That other coronaviruses circulating among the human population do not afford a lasting immunity was known before the Covid-19 pandemic reached these shores. That the government bet the farm on the assumption of immunity is one of many national scandals coming out of this epidemic. The paper that supposedly caused the government to change tack and institute a lockdown, from Imperial College epidemic modellers, is also based upon the same assumption.There is 'no evidence' that people who have survived coronavirus have immunity - WHO warns - after Britain 'paid £16m' for two million antibody tests from China that DON'T WORK
There is currently no evidence to support the belief that people who have recovered from coronavirus are immune to catching the virus again, the World Health Organisation has said. Senior WHO epidemiologists warned despite the hopes governments across the world have piled on antibody tests, there is no proof those who have been infected cannot be infected again.
The British Government has bought 3.5 million serology tests, which measure levels of antibodies in blood plasma, even though they are not definitive of growing levels of herd immunity. Many tests being developed are pin prick blood tests similar to widely used instant HIV tests and measure for raised levels of the antibodies the body uses to fight the virus.
Speaking at a press conference in Geneva, Dr Maria van Kerkhove said: 'There are a lot of countries that are suggesting using rapid diagnostic serological tests to be able to capture what they think will be a measure of immunity. 'Right now, we have no evidence that the use of a serological test can show that an individual has immunity or is protected from reinfection.' She added: 'These antibody tests will be able to measure that level of seroprevalence - that level of antibodies but that does not mean that somebody with antibodies means that they are immune.'
On another note, I do not agree with the quoted article's implication that the government should not begin widespread antibody testing until immunity is proven ("even though they are not definitive of growing levels of herd immunity"). For one thing, widespread antibody testing is useful for testing the hypothesis that there is an immunity to Covid-19 after infection. For another, it will show how far the infection has already spread in the country, which would be useful to a determination of the true infection fatality rate and reproduction number, and also for making better projections and plans.
That's an excellent assessment, and I agree with you. It seems to me that COVID-19 just keeps coming back, and that our original ideas of a vaccine may have been optimistic, to say the least.That other coronaviruses circulating among the human population do not afford a lasting immunity was known before the Covid-19 pandemic reached these shores. That the government bet the farm on the assumption of immunity is one of many national scandals coming out of this epidemic. The paper that supposedly caused the government to change tack and institute a lockdown, from Imperial College epidemic modellers, is also based upon the same assumption.
The Imperial College team used a compartmental model, or SIR model, of disease spread. The letters SIR are an abbreviation giving the 'compartments' that people are put into.
The assumption of these models is those who get infected move from the S compartment to the I compartment. When the disease runs its course in those, they move from the I compartment to the R compartment. Eventually S becomes zero, or so small that the reproduction number is insufficient to maintain transmission (the herd immunity we have all been told about), and the size of S holds steady, and all of the I is converted to R and the epidemic ends. That is, that the movement for an individual is S → I → R and then ends. Although populations are whole numbers of individuals, an assumption of these models is that when the numbers are very large, that you can model populations as continuous quantities. Also, S + I + R is a constant.
- S is the susceptible population.
- I is the infectious population (i.e. those who have the virus and are shedding, so can infect others).
- R is the removed population (those who have died of the disease, those who have been isolated and cannot infect others, or those who have had the disease, recovered and are now immune).
But if Covid-19 does not provide a lasting immunity, then the cycle through compartments might look like this: S → I → R → S → I → R → S ... Where the duration in the R compartment is of unknown length (possibly short). If there is no immunity at all, then the cycle is like this S → I → S → I → S ... until death. Existing coronaviruses are somewhat like this, where the immunity is only short-lived, or not even present, and they return seasonally.
This sort of modelling I have seen described as sophisticated in the press, by journalists who are evidently unfamiliar with mathematics. I would say that it is fairly crude, and the results you get out are tuned by an array of parameters whose values are informed by guesswork. They are useful educational tools for showing people what an epidemic trajectory looks like qualitatively, but I would not rest the fate of nations upon their results.
The very same academic unit whose model is said to have influenced the British government's policy (and the US government's) used similar modelling which lead British authorities to slaughter millions of healthy livestock in response to the 2001 foot and mouth epidemic. What is now widely viewed to have been a mistake which caused serious economic damage (at least, serious in pre-Covid-19 terms).
The whole thing goes to show that the government's mantra that its decisions have been guided 'by the science' is a nonsense. Science is not a monolithic entity. Science is a set of tools and a philosophy for discovering truths about the natural world. Science is also a collection of individuals across a vast array of disciplines, each with their own opinions about what those truths are. Scientists sometimes form consensuses on issues. Sometimes they divide into different schools of thought.
