Please note: I have added further clarification and correction to the Baker, et. al. paper. I overlooked that the paper does indicate a large difference in binding affinity and electrostatic potential between the Ad26 (J&J) as well as ChAdOx1 (AstraZeneca), so please keep in mind that although the researchers argue that binding to Adenoviral vectors by PF4 may be occurring, the extent to which it is occurring in Ad26 viral vectors should be questioned. Apologies for overlooking this error.
I have wanted to put a vector post together but my research was far less productive. There’s also very little info on what has been verified rather than assumed as far as the physical structure and in vivo behavior of the main two products.
AZ is two doses, spaced a weird amount of weeks apart. https://www.bmj.com/content/372/bmj.n421 refers to the normal 3 being adjusted to 12 during the UK rollout so I think 3 is the manufacturer's norm. E1 is knocked out, and it’s unclear to what degree this affects expression of other structural proteins. But presumably spike is still expressed, otherwise no antibodies. Except once again I’m reluctant to say this for sure, because what if there’s just leftover spike in the injection. Again, there’s no apparent lit from the manufacturers on this question.
Thanks for your comment Brian. I'll look into the vaccine scheduling. This post came from February 2021 so I think there were talks about a second dose but they ended up scrapping it stating they didn't need it. I believe that's what happened with the J&J Vaccine. I'll look it up and see check on that.
I'll check out that post. I did come across this short article, and so I wasn't sure to the extent of knockout. I certainly don't believe it was the "gutless" knockout where it left just the bare bones.
So according to the WHO it says that the 2nd dose can be given 8-12 weeks after the first, which is still a weird timeframe. I do believe that when there were talks about a second J&J shot they talked about a 3 month time-lapse for the 2nd dose so I wonder if they modeled their dosing after AstraZeneca.
Personally, I believe that all second-dosing is unnecessary. There's no magic "true immunity" benefit from front-loading more circulatory IgG that just fades out anyway...
Honestly I really still don't know where the idea for a two-dose regimen came from, aside from a "the more the better" idea. I never looked too deeply into it.
I forgot to link but this is the WHO website that mentioned the 8-12 week comment.
I would note the Baker et al. paper in your post finds a big difference in the negative-ness of ChAdOx1 and HAd26, and simulated amount of PF4 binding. Since both cause VITT, that seems to refute the suggestion that PF4 binding is a primary cause.
You're right Brian. I'll add a comment in regard to that. To the extent that it may not be a primary cause the researchers did make a comment about binding dynamics:
Ad26 has also been implicated in TTS at a similar frequency to ChAdOx1 on a per dose basis (7, 32). Using a previously published model of Ad26 (16), we performed simulations as for ChAdOx1 and observed that PF4 contacted Ad26 less frequently than ChAdOx1 (Fig. 6, A and B). However, it is important to acknowledge that BD does not account for flexibility of the proteins following the initial interaction and operates on an accelerated time scale. Therefore, no inferences can be made regarding the protein’s residency times and whether a stable complex is formed. This should be explored in future molecular dynamics simulations.
But I will add a large caveat to the post to take into account that the study is likely reflective of ChAdOx1 more than the other adenoviral vectors.
Thank you! I am grateful for your ability to present complex biochemical patterns into a readable, educational, and rewarding experience. There is so much more going on than meets the eye, and I remain curious.
Thanks Paul! I hope the information does come across in a manner that people can read. And yes, I do believe that there's more than just the spike protein at least, but the extent that the other components of the vaccine are at play should be taken into account, such as the viral vector.
Unintended consequences such as blood clotting are why vaccines typically are developed over a span of years, rather than the span of months for the SARS-CoV-2 inoculations, courtesy of Operation Warp Speed.
Speed and safety are mutually exclusive in most things, and so the accelerated pace of Operation Warp Speed necessarily entailed a sacrifice in the safety of the resulting inoculations. There simply was not time allotted to investigate these potential adverse effects early in clinical trials.
Of course, the crowning indignity of that sacrifice is that it did not result in an effective vaccine that stopped community spread of the virus--the promise that was hyped by Big Pharma, government, and the media.
What's interesting is that there has been prior evidence that adenoviruses themselves may cause clotting in severe patients. I believe there was a mouse study where adenoviral vectors led to thrombosis but I misplaced that study. So even beforehand there may have been a few signals that suggest that these may occur due to the nature of the vector themselves.
