed for the mRNA to be undetectable, then would TLR-agonists that mimic viral RNA not eliciting a cytokine response be unexpected? It seems possible that the immune system may just be "trained" to bypass this signaling pathway. Like I stated in my article on Friday a good comparison would be Novavax to see if this happens there as well. It appears Adenoviral dsDNA triggers TLR-9, so it would be interesting to consider what is actually going on.
One thing I am rather critical of is the idea that this is indicative of VAIDS. It's sort of likely someone using the acronym AIDS without understanding the progression of AIDS. If VAIDS is occurring shouldn't we be expecting many deaths related to infections? Or I guess this is when the "negative efficacy" argument comes into play. It just seems like a lot of mixed up information being spread around these days.
1. A not-very pathogenic version is better adapted to transmission,
2. Someone carries that to another local, but it takes some time, like weeks to become more pathogenic and once pathogenic, infected people are pumping out enough of the pathogenic strain that it spreads easily once established in a location and those infected with the pathogenic strain find it difficult to move to a new locale.
When it comes to flu it used to be accepted that either it must be leaping through the atmosphere or it must somehow be seeded in different places before becoming evident, there was no other way to explain how quickly it traveled (just as quickly in 1789 as today even though there were no trains, airplanes, anything). This is in the Shope link. This way of thinking about flu mostly died with Shope and Andrewes and now today we just think, "oh of course it's because airplanes." And now we don't think much about flu disappearing because usually PCR shows it to be still around in off-seasons (except not in 2020). But it used to be considered very mysterious. So an idea of one phenotype that spreads and one that causes illness is in line with how flu used to be thought about.
Kevin McKernan (you know, that guy with more than 20,000 citations) suggests that "20-30% of COVID deaths have aspergillosis. COVID isn't the issue, immune suppression is"
https://twitter.com/Kevin_McKernan/status/1703026695748653507
As often the case, this is semantic imprecision. If everyone but the really slow deer outrun the lion, you can say "slowness kills the deer" but literally the lion kills the deer. Of course older people have weaker immune systems than children. The virus is still what kills them.
I just wrote something where I mentioned your post
Regarding not having a control group in the "VAIDS" study: the authors explained that it would be "unethical" to have a control group (crazy, I know)
> Limitations include the inability to include an unvaccinated control group due to the ATAGI recommendation for all children aged 5 to 11 years to receive the BNT162b2 vaccine. It was unethical to randomise children into an unvaccinated, placebo or delayed vaccination group, given that ATAGI recommended the BNT162b2 vaccine for the age group of interest and that Melbourne was experiencing a surge in COVID-19 cases in the community during the study period.
I think that is just their way of saying "We don't want to piss off Big Pharma!"
On a different topic, it seems that there is evidence that those who have accepted the #ClotShot seem to create the Spike Protein for 69-187 days, but the upper limit is because they stopped measuring at 187 days. If you check 1B people you might find the upper range is larger.
https://onlinelibrary.wiley.com/doi/epdf/10.1002/prca.202300048
You have pointed out that what seems to be happening is DAD in many of the victims.
This means lots of dead cell detritus in the lungs and it would seem that bacteria would have a party in that case. So, why is bacterial pneumonia not an issue here?
Even with an electron microscope, you cannot see the real dynamic state.
Therefore, for the time being we have no choice but to make inferences based on supporting evidence.
I wish someone smart would invent a method that allows us to realistically observe things down to the nanometer.
I haven't gotten to writing an assessment on the immune study. It does seem like an initial exploratory study that would require an actual control. I commented that there may also be some sort of ebb and flow in our immune system where our responses may be biased by recent prior experiences, and so just as important as "weak immune system = death" is "can the immune system 'recover' or be modified by its experience". The thing to consider is that children have gotten routine illnesses, but a rather poor immune system would seem to be suggestive of an inability to recover and hence either worse outcomes or death. At least that's my assumption.
Absolutely requires a control. For all we know it is normal for kids to show log 1 swings in cytokines by season, this would still keep them well above adults in terms of innate immunity because the bigger difference needs to be looked at in immune cells in tissues anyway
Even worse - what if all the study is showing us is a quality control problem on the reagents used to stimulate cytokines. Off hand I would guess that actually they collected everything gradually and tested at the same time, but still the mere possibility of this kind of thing shows why the reader wants a control
Also, with respect to stimulation the supplementary material suggests that the samples were stimulated around 2 hours post-collection if that adds some additional context.
That's sort of my line of thought as well. Well, maybe not a QC issue, but given that the mRNA vaccines are designed for the mRNA to be undetectable, then would TLR-agonists that mimic viral RNA not eliciting a cytokine response be unexpected? It seems possible that the immune system may just be "trained" to bypass this signaling pathway. Like I stated in my article on Friday a good comparison would be Novavax to see if this happens there as well. It appears Adenoviral dsDNA triggers TLR-9, so it would be interesting to consider what is actually going on.
One thing I am rather critical of is the idea that this is indicative of VAIDS. It's sort of likely someone using the acronym AIDS without understanding the progression of AIDS. If VAIDS is occurring shouldn't we be expecting many deaths related to infections? Or I guess this is when the "negative efficacy" argument comes into play. It just seems like a lot of mixed up information being spread around these days.
If we go with the quasi-species concept, what if:
1. A not-very pathogenic version is better adapted to transmission,
2. Someone carries that to another local, but it takes some time, like weeks to become more pathogenic and once pathogenic, infected people are pumping out enough of the pathogenic strain that it spreads easily once established in a location and those infected with the pathogenic strain find it difficult to move to a new locale.
Just throwing around ideas.
When it comes to flu it used to be accepted that either it must be leaping through the atmosphere or it must somehow be seeded in different places before becoming evident, there was no other way to explain how quickly it traveled (just as quickly in 1789 as today even though there were no trains, airplanes, anything). This is in the Shope link. This way of thinking about flu mostly died with Shope and Andrewes and now today we just think, "oh of course it's because airplanes." And now we don't think much about flu disappearing because usually PCR shows it to be still around in off-seasons (except not in 2020). But it used to be considered very mysterious. So an idea of one phenotype that spreads and one that causes illness is in line with how flu used to be thought about.