Coronavirus

[Maeght]

The two positive samples of participants had to be between 20 and 60 days apart. According to Geert's talks a year ago, this is the time after the initial infection is cleared during which a suboptimal immune response occurs - short-lived antibodies specific to the antigen. These have higher affinity to the virus than innate antibodies - thus preventing the latter from binding if the person is re-exposed during this 2 month period - but do not neutralize the virus, so that it can re-infect the person.
The first infection is likely to be mild, since the innate antibodies are not inhibited as they are in the reinfection, which is likely to be more symptomatic.
After the reinfection, longer lasting immunity is built up.
The high infectiousness of Omicron makes it much more likely that a person will be re-exposed in this way.

Is there actually any evidence of this?

'Despite the fact that natural antibodies differ in their function from adaptive antibodies, they are polyreactive and they detect autoantigens and new antigenic determinants.'

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6384419/

[Spud]

These are the figures he is referring to. As usual, it is more complex than those who adopt tin foil wish to admit. Scrub that last bit - aren't bright enough to understand.

https://www.reuters.com/article/factcheck-comorbidities-coviddeaths-idUSL1N2TU22X

I was not trying to prove that the number of coronavirus deaths in the country has been significantly overstated, as your link says. I perhaps should have said that if we had vaccinated those with comorbidities (like those in the study linked to in your link), this may have reduced the deaths in those people while allowing those in good health to develop herd immunity. Like we do with the flu vaccine.

[Spud]

Is there actually any evidence of this?

'Despite the fact that natural antibodies differ in their function from adaptive antibodies, they are polyreactive and they detect autoantigens and new antigenic determinants.'

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6384419/

Good question; in his videos he talks as though it is an established fact but then on his website it is listed as a critical unanswered question. So I have sent a message asking him to clarify.
Meanwhile, just came across this:
Not so fast: adaptive suppression of innate immunity
"T cells of the adaptive immune system have now been shown to suppress overzealous early innate responses to infection that can lead to 'cytokine storm'–mediated death"

[Maeght]

Good question; in his videos he talks as though it is an established fact but then on his website it is listed as a critical unanswered question. So I have sent a message asking him to clarify.
Meanwhile, just came across this:
Not so fast: adaptive suppression of innate immunity
"T cells of the adaptive immune system have now been shown to suppress overzealous early innate responses to infection that can lead to 'cytokine storm'–mediated death"

Will be interesting to hear an answer.

[Maeght]

Good question; in his videos he talks as though it is an established fact but then on his website it is listed as a critical unanswered question. So I have sent a message asking him to clarify.
Meanwhile, just came across this:
Not so fast: adaptive suppression of innate immunity
"T cells of the adaptive immune system have now been shown to suppress overzealous early innate responses to infection that can lead to 'cytokine storm'–mediated death"

There is a lot about the innate immune system here https://www.frontiersin.org/articles/10.3389/fimmu.2012.00066/full

[Spud]

There is a lot about the innate immune system here https://www.frontiersin.org/articles/10.3389/fimmu.2012.00066/full

Rather a lot to read! Had a scan though, thanks.

[Spud]

In a recent interview, Vanden Bossche was talking about the belief that the high infectiousness of Omicron could help us build herd immunity, because so many people are catching it and becoming immune. He said this is going to put high evolutionary pressure on the virus, and a new variant that can evade this immunity will become dominant. It will be similar to the effect of having most of the population vaccinated (and generating antibodies) in a short space of time.

[ProfessorDavey]

The beneft from the vaccines is temporary.

So is the benefit from immunity derived from infection.

[Spud]

So is the benefit from immunity derived from infection.

Which is probably because the virus will be likely to have mutated before the immune system is exposed to it again, so it makes sense to have a short-lived  antibody response in the event of mild infection.
But apparently the innate immune system can retain a memory of the virus, so it will be updated each time we are exposed to a new strain.

[ProfessorDavey]

But apparently the innate immune system can retain a memory of the virus, so it will be updated each time we are exposed to a new strain.