It is quite clear that what 'the science' says depends on whom you ask. There have been great differences between what government advisers have said, and what other equally qualified people have said. 'The science' on Covid-19 also differs from country to country (q.v. disparate national advice about the use of PPE by the general population, and differing views on the importance of community testing). It would be more truthful for the government to say that its decisions have been informed by the assumptions and judgements (even in the face of a lack of real scientific information about the threat) of a few scientists. These have often not fallen on the side of caution.
On another note, I do not agree with the quoted article's implication that the government should not begin widespread antibody testing until immunity is proven ("even though they are not definitive of growing levels of herd immunity"). For one thing, widespread antibody testing is useful for testing the hypothesis that there is an immunity to Covid-19 after infection. For another, it will show how far the infection has already spread in the country, which would be useful to a determination of the true infection fatality rate and reproduction number, and also for making better projections and plans.
Yeah, that's what I think. Unfortunately, I agree with AD1184, who made a good point that Japan may not be seeing a second wave, but rather a delayed 1st wave, and I think we're about to get smacked down hard.No matter how you crunch the numbers, this pandemic is only just getting started
People are understandably looking for good news. But the truth is, we’re nowhere near controlling coronavirus.
(More on the link)
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But Nivek, if you test everyone, you're only going to find that almost everybody has it ...except, as you mention, a very small number of truly immune.Things keep pointing back to this, the need to test everyone and as promptly as we can across the world, we could know so much more about this virus as you mentioned and we need this information, especially we need to know if there is a true immunity to Covid-19 after infection, if there's not then our uphill battle against this virus will be obviously even more difficult...IMO
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This was such an alarming statement that I spent a couple of hours today checking it out, and it's not true - virologists discovered that the SARS and MERS coronaviruses induce antibodies that are detectable in the patient's blood for about 24 and 18 months [1], and it's believed that these antibodies confer immunity during that time, but this assumption is untested. It is reasonable to tentatively conclude however that since the patients did recover from the virus, the antibodies played a role in their recovery.That other coronaviruses circulating among the human population do not afford a lasting immunity was known before the Covid-19 pandemic reached these shores. That the government bet the farm on the assumption of immunity is one of many national scandals coming out of this epidemic. The paper that supposedly caused the government to change tack and institute a lockdown, from Imperial College epidemic modellers, is also based upon the same assumption.
The results just came in from a random sampling of 3,000 residents of Santa Clara, California, and they found that only 2.5% - 4.2% of that population had been exposed to the virus (they tested positive for the antibodies to the SARS-CoV-2 virus) - that's far more than the official counts indicated, but nowhere near the entire population:But Nivek, if you test everyone, you're only going to find that almost everybody has it ...except, as you mention, a very small number of truly immune.
There is this study here from 1990:This was such an alarming statement that I spent a couple of hours today checking it out, and it's not true - virologists discovered that the SARS and MERS coronaviruses induce antibodies that are detectable in the patient's blood for about 24 and 18 months [1], and it's believed that these antibodies confer immunity during that time, but this assumption is untested. It is reasonable to tentatively conclude however that since the patients did recover from the virus, the antibodies played a role in their recovery.
However early clinical results have indicated that the convalescent plasma havrested from recovered COVID-19 patients is effective in treating severely ill patients, and several studies are going on right now to quantify the benefits and any associated risks:
The time course of the immune response to experimental coronavirus infection of man.
K. A. Callow, H. F. Parry, M. Sergeant, and D. A. Tyrrell
Abstract
After preliminary trials, the detailed changes in the concentration of specific circulating and local antibodies were followed in 15 volunteers inoculated with coronavirus 229E. Ten of them, who had significantly lower concentrations of pre-existing antibody than the rest, became infected and eight of these developed colds. A limited investigation of circulating lymphocyte populations showed some lymphocytopenia in infected volunteers. In this group, antibody concentrations started to increase 1 week after inoculation and reached a maximum about 1 week later. Thereafter antibody titres slowly declined. Although concentrations were still slightly raised 1 year later, this did not always prevent reinfection when volunteers were then challenged with the homologous virus. However, the period of virus shedding was shorter than before and none developed a cold. All of the uninfected group were infected on re-challenge although they also appeared to show some resistance to disease and in the extent of infection. These results are discussed with reference to natural infections with coronavirus and with other infections, such as rhinovirus infections.
I'm very encouraged to see that small-scale study reporting successful outcomes with convalescent plasma: it sounds like they were able to pull several of those ten people back from the brink with just one injection. That's exactly what we need: a treatment that we can give to the most severe cases, and ideally reduce the chances of death in severe cases down to a few percent or less. Because that's what's really scaring the shit out of everyone: knowing that if this virus hits you hard and you get ARDS, then there's nothing they can do but put you on a ventilator and you'll have about a 20% chance of surviving. Yikes, y'know?There is this study here from 1990:
The time course of the immune response to experimental coronavirus infection of man.
