Covid

[Danny]

Dec 22, 2023 9:06:18 GMT moby said:

Dec 16, 2023 17:56:48 GMT alec said:

Another positive sign on nasal vaccies - www.nature.com/articles/s41586-023-06951-3

This is the full version of a previous preprint, and has positive results from trials in monkeys. The issue of longevity of protection remains to be answered, and may well be the flaw in any vaccine approach, but this is more encouraging.

I had Covid for the first time a few months back, given your interest I'd be grateful for any advice going forward. I have no symptoms of long covid but am aware of increased risks re. other health conditions? I have good health generally.

How do you know this was the first time? And what does it mean to say 'I have covid'? What it generally means is someone has an illness sufficiently bad that they notice there is something wrong with their health. But we get infected with all sorts of stuff every day. We just eliminate it without noticing.  By now, statistically we have all been infected with covid many, many times.

This is important, because claims such as Alec's about the liklihood of serious harm from covid only make sense if they are  compared to the real prevalence of the disease. The whole story of covid has been exaggeration of the risk it produces because of lack of knowledge of the real extent of infection.

[alec]

Slightly alarming - www.medrxiv.org/content/10.1101/2023.12.24.23300512v1.full.pdf

This is a US based study, quite small, but still worrisome. It tested the efficacy of the XBB 1.5 boosters (different, more updated booster than those used in the UK) and found just 60% protection against severe outcomes (hospitalisation)after 30 days compared to not having the booster. More worryingly, they also checked the risks of those who had been previously vaccinated but not with the XBB booster against the risks for the completely unvaccinated and found zero protection.

This isn't quite as bad as it sounds, as (presumably) the unvaccinated have also been infected, so there will be some protection in that comparison cohort, but it's overall pretty alarming, especially as the booster only offers very partial additional protection against severe outcomes.

[leftieliberal]

As we know there are four other circulating coronaviruses OC43, NL63, HKU-1 and 229E. The consensus is that these viruses are also descendants of past pandemics and that Sars-CoV-2 is just the latest member of their club. theconversation.com/some-believe-the-1889-russian-flu-pandemic-was-actually-caused-by-a-coronavirus-heres-why-thats-unlikely-220484

It now looks like OC43 caused a pandemic in 1899-1900 but the outbreak of pneumonia at that time was attributed to a late wave of Russian flu. So it looks like we are going to have to live with Covid for nearly a century. 

[alec]

leftieliberal - it's quite common to read about comparisons between SARS-CoV-2 and the other 4 circulating HCoVs, but it's misleading and somewhat dangerous. While they are all HCoVs, the classification is merely a human construction, based on effectively what they look like under an electron microscope. The real comparison is with the other SARS type coronaviruses - SARS1 and MERS. These are in a completely different class, in terms of functional impact.

There is absolutely no reason why SARS-CoV-2 should follow the pattern of the 4 'normal' HCoVs. No reason whatsoever. We've already seen a shift to greater severity, and the mechanisms of cell entry are completely different. Given what we are now seeing in terms of impacts on male fertility, it's not beyond the realms of possibility (although very slender odds) that SARS-CoV-2 becomes an extinction level event.

SARS-CoV-2 is a coronavirus in the same way that the field mushroom and the death cap are both in the same family of fungi. That really doesn't provide any reason to imagine the functional effects are remotely similar.

[leftieliberal]

Jan 10, 2024 8:14:40 GMT alec said:

leftieliberal - it's quite common to read about comparisons between SARS-CoV-2 and the other 4 circulating HCoVs, but it's misleading and somewhat dangerous. While they are all HCoVs, the classification is merely a human construction, based on effectively what they look like under an electron microscope. The real comparison is with the other SARS type coronaviruses - SARS1 and MERS. These are in a completely different class, in terms of functional impact.

There is absolutely no reason why SARS-CoV-2 should follow the pattern of the 4 'normal' HCoVs. No reason whatsoever. We've already seen a shift to greater severity, and the mechanisms of cell entry are completely different. Given what we are now seeing in terms of impacts on male fertility, it's not beyond the realms of possibility (although very slender odds) that SARS-CoV-2 becomes an extinction level event.

SARS-CoV-2 is a coronavirus in the same way that the field mushroom and the death cap are both in the same family of fungi. That really doesn't provide any reason to imagine the functional effects are remotely similar.

You obviously didn't bother to read the article before responding:
Examination of the total excess deaths per million of population in England and Wales over 1899 and 1900 gave a figure of 1,576 deaths per million, less than the 2,275 deaths per million for the Russian influenza, but only just short of the 1,866 deaths per million for the two worst COVID years of 2020 and 2021.
OC43 caused almost as many excess deaths per million over the same period as  SARS-CoV-2. It is not correct to call it a "field mushroom".

As usual you are ignorant of biological taxonomy: the Field Mushroom is of the family Agaricaceae; the Death Cap is of the family Amanitaceae. They are not in the same family of the fungi as you claim.

[alec]

Quite correct - they are in the same order, not the same family. But the point still stands. There is no real functional similarity between the SARS viruses and the other HCoVs, and their classification as coronaviruses is a completely human designation, based in no small part by their appearance.

