A "more virulent" coronavirus does not have any coherent mechanistic basis. Low doses are repelled with toll receptor detection and natural killer cells, higher dose challenges result in a cold. The virus gets what it wants (transmission) without killing the host even running with the dials "at 11." Severe disease from infection with SAR…
A "more virulent" coronavirus does not have any coherent mechanistic basis. Low doses are repelled with toll receptor detection and natural killer cells, higher dose challenges result in a cold. The virus gets what it wants (transmission) without killing the host even running with the dials "at 11." Severe disease from infection with SARS-CoV-2 seems to have more to do with previously primed inflammation / enhancement than with how "contagious" or "fast multiplying" SARS-CoV-2 is. Kids have no trouble with this virus, we should not be afraid of it.
The covid vaccinated do not have infection / transmission efficacy after 4 months and thus are not placing any kind of evolutionary pressure on the virus anyways. "Boosting" might re-accelerate pressure, but that still doesn't get to "more virulent."
I really, really hope you are right. I have an open bet about a dinner with Luigi Warren, he says Marek will hit first, me and Orwell2024 think ADE will be the clear winner. The data is signalling more towards ADE than anything else.
Without boosting, you would already be guaranteed at least a draw. With boosting it's like the "Vaccine GoF" team gets multiple innings per round; we'll see if it makes a difference.
With the “broken-through” vaccinated all challenging the virus with sub-optimal legacy spike antibodies, how is that not submitting the virus to evolutionary pressure and training it to evade or even utilize this response to its advantage? Yes, it’s all working out just swimmingly right now with some protection against severe disease, but what happens when the virus obtains the passwords it needs to hack the vaxxed immune systems?
The residual. antibodies are not challenging / pressuring the virus after ~4 months. If anything, they appear to be aiding it in a sort of low-grade enhancement way that aligns with vanden Bossche's prediction - namely, they are disabling innate immunity (natural antibodies and Natural Killer Cells). As soon as mucosal IgA antibodies fade out, "sterilizing" immunity is gone and there is no more screening for antibody evasion (IgG humoral antibodies continue to provide protection against severe outcomes but do not impair transmission and thus do not place pressure on the virus).
The coronavirus can't benefit from that logic. There is no mechanistic basis.
Herpes viruses dedicate the majority of their genome to sophisticated immune evasion timers that turn off after infiltrating various niches within the body, and even appear to enhance immune function against other viruses (to me; most of the research interprets this behavior negatively in spite of the fact that we're all walking around with these viruses all our lives and are perfectly fine). It is these sophisticated timer genes which get distorted by passage through "leaky" immunity, leading to unvaccinated host death.
There's nothing like that in the coronavirus phenotype.
then how do you explain why the CFR of delta is spiking since vaccine fade started and that it's affecting the vaccinated and unvaccinated equally?
it's not ADE. it's not OAS. that would only be affected the vaxxed.
this looks to be vaccine mediated evolution to hotter strains.
delta is behaving in a completely new (and maladaptive in the absence of non-sterilizing but protective vaccines) fashion from other variants and variant jumps.
I think cpalmer's figures above suggest a pretty steady impact on the unvaccinated in the UK, with the Covid vaccinated driving higher overall CFR by aging up the pool of infection-susceptible. (I've mentioned before that figures in the US are poisoned by shoddy reporting and an essentially murderous treatment protocol.) I agree there is no signal for ADE yet (except in driving more infection, but not severe outcomes).
Unless a virus phenotype includes immune evasion (sabotaging cellular immunity) / dormancy, I don't think Marek's applies. Coronavirus probably has intracellular immune evasion but this is not influenced by adaptive immunity, so vaccines can't futz with the dials. Otherwise, what exactly is the vaccine going to train the coronavirus genome to do? Make spikes faster? Again, I propose that it is already running with all relevant dials at 11.
I am sure I know about 1/1000th of the biology you do, but are you suggesting that the old & vulnerable are the 1st to come out of the protective vaccine window & therefore the CFR is being boosted because those folks are re-entering danger zone? This is what I have surmised (with no biology, simply trying to understand the data). Wrote a single substack post with some charts there.
Regarding the absolute increase in cases (and therefor hospitalizations and deaths, despite severe outcome efficacy) mentioned in your post, that falls back under the vaccines appearing to have "negative infection efficacy" due to disabling innate immunity. See my "Forever Spike" post - https://unglossed.substack.com/p/forever-spike#footnote-anchor-13
Right, when infection efficacy was still holding in June, only the best players (the young) were out on the field. Now the elderly have come out from the bench. Even if the elderly are stronger players than they would be without the vaccine, the virus gets more runs.