Non-sense - the whole point about the innate immune system is that it non-specific and isn't adaptive - hence the distinction between innate immune system and the adaptive immune system.

And of course the other issue is that the innate immune system is pretty poor as a line of defence, hence the need for adaptive immunity.

So you will always get an innate immune response to a new viral infection, but that alone will provide a poor barrier to serious infection, disease and death. You will also always get an adaptive immune response which is better but takes time to kick in resulting in the risk of severe disease. Hence the benefit of vaccination which kicks the adaptive immune system into action decoupled from viral infection, meaning that if the virus is encountered you get a more rapid and stronger adaptive immune response which will reduce the likelihood of infection taking hold, reduce the likelihood of severe disease and reduce the likelihood of death.

But another massive benefit of being vaccinated is that the earlier and more robust immune response will reduce the number of viral replicative events and this number is directly related to the likelihood of mutations during replication, some of which may confer the virus to be more transmissible or more virulent and therefore be variants of concern.

[Maeght]

Which is probably because the virus will be likely to have mutated before the immune system is exposed to it again, so it makes sense to have a short-lived  antibody response in the event of mild infection.
But apparently the innate immune system can retain a memory of the virus, so it will be updated each time we are exposed to a new strain.

You haven't been reading the links I've provided f you think that Spud.

[Maeght]

Non-sense - the whole point about the innate immune system is that it non-specific and isn't adaptive - hence the distinction between innate immune system and the adaptive immune system.

And of course the other issue is that the innate immune system is pretty poor as a line of defence, hence the need for adaptive immunity.

So you will always get an innate immune response to a new viral infection, but that alone will provide a poor barrier to serious infection, disease and death. You will also always get an adaptive immune response which is better but takes time to kick in resulting in the risk of severe disease. Hence the benefit of vaccination which kicks the adaptive immune system into action decoupled from viral infection, meaning that if the virus is encountered you get a more rapid and stronger adaptive immune response which will reduce the likelihood of infection taking hold, reduce the likelihood of severe disease and reduce the likelihood of death.

But another massive benefit of being vaccinated is that the earlier and more robust immune response will reduce the number of viral replicative events and this number is directly related to the likelihood of mutations during replication, some of which may confer the virus to be more transmissible or more virulent and therefore be variants of concern.

Absolutely. Was going to write something similar but you did it much better than I could have, so won't try to repeat it.

[Spud]

Non-sense - the whole point about the innate immune system is that it non-specific and isn't adaptive - hence the distinction between innate immune system and the adaptive immune system.

FYI, innate training
"activation of the innate immune system can also result in enhanced responsiveness to subsequent triggers. This process has been termed ‘trained immunity’, a de facto innate immune memory. "

[Maeght]

FYI, innate training
"activation of the innate immune system can also result in enhanced responsiveness to subsequent triggers. This process has been termed ‘trained immunity’, a de facto innate immune memory. "

A lot of interesting ideas there and a lot more to be found about it on the internet of course. Interesting that it talks about giving vaccines early to train the innate immune response.

Edit: Read this article https://www.frontiersin.org/articles/10.3389/fimmu.2018.00799/full

' In general, although debatable, innate memory is considered as a non-specific short-lived phenomenon, as opposed to adaptive memory that is long-lived and highly specific.'

[Spud]

Is there actually any evidence of this?

Back to this question; I haven't had a reply to my email yet, but I had some thoughts.

The reason he has concluded that antigen-specific antibodies can suppress innate antibodies from binding to covid-19, seems to be related to the observation that during the first phase of the pandemic, children were always asymptomatic when infected, but when infected later on they developed symptoms and illness.

Children were not symptomatic early on because they have high levels of natural antibodies. Because these can recognize a wide range of pathogens they are able to bind to covid-19.

Because they had no previous exposure to Covid-19, they hadn't yet made antigen-specific antibodies. But upon first exposure they did then mount a suboptimal antibody response, and these antibodies would be gone within 2 months, as occurs after a first vaccination.