I also didn't see the link to the article for some reason, as it doesn't appear on my laptop. I've seen these claims previously, and they are quite interesting, although contested. One of the interesting aspects of the 4 existing HCoVs is that they are actually worse infections than what we normally refer to as 'common colds', and they do tend to produce heavier symptoms than the 200 or so rhinoviruses. I've also seen some research predating the pandemic that found the 4 HCoVs had the ability to enter the brain, and were being linked with later neurological conditions, with several authors suggesting that we need to be taking these more seriously as health threats.

One of the things I do expect to come out of the pandemic is a greater appreciation of the long term health effects of viral infections. It's something we already know about. Lyme's and HIV are both accepted as persistent infections that have very mild acute phases but can be deadly long terms (Lyme's is a bacteria though) but we're also firming up understanding of EBV for example, as a major contributor to MS. It looks like researchers are increasingly coming round to an acceptance that we've been stuck on the acute phase symptoms of viruses, whereas the long term effects are often much worse.

[Danny]

Jan 10, 2024 8:14:40 GMT alec said:

leftieliberal - it's quite common to read about comparisons between SARS-CoV-2 and the other 4 circulating HCoVs, but it's misleading and somewhat dangerous. While they are all HCoVs, the classification is merely a human construction, based on effectively what they look like under an electron microscope. The real comparison is with the other SARS type coronaviruses - SARS1 and MERS. These are in a completely different class, in terms of functional impact.

and yet they all confer a degree of cross immunity? So catching the now tamed ones helped protect us from the new covid. You keep campaigning to try to eradicate all of them, leaving us susceptible to whole new waves of serious epidemic when they eventually escape back into cirulation.

There is absolutely no reason why SARS-CoV-2 should follow the pattern of the 4 'normal' HCoVs. No reason whatsoever. We've already seen a shift to greater severity, and the mechanisms of cell entry are completely different.

There has never been an infectious agent which did not fade in severity over time. Thats the obvious reason why it will fade, because they always do. Some have been more resistant to this, but as a class corona viruses all have followed this trend of adapting to be less severe illnesses but ubiquitous in society. The tradeoff suits them.

[Danny]

I gather death cap mushrooms are beneficial to some trees because they form a symbiotic relationship where the mushroom provides the tree with chemicals protective against other harmful agents. And they are being investigated for anti cancer chemicals. Also rabbits can eat them fine, which maybe suggests they have adapted to be able to do so after years of exposure. Evolution in action.

[alec]

Danny - "There has never been an infectious agent which did not fade in severity over time."

Absolutely, completely and utterly untrue. You're talking total bollocks and absolutely haven't the first clue about anything you're talking about here. It's just utter tripe.

There are dozens of examples, from human to animal pathogens, where infectious agents have demonstrated increased severity over time. Smallpox is the classic example from human pathogens. That went from being a minor illness to a global killer, with absolutely no move towards reduced severity over a time span of centuries. HIV/AIDS has recently become more severe and Dengue has been developing new serotypes with enhanced severity for a couple of decades. In the animal world, the current devastation of bird flu comes from a strain that has been around for a quarter of a century and then suddenly become savagely dangerous, and then there's the well known shift of Marek's disease from a non serious illness to a near total lethality pathogen, the example of myxomatosis in rabbits which overcame initial population resistance to become much more severe, etc etc. The examples are legion.

I really do wish you could put away your belligerent myth making and just open your mind to being able to learn. You're stuck in this mental dead end where you believe conspiracy theory nonsense and invent facts that suit your worldview. You're completely wrong, and I continually present you with actual facts, yet you never, ever seem to have the capacity to understand reality.

No, there is absolutely no natural path that ensures pathogens become less severe. They can do, they can maintain the same severity, or they can become far worse. We have abundant examples of all three pathways.

[leftieliberal]

Jan 10, 2024 14:53:41 GMT alec said:

Quite correct - they are in the same order, not the same family. But the point still stands. There is no real functional similarity between the SARS viruses and the other HCoVs, and their classification as coronaviruses is a completely human designation, based in no small part by their appearance.

I also didn't see the link to the article for some reason, as it doesn't appear on my laptop. I've seen these claims previously, and they are quite interesting, although contested. One of the interesting aspects of the 4 existing HCoVs is that they are actually worse infections than what we normally refer to as 'common colds', and they do tend to produce heavier symptoms than the 200 or so rhinoviruses. I've also seen some research predating the pandemic that found the 4 HCoVs had the ability to enter the brain, and were being linked with later neurological conditions, with several authors suggesting that we need to be taking these more seriously as health threats.

One of the things I do expect to come out of the pandemic is a greater appreciation of the long term health effects of viral infections. It's something we already know about. Lyme's and HIV are both accepted as persistent infections that have very mild acute phases but can be deadly long terms (Lyme's is a bacteria though) but we're also firming up understanding of EBV for example, as a major contributor to MS. It looks like researchers are increasingly coming round to an acceptance that we've been stuck on the acute phase symptoms of viruses, whereas the long term effects are often much worse.

alec I refer you to www.ncbi.nlm.nih.gov/pmc/articles/PMC8930171/

While these viruses belong to the same family, there are many similarities and dissimilarities between the pathogenesis and clinical features of their respective diseases. SARS-CoV-2 is much less pathogenic as compared to MERS-CoV and SARS-CoV.