And honestly, a vaccine that targets the upper respiratory tract just seems a bit farfetched, especially since it hasn't happened to a high degree of effectiveness so far with other vaccines.
A study on SARSr-CoV viruses by Shi Zhengli (China's infamous "Bat Lady") noted that antibodies against SARS and related pathogens don't hang around long.
I'll be candid and say that I haven't concerned myself with "transhumanist" ideas with these vaccines. Especially with many of these genetic material it would be easy to sequence and see any information that's available. Also, even if these vaccines are able to incorporate into our genome, it's likely targeting somatic cells alone, and a sparse number at that, which is not an easy way to hope to change people's genetic makeup. For me, it's a bit much to ask to reach the idea that they are changing our genetic material to such a degree that we should be riling ourselves up into hysteria.
You said "likely targeting somatic cells alone," but has anyone done any studies on germ cells?
And yes the genetic material would be easy to sequence, again, but, all this stuff they are doing and they don't see to care if we know.
"They know we know they know we know, and still they lie."
--Sundance
I agree human genome tampering is a stretch, but look at all the other things that just five years ago we would have said is a stretch. With the recent revelations, we just cannot 'assume" anything anymore.
No we don't know the effects on germ cells, but there are a lot more caveats to germ cells that would need to be considered.
I don't mind that people speculate on what may be happening, but for me personally I just need a good deal more evidence before I come to the same conclusions or speculations as others are.
Please note: I have added further clarification and correction to the Baker, et. al. paper. I overlooked that the paper does indicate a large difference in binding affinity and electrostatic potential between the Ad26 (J&J) as well as ChAdOx1 (AstraZeneca), so please keep in mind that although the researchers argue that binding to Adenoviral vectors by PF4 may be occurring, the extent to which it is occurring in Ad26 viral vectors should be questioned. Apologies for overlooking this error.
Fantastic.
I have wanted to put a vector post together but my research was far less productive. There’s also very little info on what has been verified rather than assumed as far as the physical structure and in vivo behavior of the main two products.
AZ is two doses, spaced a weird amount of weeks apart. https://www.bmj.com/content/372/bmj.n421 refers to the normal 3 being adjusted to 12 during the UK rollout so I think 3 is the manufacturer's norm. E1 is knocked out, and it’s unclear to what degree this affects expression of other structural proteins. But presumably spike is still expressed, otherwise no antibodies. Except once again I’m reluctant to say this for sure, because what if there’s just leftover spike in the injection. Again, there’s no apparent lit from the manufacturers on this question.
I think JJ is same gene knocked out, let me check. Doorlesscarp also did a resource hub for the vectors here https://doorlesscarp953.substack.com/p/adenovirus-hepatitis-in-children
Thanks for your comment Brian. I'll look into the vaccine scheduling. This post came from February 2021 so I think there were talks about a second dose but they ended up scrapping it stating they didn't need it. I believe that's what happened with the J&J Vaccine. I'll look it up and see check on that.
I'll check out that post. I did come across this short article, and so I wasn't sure to the extent of knockout. I certainly don't believe it was the "gutless" knockout where it left just the bare bones.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7937504/
So according to the WHO it says that the 2nd dose can be given 8-12 weeks after the first, which is still a weird timeframe. I do believe that when there were talks about a second J&J shot they talked about a 3 month time-lapse for the 2nd dose so I wonder if they modeled their dosing after AstraZeneca.
And EMA says given as 2 doses, anywhere from 4 to 12 weeks apart - https://www.ema.europa.eu/en/medicines/human/EPAR/vaxzevria-previously-covid-19-vaccine-astrazeneca
Personally, I believe that all second-dosing is unnecessary. There's no magic "true immunity" benefit from front-loading more circulatory IgG that just fades out anyway...
Honestly I really still don't know where the idea for a two-dose regimen came from, aside from a "the more the better" idea. I never looked too deeply into it.
I forgot to link but this is the WHO website that mentioned the 8-12 week comment.
https://www.who.int/news-room/feature-stories/detail/the-oxford-astrazeneca-covid-19-vaccine-what-you-need-to-know
I would note the Baker et al. paper in your post finds a big difference in the negative-ness of ChAdOx1 and HAd26, and simulated amount of PF4 binding. Since both cause VITT, that seems to refute the suggestion that PF4 binding is a primary cause.