A "more virulent" coronavirus does not have any coherent mechanistic basis. Low doses are repelled with toll receptor detection and natural killer cells, higher dose challenges result in a cold. The virus gets what it wants (transmission) without killing the host even running with the dials "at 11." Severe disease from infection with SARS-CoV-2 seems to have more to do with previously primed inflammation / enhancement than with how "contagious" or "fast multiplying" SARS-CoV-2 is. Kids have no trouble with this virus, we should not be afraid of it.
The covid vaccinated do not have infection / transmission efficacy after 4 months and thus are not placing any kind of evolutionary pressure on the virus anyways. "Boosting" might re-accelerate pressure, but that still doesn't get to "more virulent."
i do not think this is correct. the mechanism is clear and coherent:
it's what leaky vaccines that offer severity protection do.
previous examples abound, just not in humans because we've never used a leaky vaccine at scale before.
you should read this.
https://boriquagato.substack.com/p/are-leaky-vaccines-driving-delta
I really, really hope you are right. I have an open bet about a dinner with Luigi Warren, he says Marek will hit first, me and Orwell2024 think ADE will be the clear winner. The data is signalling more towards ADE than anything else.
Without boosting, you would already be guaranteed at least a draw. With boosting it's like the "Vaccine GoF" team gets multiple innings per round; we'll see if it makes a difference.
With the “broken-through” vaccinated all challenging the virus with sub-optimal legacy spike antibodies, how is that not submitting the virus to evolutionary pressure and training it to evade or even utilize this response to its advantage? Yes, it’s all working out just swimmingly right now with some protection against severe disease, but what happens when the virus obtains the passwords it needs to hack the vaxxed immune systems?
The residual. antibodies are not challenging / pressuring the virus after ~4 months. If anything, they appear to be aiding it in a sort of low-grade enhancement way that aligns with vanden Bossche's prediction - namely, they are disabling innate immunity (natural antibodies and Natural Killer Cells). As soon as mucosal IgA antibodies fade out, "sterilizing" immunity is gone and there is no more screening for antibody evasion (IgG humoral antibodies continue to provide protection against severe outcomes but do not impair transmission and thus do not place pressure on the virus).
I agree with you, I think there’s a very logical process by which the vaccines cause an evolutionary pressure that may make the virus more virulent
The coronavirus can't benefit from that logic. There is no mechanistic basis.
Herpes viruses dedicate the majority of their genome to sophisticated immune evasion timers that turn off after infiltrating various niches within the body, and even appear to enhance immune function against other viruses (to me; most of the research interprets this behavior negatively in spite of the fact that we're all walking around with these viruses all our lives and are perfectly fine). It is these sophisticated timer genes which get distorted by passage through "leaky" immunity, leading to unvaccinated host death.
There's nothing like that in the coronavirus phenotype.
then how do you explain why the CFR of delta is spiking since vaccine fade started and that it's affecting the vaccinated and unvaccinated equally?
it's not ADE. it's not OAS. that would only be affected the vaxxed.
this looks to be vaccine mediated evolution to hotter strains.
delta is behaving in a completely new (and maladaptive in the absence of non-sterilizing but protective vaccines) fashion from other variants and variant jumps.
i very much doubt it's a coincidence
I think cpalmer's figures above suggest a pretty steady impact on the unvaccinated in the UK, with the Covid vaccinated driving higher overall CFR by aging up the pool of infection-susceptible. (I've mentioned before that figures in the US are poisoned by shoddy reporting and an essentially murderous treatment protocol.) I agree there is no signal for ADE yet (except in driving more infection, but not severe outcomes).
Unless a virus phenotype includes immune evasion (sabotaging cellular immunity) / dormancy, I don't think Marek's applies. Coronavirus probably has intracellular immune evasion but this is not influenced by adaptive immunity, so vaccines can't futz with the dials. Otherwise, what exactly is the vaccine going to train the coronavirus genome to do? Make spikes faster? Again, I propose that it is already running with all relevant dials at 11.
I am sure I know about 1/1000th of the biology you do, but are you suggesting that the old & vulnerable are the 1st to come out of the protective vaccine window & therefore the CFR is being boosted because those folks are re-entering danger zone? This is what I have surmised (with no biology, simply trying to understand the data). Wrote a single substack post with some charts there.
Regarding the absolute increase in cases (and therefor hospitalizations and deaths, despite severe outcome efficacy) mentioned in your post, that falls back under the vaccines appearing to have "negative infection efficacy" due to disabling innate immunity. See my "Forever Spike" post - https://unglossed.substack.com/p/forever-spike#footnote-anchor-13
Right, when infection efficacy was still holding in June, only the best players (the young) were out on the field. Now the elderly have come out from the bench. Even if the elderly are stronger players than they would be without the vaccine, the virus gets more runs.