Bearing in mind that medical treatment (particularly keeping patients alive) is rather better now than at the turn of the 20th century it is likely that OC43 would have caused a lower fatality rate if it had happened a century after it did. Nevertheless it is a better comparator for covid-19 than either SARS or MERS, both of which are highly pathogenic.

[alec]

leftieliberal - I personally think we're in the same area as that old saying about autistic people; if you've met one autistic person, you've met one autistic person.

Viruses are all different, and I'm not sure we should go too far down the route of labeling them as like other viruses. I think the biggest mistake we made was to assume covid will now be like 'the common cold'. Equally, it's not 'airborne aids', although there are some similarities in the way it attacks some parts of the immune system.

I would also caution against drawing any conclusions about the pathogenesis of Covid. If people had been writing about the pathogenesis of HIV four years after the first human infection, they would be saying it's like a 'common cold', with mild flu like symptoms which resolve rapidly with no lasting effects. It was only after 5 - 8 years or so post infection that it's devastating consequences were truly identified, with effectively 100% fatality.

I'm not saying that this is a likely outcome with Covid, but given what we do know regarding viral persistence, mitochondrial damage, and the signals for substantial increases in numerous other clinical conditions after Covid infection, I think it's far too premature to make any conclusions about Covid pathogenesis. The best we can say is that in it's acute phase, it's very serious but nowhere near as lethal as SARS1 and MERS. Beyond that, we're waiting for data.

[leftieliberal]

Jan 11, 2024 23:19:09 GMT alec said:

leftieliberal - I personally think we're in the same area as that old saying about autistic people; if you've met one autistic person, you've met one autistic person.

Viruses are all different, and I'm not sure we should go too far down the route of labeling them as like other viruses. I think the biggest mistake we made was to assume covid will now be like 'the common cold'. Equally, it's not 'airborne aids', although there are some similarities in the way it attacks some parts of the immune system.

I would also caution against drawing any conclusions about the pathogenesis of Covid. If people had been writing about the pathogenesis of HIV four years after the first human infection, they would be saying it's like a 'common cold', with mild flu like symptoms which resolve rapidly with no lasting effects. It was only after 5 - 8 years or so post infection that it's devastating consequences were truly identified, with effectively 100% fatality.

I'm not saying that this is a likely outcome with Covid, but given what we do know regarding viral persistence, mitochondrial damage, and the signals for substantial increases in numerous other clinical conditions after Covid infection, I think it's far too premature to make any conclusions about Covid pathogenesis. The best we can say is that in it's acute phase, it's very serious but nowhere near as lethal as SARS1 and MERS. Beyond that, we're waiting for data.

What has this got to do with autism? You are turning into Danny. SARS is just an abbreviation for Severe acute respiratory syndrome, MERS is just an abbreviation for Middle East respiratory syndrome. Both reference the principal symptoms of the disease, they don't tell us anything about what virus caused it and it doesn't mean that the SARS-CoV-2 virus is closer to SARS-CoV-1 than it is to any other named coronavirus. This report on a OC43 outbreak in British Columbia in 2003 www.ncbi.nlm.nih.gov/pmc/articles/PMC2095096/ showed cross-reactivity with SARS-CoV-1 which indicated a similar nucleic acid sequence in the two viruses.

[alec]

leftieliberal - "What has this got to do with autism?"

Nothing at all, but the phrase "if you've met one autistic person, you've met one autistic person", is a standard rhetorical device in discussions around understanding neurodivergent people, based on the idea that you should avoid drawing conclusions from one person to another, because everyone is different. I just applied the same thinking to viruses, and it's nothing whatsoever to do with being like Danny. I'm saying the same thing as I think you are saying; that we should be careful making too many assumptions about whether different viruses will behave in similar ways or not.

What I would say though is that technically, SARS-2 really is closer to SARS than any other coronavirus. That's why it was named as such. It's been classified in the subgenus of Sarbecoviruses, whereas OC43 is an embecovirus. The sarbecoviruses are distinguished by specific structural factors, and it's thought these split from the other betacoronaviruses (which includes the embecoviruses) to form a distinct, structurally different subgenus. The 'SARS' name was given to this virus based on this classification, not because of any symptoms - "ICTV announced “severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)” as the name of the new virus on 11 February 2020. This name was chosen because the virus is genetically related to the coronavirus responsible for the SARS outbreak of 2003. " (from www.who.int/emergencies/diseases/novel-coronavirus-2019/technical-guidance/naming-the-coronavirus-disease-(covid-2019)-and-the-virus-that-causes-it )

Where I think it is relevant to talk of the symptoms leading to the name selection is with the origin of the SARS name itself in 2003 (and, presumably, the sarbecovirus subgenus name). If SARS had caused a minor skin rash, it obviously would not have been termed a 'severe acute respiratory' virus, but once we had named that one, when a structurally similar bat virus came along, it had to be given the same name. Indeed, I think recent published research has identified something like 150 distinct sarbecoviruses in bats, and these are termed SARSr-CoVs (as in 'SARS related') and SARS2r-CoVs (SARS2 related), so the 'SARS' bit of the name is used regardless of whether they infect humans, but entirely due to the structural similarity.