Some children would be re-exposed to the virus while they had these suboptimal antibodies. At this point the children developed symptoms and illness. He says that the reason for this must be that the higher strength of binding of the antigen-specific antibodies enabled them to bind better than the less specific innate antibodies could do.

While suppressing the innate antibodies, the antigen-specific antibodies, being of low quality and quantity, failed to neutralize the virus and thus allowed it to bind to ACE2 and infect host cells, so that these children developed symptomatic illness.

We do have evidence that suboptimal antibodies can bind to a virus but not neutralize it. They are called 'non-neutralizing antibodies'.

[ProfessorDavey]

The reason he has concluded that antigen-specific antibodies can suppress innate antibodies from binding to covid-19, seems to be related to the observation that during the first phase of the pandemic, children were always asymptomatic when infected, but when infected later on they developed symptoms and illness.

You do realise how non-sensical that is.

In the first phase of the pandemic we didn't have testing (certainly not widespread testing), so the only way we 'knew' someone was infected was because of their symptoms. So the notion that in the first phase of the pandemic you could know who was infected by asymptomatic is non-sense. You simply didn't know as firstly there was no testing (and therefore you couldn't know unless someone was symptomatic) and then testing was limited to confirming infection in symptomatic cases - so again you never have a positive test for an asymptomatic case.

So Spud, you are just talking non-sense.

[Spud]

Professor,
It doesn't matter. The point is that children weren't affected at the start of the pandemic
 This would be explained by their good innate immunity.
Do stop being so patronising 

[ProfessorDavey]

Professor,
It doesn't matter. The point is that children weren't affected at the start of the pandemic
 This would be explained by their good innate immunity.
Do stop being so patronising 

I'm not being patronising - I am simply pointing out that it is completely non-sensical to claim that infected children at the start of the pandemic were asymptomatic as we couldn't know that they were infected as we had no tests and were relying on symptoms, or slightly later tests were only used to confirm symptomatic cases.

It does matter, as you cannot make a claim about whether children were or not symptomatic early on if you could not know whether they were infected or not. How would you tell between an infected asymptomatic kid and a non infected asymptomatic kid? You couldn't.

And i think you are also adding two and two and making about one thousand. Sure there is evidence that more recently children represent a larger proportion of those with reasonably severe symptoms or even being hospitalised. But remember this is proportional and the obvious explanation is not that children (who were the last to be vaccinated and many still aren't) are being more affected, but that the adult population (who are by and large vaccinated) are being less affected, hence the proportion of children gets larger.

The data suggest (as all the data do) that the vaccine is positive, not negative.

[ProfessorDavey]

The point is that children weren't affected at the start of the pandemic

But they were - it is just that the numbers were being overwhelmed by older and particularly vulnerable people being hospitalised and dying. Now that vaccination has reduced the severity for most of the population, we perhaps become more aware of children getting covid. This doesn't mean there are more cases in children nor that they are more severe - indeed the evidence seems to be the opposite - e.g. this from the BMJ on the very youngest children from Jan 2022:

'And the indications are that children admitted to hospital with omicron are even less sick, as they require less support than children admitted earlier in the pandemic and are discharged earlier. Oxygen use by children aged under 1 admitted in the past four weeks for whom data are available was 12%, compared with 22.5% in the first wave of the pandemic. Admission to intensive care was 9.9% (v 14%), use of mechanical ventilation was 2% (v 5.8%), use of non-invasive ventilation was 2% (v 7.2%), and mean length of stay was 1.7 days (v 6.6 days).

This would be explained by their good innate immunity.

This could be an explanation if the underlying assumption were true (that children are being affected more severely by covid now compared to earlier in the pandemic) but that doesn't seem to be the case. And even if it were there are many other explanations that are more likely explanations that some scientifically illiterate appeal to declining innate immunity.