You're right Brian. I'll add a comment in regard to that. To the extent that it may not be a primary cause the researchers did make a comment about binding dynamics:
Ad26 has also been implicated in TTS at a similar frequency to ChAdOx1 on a per dose basis (7, 32). Using a previously published model of Ad26 (16), we performed simulations as for ChAdOx1 and observed that PF4 contacted Ad26 less frequently than ChAdOx1 (Fig. 6, A and B). However, it is important to acknowledge that BD does not account for flexibility of the proteins following the initial interaction and operates on an accelerated time scale. Therefore, no inferences can be made regarding the protein’s residency times and whether a stable complex is formed. This should be explored in future molecular dynamics simulations.
But I will add a large caveat to the post to take into account that the study is likely reflective of ChAdOx1 more than the other adenoviral vectors.
Thank you! I am grateful for your ability to present complex biochemical patterns into a readable, educational, and rewarding experience. There is so much more going on than meets the eye, and I remain curious.
Aloha
Thanks Paul! I hope the information does come across in a manner that people can read. And yes, I do believe that there's more than just the spike protein at least, but the extent that the other components of the vaccine are at play should be taken into account, such as the viral vector.
Unintended consequences such as blood clotting are why vaccines typically are developed over a span of years, rather than the span of months for the SARS-CoV-2 inoculations, courtesy of Operation Warp Speed.
Speed and safety are mutually exclusive in most things, and so the accelerated pace of Operation Warp Speed necessarily entailed a sacrifice in the safety of the resulting inoculations. There simply was not time allotted to investigate these potential adverse effects early in clinical trials.
Of course, the crowning indignity of that sacrifice is that it did not result in an effective vaccine that stopped community spread of the virus--the promise that was hyped by Big Pharma, government, and the media.
What's interesting is that there has been prior evidence that adenoviruses themselves may cause clotting in severe patients. I believe there was a mouse study where adenoviral vectors led to thrombosis but I misplaced that study. So even beforehand there may have been a few signals that suggest that these may occur due to the nature of the vector themselves.
And honestly, a vaccine that targets the upper respiratory tract just seems a bit farfetched, especially since it hasn't happened to a high degree of effectiveness so far with other vaccines.
The SARS-CoV-2 vaccine was always implausible.
A study on SARSr-CoV viruses by Shi Zhengli (China's infamous "Bat Lady") noted that antibodies against SARS and related pathogens don't hang around long.
https://link.springer.com/article/10.1007/s12250-018-0012-7
If the antibodies are of relatively short duration, a vaccine based on triggering antibody production is only going to have short term impact.
That coupled with the high rates of mutation observed for the SARS-CoV-2 virus and a vaccine is an uphill battle on a good day.
"So, Iet's say
you want to change
the human body."
"You want to fix a mistake."
"You want to repair something,
improve something."
"Well, if you're going
to reprogram human
genetic materiaI,
you need a deIivery
system, and nothing
works better than virus."
"It's Iike a suitcase."
"You pack in genetic mutation,
infect the body
and the vector unIoads
into the target cells."
"But getting it
where you want it,
how you want it,
is the nightmare."
I'll be candid and say that I haven't concerned myself with "transhumanist" ideas with these vaccines. Especially with many of these genetic material it would be easy to sequence and see any information that's available. Also, even if these vaccines are able to incorporate into our genome, it's likely targeting somatic cells alone, and a sparse number at that, which is not an easy way to hope to change people's genetic makeup. For me, it's a bit much to ask to reach the idea that they are changing our genetic material to such a degree that we should be riling ourselves up into hysteria.
You said "likely targeting somatic cells alone," but has anyone done any studies on germ cells?
And yes the genetic material would be easy to sequence, again, but, all this stuff they are doing and they don't see to care if we know.
"They know we know they know we know, and still they lie."
--Sundance
I agree human genome tampering is a stretch, but look at all the other things that just five years ago we would have said is a stretch. With the recent revelations, we just cannot 'assume" anything anymore.
No we don't know the effects on germ cells, but there are a lot more caveats to germ cells that would need to be considered.
I don't mind that people speculate on what may be happening, but for me personally I just need a good deal more evidence before I come to the same conclusions or speculations as others are.