Does make me feel a bit wobbly though, thinking there are 150 SARS like viruses out there.....

[Danny]

Jan 11, 2024 15:38:53 GMT leftieliberal said:

Bearing in mind that medical treatment (particularly keeping patients alive) is rather better now than at the turn of the 20th century it is likely that OC43 would have caused a lower fatality rate if it had happened a century after it did. Nevertheless it is a better comparator for covid-19 than either SARS or MERS, both of which are highly pathogenic.

Well i dont know about that. Covid has beautifully exemplified that it only killed already immunologically weak individuals. Obvious correlation with age, but that seems likely mediated by the accumulation of bodily infirmity with age, and then stronger effects on younger people with risk factors. Medical treatment mitigated the death rate somewhat, and there is an argument the Uk behaved worse than some equivalent european countries because it had weaker medical infrastructure, but the great majority of people survived covid and were never at serious risk because of their own immune systems. So the determinant of death rate would be the proportion of at risk people in the population.

On the one hand 100 years ago people died younger and there was more debilitating disease about, which could have increased the numbers of weakened individuals and surely would have increased the numbers at younger ages. But on the other hand, people would have died younger before they became bodily infirm with age, and then died more quickly once debilitated. So its arguable the population of suscepitble people might have been much smaller and the death toll therefore much smaller. Its possible our recent covid would hardly have been noticed 100 years ago, though of course its effects were hugely hyped just recently anyway.

Similarly, its possible the 1918 flu would have been very much worse had it happened now because of a far greater population of susceptible old people today. Although it had a big impact on younger people, which in many respects is far worse in terms of life years lost. So it also depends how you measure harm, in terms of numbers dying or life years lost.

[alec]

Danny - "Covid has beautifully exemplified that it only killed already immunologically weak individuals. Obvious correlation with age, but that seems likely mediated by the accumulation of bodily infirmity with age, and then stronger effects on younger people with risk factors. Medical treatment mitigated the death rate somewhat, and there is an argument the Uk behaved worse than some equivalent european countries because it had weaker medical infrastructure, but the great majority of people survived covid and were never at serious risk because of their own immune systems. So the determinant of death rate would be the proportion of at risk people in the population."

Once again you demonstrate your inability to think clearly and logically. Despite repeated efforts to educate you on this matter, you still persist in falsely restricting your 'analysis' to the acute phase of the virus, despite abundant evidence that the chronic effects of Covid are likely to be substantial.

Just try, for once, to step outside your own mind, and look at some factual evidence that is uncomfortable for your theories. Take Lymes disease (a zoonotic bacteria, not transmissible human to human). If you wanted to assess the severity of this by restricting your analysis to the acute phase, you would conclude that it causes a very minor cold like illness in most individuals, something more like a mild dose of 'flu in a minority of others, accompanied in around half of all cases by a strange, point specific rash. However - and this is really what you need to understand - left untreated, Lymes can resolve but for some it becomes a life changing autoimmune condition that can ultimately be fatal, years or decades after the initial 'mild' infection.

If you want an example of a virus that presents as supremely mild in the acute phase, shows zero symptoms for a couple of years, and then has a very high fatality rate thereafter, look no further than HIV. Yet you persist on only addressing Covid in terms of the acute phase. Covid's acute phase is actually way more severe than HIV. We've just got to hope that the observed immune system disregulation seen in long covid patients, and the very strong signal for sever heart issues post acute infection, are restricted to a section of the population with a genetic predisposition, because if it isn't, and - as some claim - it's more a function of the number of infections, then we're in for a very long and severe Covid induced health impact that goes way beyond the more vulnerable being hit in the acute phase. Neither you nor I, nor anyone else, knows yet how this will end.

[Danny]

Jan 15, 2024 9:59:23 GMT alec said:

Once again you demonstrate your inability to think clearly and logically. Despite repeated efforts to educate you on this matter, you still persist in falsely restricting your 'analysis' to the acute phase of the virus, despite abundant evidence that the chronic effects of Covid are likely to be substantial.

Well there isnt any! Sure, evidence people badly affected by covid were susceptible to longer term effects impacting their health. But frankly no evidence this is a significant effect on long term population health. 

The biggest problem is that I am proceeding from the assumption we achieved herd immunity to two strains of covid, basically everyone caught it who would ever have done so naturally. Whereas most studies assume only those formally recorded by doctors ever caught it. The difference to the impact on populations is massive depending which assumption you make. Lockdown was only justifiable on the asumption it saved very much illness and death, and there is really no evidence it did. Even people like Johnson could see from the evidence they were getting autumn 2020 that this was true.

There seems to be an analogy here with what happened over the post office horizon scheme. Political need to be seen to have made a good choice plus commercial interest to make money from the software overrode concerns about real harm being caused. Here, the commercial medical companies have made vast fortunes from covid interventions, while experts and politicians once committed to a course of action could never admit they had been mistaken, or that initially it might have been just a tossup whether to do all that lockdown or not.