[ProfessorDavey]

The point is that children weren't affected at the start of the pandemic

Nope

https://www.newscientist.com/article/2304688-why-omicron-isnt-more-severe-in-kids-despite-rise-in-hospitalisations/

[Aruntraveller]

Remember it's all over. At least that's what the government wants you to think:

https://www.theguardian.com/world/2022/apr/05/i-lowered-my-guard-four-people-on-catching-covid-for-the-first-time

"Living with Covid" is a useless piece of spin if you don't do anything to facilitate living with Covid.

[Maeght]

Back to this question; I haven't had a reply to my email yet, but I had some thoughts.

The reason he has concluded that antigen-specific antibodies can suppress innate antibodies from binding to covid-19, seems to be related to the observation that during the first phase of the pandemic, children were always asymptomatic when infected, but when infected later on they developed symptoms and illness.

Children were not symptomatic early on because they have high levels of natural antibodies. Because these can recognize a wide range of pathogens they are able to bind to covid-19.

Because they had no previous exposure to Covid-19, they hadn't yet made antigen-specific antibodies. But upon first exposure they did then mount a suboptimal antibody response, and these antibodies would be gone within 2 months, as occurs after a first vaccination.

Some children would be re-exposed to the virus while they had these suboptimal antibodies. At this point the children developed symptoms and illness. He says that the reason for this must be that the higher strength of binding of the antigen-specific antibodies enabled them to bind better than the less specific innate antibodies could do.

While suppressing the innate antibodies, the antigen-specific antibodies, being of low quality and quantity, failed to neutralize the virus and thus allowed it to bind to ACE2 and infect host cells, so that these children developed symptomatic illness.

We do have evidence that suboptimal antibodies can bind to a virus but not neutralize it. They are called 'non-neutralizing antibodies'.

I'd rather see some direct evidence rather than something inferred from incomplete data.

[Spud]

.....

I'm pretty sure children were not susceptible to covid19 disease at the beginning of the pandemic. If they were, we would have seen them in the hospitals with the adults.
Now however they are susceptible and are being admitted to hospital more often. What is the explanation for this, if not that the virus is now more infectious and there is more chance of secondary exposure with innate abs suppressed by suboptimal s-specific abs.

[Maeght]

I'm pretty sure children were not susceptible to covid19 disease at the beginning of the pandemic. If they were, we would have seen them in the hospitals with the adults.
Now however they are susceptible and are being admitted to hospital more often. What is the explanation for this, if not that the virus is now more infectious and there is more chance of secondary exposure with innate abs suppressed by suboptimal s-specific abs.

'Experts believe the jump in pediatric hospitalizations is likely the result of a confluence of factors. One of them is Omicron’s more contagious nature, and another may be the variant’s newfound preference for airway passages above the lungs, which can be more easily blocked in small children.'

https://www.scientificamerican.com/article/why-omicron-is-putting-more-kids-in-the-hospital/

' children have relatively small nasal passageways that can easily be blocked, so paediatric upper respiratory infections sometimes warrant extra attention compared with those in adults. Roberta DeBiasi, who heads the division of paediatric infectious diseases at the Children’s National Hospital in Washington DC, says that she and her colleagues have noticed an increase in the number of children with ‘COVID croup’, which is an inflammation of the upper airway that produces a characteristic ‘barking’ cough. That adds credence to the theory that Omicron might infect children differently from adults.' '

https://www.nature.com/articles/d41586-022-00309-x

[Udayana]

Remember it's all over. At least that's what the government wants you to think:

https://www.theguardian.com/world/2022/apr/05/i-lowered-my-guard-four-people-on-catching-covid-for-the-first-time

"Living with Covid" is a useless piece of spin if you don't do anything to facilitate living with Covid.

Indeed. Worse than useless.

After two years of trying to deal with it we want say it's all over and carry on in the (generally stupid) way we did before. But it has not been dealt with ... here ... let alone worldwide, where vaccines were not made available for a variety of short sighted reasons.

Deaths will decrease but we are likely to see wave after wave of variants that, though they may not be as severe, will act as a constraint on economic and environmental actions that need to be taken and impede progress generally.