[Danny]

Jan 12, 2024 14:19:16 GMT leftieliberal said:

This report on a OC43 outbreak in British Columbia in 2003 www.ncbi.nlm.nih.gov/pmc/articles/PMC2095096/ showed cross-reactivity with SARS-CoV-1 which indicated a similar nucleic acid sequence in the two viruses.

hence why past exposure to other related viruses created immunity to covid this time round before it had even arrived. obviously, this would have varied country to country depending on their histories of other viruses.

The irony is that while china had one of the lowest death rates in the whole world, and it attributed this to lockdown, when lockdown was finally released nothing much happened. In reality its likely China already had one of the better immunity levels to covid before the outbreak began and therefore both was always going to have one of the lowest death rates, and never got any benefit from lockdown (except to asist its rulers expand political population control measures). This is rather unsurprising if the origin of covid was from local animal populations, and would therefore have been infecting locals in a low key way forever.

The sad truth is that those in the Uk who had most corona virus infections beforre covid, had fewest deaths during the epidemic.

[alec]

Danny - "Well there isnt any! Sure, evidence people badly affected by covid were susceptible to longer term effects impacting their health. But frankly no evidence this is a significant effect on long term population health."

Sigh...Patiently explaining to those too stubborn to accept new data...

Completely wrong. Study after study has demonstrated that longer term impacts are not restricted and often don't correlate at all with the severity of the acute infection. We also have mounting evidence that repeat infections increase the risk of more severe long term outcomes. So this suggests the idea of a naturally susceptible pool is incorrect. But we do have strong evidence of adverse impacts on long term population health.

"The biggest problem is that I am proceeding from the assumption we aiheved herd immunity to two strains of covid, basically everyone caught it who would ever have done so naturally. Whereas most studies assume only those formally recorded by doctors ever caught it."

Again, as has been pointed out to you sooo many times, you are completely wrong. There are now thousands of studies based on: Random PCR testing survey; wastewater prevalence data; modeled infection data; real world cohort based mass testing data. I'm afraid you simply don't know what you are talking about, because you refuse to read the evidence. So no, most studies don't assume recorded infections are the only ones infected. But yes, I can see how you've become completely stuck because you have rigidly adhered to a false assumption, despite all the evidence.

"The irony is that while china had one of the lowest death rates in the whole world, and it attributed this to lockdown, when lockdown was finally released nothing much happened."

This will probably be one of your more stupid comments of 2024, and we're only just into the third week. It's completely wrong.

China engaged in a massive state backed data suppression exercise, claiming around 100,000 deaths only, where independent researchers looking at subsequent deaths data came to the conclusion that around 2m died in a short period of time. It was the biggest single death toll of the pandemic to date. The Chinese experience backs up the efficacy of vaccines. They wasted their time and released restrictions without adequate vaccine coverage, and paid a heavy price.

"The sad truth is that those in the Uk who had most corona virus infections beforre covid, had fewest deaths during the epidemic."

I'm assuming you have evidence for this assertion? Actual, measurable data? Otherwise you wouldn't say it, because that would just be making stuff up. So provide the link to the evidence and everyone will be happy.

There was this paper - www.ncbi.nlm.nih.gov/pmc/articles/PMC7590640/ from December 2020 which suggested prior HCoV infection reduced Covid risks, but this was based only on a presumption that prior reported symptoms were HCoVs, and none of the cohort were tested to confirm the original pathogen. This study, from Feb 2021 - www.cell.com/cell/fulltext/S0092-8674(21)00160-4?_returnURL=https%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS0092867421001604%3Fshowall%3Dtrue

found that seasonal HCoV antibodies were cross reactive with SARS-CoV-2 but that this didn't offer any protection against Covid, while this study, from Aug 2022 pubmed.ncbi.nlm.nih.gov/35091739/
found that anti-S SARS-CoV-2 IgG (antibody) levels were highly correlated with IgG antibodies against OC43 and HKU1 S proteins (eg prior infection with these two HCoVs gives you elevated antibodies against Covid) but "High anti-OC43 and anti-S2 antibody levels were associated with both a rapid anti-SARS-CoV-2 antibody response and increased disease severity. Subjects with increased sequential organ failure assessment (SOFA) scores developed a higher ratio of S2- to S1-reactive antibodies."

In other words, the exact opposite of what you are claiming. Prior HCoV infection was associated with markedly worse outcomes to Covid.

Like I say, you must have evidence for your claims, so let's see why you said that.

[alec]

lens - this might be of interest - www.nature.com/articles/s41586-023-06952-2

It's a paper using the NHS app data to calculate the odds of getting infected after a contact. I haven't got the time today to pick through the methodology in detail, but one sentence caught my eye in the pre edit PDF version - "We demonstrate that the NHS COVID-19 app accurately translated proximity and duration of exposure into a meaningful epidemiological risk score and we quantify how these factors affected the actual probability of transmission."

I appreciate what you said previously about the success of tracing apps, but this appears to suggest that the app was able to identify contacts that were correlated with subsequent infections, possibly suggesting that the app was most effective?

As I say, I haven't the time to study this in detail, and wasn't looking to get into a debate on the issue, but I thought it might be of general interest.

[alec]

Not sure if this is relevant for anyone, but there have been some significant developments in the availability of accurate covid testing kit in recent months. There is now the capacity to purchase a portable PCR testing kit, which can test Covid + flu (if you buy the right swabs) giving results in 10 - 35 minutes. (+ve tests usually report within 15mins, -ve confirmed after 35 mins). The kit costs around £260, less if you can reclaim the VAT, plus the costs for the test swabs.

altruan.com/en/products/pluslife-pcr

These are very accurate - pubmed.ncbi.nlm.nih.gov/37962934/ Independent testing showed them to be as good or better than lab based systems for ready to use swabs, slightly less effective if swabs had been frozen.

This isn't quite a domestic scale testing kit, and it is a bit pricey, although we are at last seeing the first steps in affordable rapid accurate testing emerge. I'm not yet investing in one of these, partly because my infection control points mean that there are few scenarios when I could use this, although I may well consider this so I can have guaranteed safe visitors at home and drop other precautions. However, the reason I'm not buying just yet is that other, cheaper options might come to the market.

But it's good to see how technology is moving, and the points to a safer future for everyone.

[Danny]

Jan 15, 2024 13:14:33 GMT alec said:

"The sad truth is that those in the Uk who had most corona virus infections beforre covid, had fewest deaths during the epidemic."

I'm assuming you have evidence for this assertion? Actual, measurable data? Otherwise you wouldn't say it, because that would just be making stuff up. So provide the link to the evidence and everyone will be happy.

Perhaps its a question of how we were educated. I followed a largely science side education, where I was taught to look at boundary conditions and worry less about what is happening inside the black box. Thats because in many mathematical or physics problems we dont know whats happening inside. The medical experts did something of the sort in the late covid epidemic, where they claimed exponential growth had begun and would therefore engulf the nation. They applied the procedure wrongly, the problem with using fundamental and simplified principles, is to apply them properly. They assumed 100% of the nation was susceptible to covid, that largely 0% of the population had had covid, that exponential growth was therefore inevitable given it was already in the community. Whereas the true figures could have been more like only 60% was ever  susceptible, 30% had already had covid by the time they made their pronouncements, with the upshot it had actually nearly reached the point of exhausting the available susceptible people and ending anyway. This is supported by the evidence of covid cases/deaths in local regions of the Uk which had covid early, before any restrictions were imposed. It still peaked and failed to exponentially rise despite nothing being done.

In this particular case, I simply juxtaposed two known facts which I hope you agree with.
1)Most people who died from covid were old.
2)Most people who caught corona virus diseases prior to the covid epidemic were young. The obvious reason for this is that children are always the group catching commonly circulating diseases most frequently, because we lump them together in classrooms where thousands are crammed into the same building most days. Thats why schools were closed to stop community spread, and SAGE figures anticipated this would cut total cases by 1/3, and also implied that ALL OTHER MEASURES combined would only reduce it by a similar amount. An expert on corona virus infections who had studied their incidence reported kids got 3 or 4 such infections a year, and I dont see you have disputed this number, nor do any of the research reports you cite elsewhere. I dont think they comment on frequency of such infections, or that it declines with age. The expert said in old age corona infections were more like 1 every ten years.

Given 1 and 2, then its a very simple deduction that the group in the UK which had the highest frequency of corona virus infections before the epidemic also had the lowest death rate. Which is what I said.

Now, the papers you cited were seeking to determine whether this was causal. I havnt had time to read them in detail to see what I make of their case. They seem to be rather mixed, one for example concludes that having  more respiratory infections (without identifying what they were) prior to covid made you less likely to have bad covid. They confirm that in lab tests corona infections do create cross immune reactions against covid, and actually that a covid infection boosts circulating antibodies which work against other corona viruses. They are less clear whether this is effective protection, but do say covid stimulates the body to produce antibodies from stored patterns which were laid down against other corona viruses. The strongest response seemed to be to internal capsid proteins rather than spike, which could very well be what you might expect from other stuff you mentioned, that covid has a unique infection mechanism with its spike,  but antibodies created against the capsid contents of other corona viruses had more in common to work against covid.  There is a suggestion that previous corona infections behaved just like the covid vaccines, in that the vaccines are now considered only to protect against serious disease, not against repeat infections numerically.

Its also possible of course that older people dont get  these infections so frequently not simply because they have less social contact, but because after a lifetime experiencing corona infections they have lots more stored immunity.  The real problem why people died from covid seems to have been they had impaired immune response compared to a fully healthy human. This being the case, a fully naive healthy human was always safe, as we saw happen. But a human with impaired immune system could never be safe whether they had past exposure creating immunity, or a vaccine (which works the same way). 

[alec]

Danny - OK - it's good that you're being polite and putting lengthy responses on the Covid thread, as we have continually asked you do, but what you've actually written is less good - more of the same pretentious guff I'm afraid. In a nutshell, you taken 736 words to say 'I have no evidence for my false assertion'.

Dribbling on about what you think, how you were educated (badly, I'd say, in terms of critical thinking at least) doesn't constitute evidence. You made an assertion, which must be backed up by evidence, otherwise it's just your opinion, and we know that your opinions on this are factually incorrect.

"I havnt had time to read them in detail to see what I make of their case."

But you have had time to write 736 meaningless words?

That sums you up I'm afraid.

[Danny]

The situation is even simpler and therefore more obvious than I explained, and yet you made no attempt to dispute it in the sense you seem to insist of posters, detailed referenced evidence.

Systematically before and after the arrival of the covid epidemic, young people get more corona virus infections than old ones. Thats because young people get more respiratory illnesses than old ones, simply because they get out and about more and so catch them more often from other people.

Overwhelmingly those who died from covid were old. Average age about 80.

The group which had most corona virus infections had the fewest deaths.

[Danny]

Feb 2, 2024 10:25:22 GMT alec said:

A couple of fascinating covid snippets: In the US, the CDC has put out a new public information campaign aimed at encouraging uptake of boosters, with the headline " your next covid infection could be your worst".

Bit of a contrast to the HIV campaign under Thatcher, whose slogan was 'AIDS, dont die of ignorance'. We have abandoned using truth to persuade people to act, instead the government embarked on a propaganda campaign, for which we now have proof thanks to the enquiry that they deliberately lied. Quite apart from where they simply promoted falsehoods in ignorance.

I was reminded of that having caught a film yesterday, somewhat on the lines of the recent 'its a sin' By Russel Davies. Both about what happened to in particular gay youth and drug users in that epidemic. In other countries of course, this became a massive epidemic spreading throughout the whole heterosexual population with truly high death tolls. The government policy of honesty on that occasion worked to safeguard the majority of the population, by honestly explaining the risk and actually where there was no risk. Whereas this time, frankly we totally failed to exploit the potential from splitting our approach between those truly at risk, the old, and those essentially safe, the young.

And here you are, still trying to scare nations into bankruptcy.



There was another lesson from what happened. When all this was unrolling, I was at prime age to be involved. Russel Davies was interviewed and asked similarly whether any of his drama was based upon his own experience. He replied he had been way too timid, though of course he made the point where one of his character who was hardly involved in anything ended up catching HIV and dying. Similarly I was also rather too timid. But even so I once dated a guy who had a couple of friends die, another whose partner died but who himself survived long enough for the drugs to arrive which can now fairly straightforwardly control the disease, albeit not cure it. Rather like high blood pressure. Another guy still living with HIV, and another way back then who suspected he might have it. I was once scared nearly to death by a doctor when being tested, you then had to come back a week later for results, who was going on so much about the disease that I spent a week thinking he knew something more which I didnt, which made him think I had it. On the whole I was pretty cautious based on the advice how to stay safe, and I was. fine. But the point is, this was a swathe of young people dying from a truly dangerous disease. At that time I thought about this and concluded it is simply no good ending your life voluntarily by hiding at home. Better to live it, risks and all.

Some people objected publicly to lockdown this time round, was one Ken Clarke? I suspect anyone who lived through a war might have had this same feeling, its absurd to hide at home cowering from something which could end your life, but instead end it anyway yourself by just hiding. And in this case, the evidence suggests we did totally the wrong thing, Government lied, government fell victim to 'the precautionary principle', which is a sure way to ruin lives.

That's a very significant departure from the previous received wisdom that infections get less severe with repeat bouts,

Theres no evidence covid is becoming more severe. Rather it seems authorities faced with the disease fading away are resorting to shouting 'FIRE' louder and louder. Possibly because the scale and cost of the errors made during this epidemic are so vast no one dares admit to them. It was clear from Johnsons testimony he understood lockdown was pointless back in autumn 2020, yet he declined to take this line in his own defence. Its just too big a disaster to admit to causing.

There has also been a new study that found what's described as 'silent organ damage' is at least one organ system detected in 60% of long covid sufferers,

You keep stating the obvious. If someone has 'long' disease, then obviously the disease is still at work and has caused longer lasting damage. Which still doesnt say they will never recover, just it will take longer, nor does it say that the numbers involved and extent of illness is significant nationally. Why dont you just let us all get on with living?

[alec]

Danny - much better Danny. Do try to keep your lengthy diatribes isolated here on the right thread.

I've not bothered reading it through because skimming it I noticed a couple of massive mistakes you've made. You've learned nothing, from all the evidence I've handed to you. It's not worth my time trying to educate someone who revels in ignorance as a personal choice.

[Danny]

So basically Alec, we have reached te stage where you wont even say what you disagree with any more in case I substantiate it further? Its as if Starmer got up and said we think con are wrong, but we will not tell you just where they are wrong? Convincing not?

[alec]

Danny - "So basically Alec, we have reached te stage where you wont even say what you disagree with any more in case I substantiate it further?"

No Danny. We've reached the point where I can't be bothered wasting my time on a time waster who has no interest in learning and is deliberately spouting nonsense. You're a troll, pure and simple. You repeatedly lie about what I say, you lie about basic facts, and you never, ever take up challenges to substantiate your claims.

[lens]

Jan 18, 2024 13:20:52 GMT alec said:

lens - this might be of interest - www.nature.com/articles/s41586-023-06952-2

It's a paper using the NHS app data to calculate the odds of getting infected after a contact. I haven't got the time today to pick through the methodology in detail, but one sentence caught my eye in the pre edit PDF version - "We demonstrate that the NHS COVID-19 app accurately translated proximity and duration of exposure into a meaningful epidemiological risk score and we quantify how these factors affected the actual probability of transmission."

I appreciate what you said previously about the success of tracing apps, but this appears to suggest that the app was able to identify contacts that were correlated with subsequent infections, possibly suggesting that the app was most effective?

As I say, I haven't the time to study this in detail, and wasn't looking to get into a debate on the issue, but I thought it might be of general interest.

Well, I've been away for a few weeks and am catching up with a lot of things, so no - I won't look at this in detail either. But a few words.

Firstly, it seems to be another study with a vested interest in talking up the app for partisan reasons. Which is not to say anything within it is untrue...... but there is such as thing as being selectively positive with facts presented.

It would be highly unlikely for the app to show *no* correlation at all, but that's really the wrong question to be (practically) asking in the first place. To be useful it's a question of how big a correlation and how effective any such is at preventing any transmission. (Encouraging isolation when a person may have become infected and likely to pass on.) So timelines are critical. It's already been discussed about when an exposure may result within a family group - the subject will be only too well aware of the other persons infection by word of mouth, so any "ping" after that person sends their notification won't do any good, it's too late. It's an example where statistical correlation will be shown (between notification and a true contact) but one which is practically useless.

I also wonder about some of the assumptions made in that study. As example: "Across all contacts, most exposures are brief (median duration 40 min) yet most detected exposures that result in transmission last several hours (median duration 6 h; 82% last more than 1 h......" Well, maybe. But could there be an alternative explanation? Could it be that such a 6hour duration indicates more a person in settings with a lot of interpersonal interactions? With the infection coming from somewhere else? Maybe the "6hour interaction" was with another phone the other side of a partition, and the infection was due to a fellow passing worker (who had left their phone on the desk) giving the contact a peck on the cheek (and Covid) without any app registration at all? OK, somewhat facetious, but in principle......?

I'm somewhat staggered that your link seems to assume that a) it's possible to always accurately assess distance from Bluetooth signals in the first place, and b) that no consideration seems to be given to the circumstances of the contact - whether directly face to face, in open or closed environment, ventilation, or even whether separated by a partition! Transmission of radio waves and transmission of viruses simply do not follow the same rules, and that's the elephant that this and other studies just don't seem to want to acknowledge.

And the other consideration is even if some beneficial early warnings may result from app usage, are such outweighed by the downsides? The previous study seemed to indicate a figure of overall about 5% testing positive after an app notification, but such ignores the situations (eg family infection) where someone is aware of an exposure BEFORE any app notification, maybe bringing the figure down to more like only 1-2% of unique notifications really then deserving isolation. Which begs the question if the 98/99% of unnecessary isolations and the economic hit thereby caused are worth it? It's certainly a long way from the glowing scenarios first promoted when the app was originally being spoken of.

And - I've been travelling, which involved more than one very long flight, regrettably in economy class. Such was an endurance test in itself, and there was no way I intended to wear a mask throughout. And fortunately no ill effects. A friend also recently had to undertake a couple of long haul flights, and had valid reasons for being very keen to avoid Covid, and decided to wear a N95 mask throughout. You've guessed it. In spite of the inconvenience he tested positive a few days after arrival. Fortunately, it was mild, and cleared before it was a problem, but doesn't say much for the efficacy of masks in general settings. I wouldn't dispute they may improve ones chances a little - but personally the downsides well outweigh any slight benefit.

[alec]

lens - like I say, I'm not familiar with the contact tracing app stuff, so I find it interesting, but I'm not really able to comment other than to note that contact tracing itself has been proven to be a brilliant and irreplaceable method of reducing infectious disease. I would have thought that in due course, technology will play a role in enhancing and refining this ability, but can accept that we might not be there just yet.

As for your friend in the N95, indeed, they're not infallible. But if the entire plane was wearing them they would have almost certainly been OK, or better still, if the sick person who spread it had been prevented from joining the flight, and if the plae had high grade HEPA filters etc etc. You also betray a slight prejudice in your concerns over masking; you don't know whether you have inadvertently killed someone because you didn't wear a mask yourself. Unlikely, perhaps, but certainly not impossible. Masking is more about everyone else, and not so much about you. That's why your friend got infected.

[leftieliberal]

COVID: there’s a strong current of pandemic revisionism in the mainstream media, and it’s dangerous

There is no clearer marker that we are now in the “after” phase of the pandemic, than the proliferation of public inquiries, reports on lessons learned and post hoc analyses. To reassess and agonise over how reasonable lockdown was is now a near-constant in the media, particularly in the UK.

However, against the backdrop of the continuing COVID inquiry, fringe views are making their way into the mainstream. And online debates have abandoned much of the ethical and political nuance they deserve.

Containing COVID was an imperfect and difficult task that required weighing health, social, ethical, psychological, economic and political interests in the face of a rapidly spreading novel virus in 2020. Yet, with increasing distance, the thorny, difficult issues tend to be flattened to false narratives and a history of simple choices. In other words, “pandemic revisionism”.

A good, balanced article from The Conversation.