The researchers inoculated 15 volunteers with coronavirus 229E, ten became infected, eight developed colds. 14 of these were able to return a year later to be re-inoculated. The group of five originally uninfected became infected this time, and one developed a cold. Of 9 returning volunteers in the infected group, six became infected on inoculation and shed virus, but did not develop disease (i.e. they were potentially asymptomatic spreaders).
I think that the degree and duration of immunity conferred by antibodies will vary across the population because not everyone has the same immune response. Some diseases have a much better immune response that is more uniform across the population than others.
For the results in regards to SARS-Cov-2, there was this report on a medical pre-print from China that I posted a couple of weeks ago:
Low antibody levels raise questions about coronavirus reinfection risk
The pre-print is here:
Neutralizing antibody responses to SARS-CoV-2 in a COVID-19 recovered patient cohort and their implications
Researchers measured SARS-Cov-2-specific neutralizing antibody levels in recovered mild Covid-19 cases. They found that a third had levels that might be insufficient to prevent re-infection, and in some patients they could not detect antibodies. The researchers excluded severe cases because they could have been in receipt of antibody-containing blood plasma. The older patients tended to have a greater presence of neutralizing antibodies than younger ones.
The idea that those vulnerable to the severe illness will be able to rely upon the herd immunity offered by those less vulnerable therefore seems questionable to me. It also makes a vaccine's likelihood of succeeding similarly questionable. Some vaccines are able to prevent disease in an individual, but not infection, allowing them to keep spreading it. This was the cause of an argument between the WHO and China about 15 years ago, because the Chinese were vaccinating chickens against avian influenza, but their vaccines were only able to prevent disease in chickens, and not infection. This enabled asymptomatic spread and provided a breeding ground for avian flu to mutate into more dangerous strains.
We can only hope that there are other immune mechanisms at work that provide immunity to SARS-Cov-2 and that a vaccine will be successful, but assuming things is dangerous.
I don't think this is true. Why do you think this is true?But Nivek, if you test everyone, you're only going to find that almost everybody has it ...except, as you mention, a very small number of truly immune.
I'm very encouraged to see that small-scale study reporting successful outcomes with convalescent plasma: it sounds like they were able to pull several of those ten people back from the brink with just one injection. That's exactly what we need: a treatment that we can give to the most severe cases, and ideally reduce the chances of death in severe cases down to a few percent or less. Because that's what's really scaring the shit out of everyone: knowing that if this virus hits you hard and you get ARDS, then there's nothing they can do but put you on a ventilator and you'll have about a 20% chance of surviving.
But Nivek, if you test everyone, you're only going to find that almost everybody has it ...except, as you mention, a very small number of truly immune.
There is this study here from 1990:
The time course of the immune response to experimental coronavirus infection of man.
The researchers inoculated 15 volunteers with coronavirus 229E, ten became infected, eight developed colds. 14 of these were able to return a year later to be re-inoculated. The group of five originally uninfected became infected this time, and one developed a cold. Of 9 returning volunteers in the infected group, six became infected on inoculation and shed virus, but did not develop disease (i.e. they were potentially asymptomatic spreaders).
I think that the degree and duration of immunity conferred by antibodies will vary across the population because not everyone has the same immune response. Some diseases have a much better immune response that is more uniform across the population than others.
For the results in regards to SARS-Cov-2, there was this report on a medical pre-print from China that I posted a couple of weeks ago:
Low antibody levels raise questions about coronavirus reinfection risk
The pre-print is here:
Neutralizing antibody responses to SARS-CoV-2 in a COVID-19 recovered patient cohort and their implications
Researchers measured SARS-Cov-2-specific neutralizing antibody levels in recovered mild Covid-19 cases. They found that a third had levels that might be insufficient to prevent re-infection, and in some patients they could not detect antibodies. The researchers excluded severe cases because they could have been in receipt of antibody-containing blood plasma. The older patients tended to have a greater presence of neutralizing antibodies than younger ones.
The idea that those vulnerable to the severe illness will be able to rely upon the herd immunity offered by those less vulnerable therefore seems questionable to me. It also makes a vaccine's likelihood of succeeding similarly questionable. Some vaccines are able to prevent disease in an individual, but not infection, allowing them to keep spreading it. This was the cause of an argument between the WHO and China about 15 years ago, because the Chinese were vaccinating chickens against avian influenza, but their vaccines were only able to prevent disease in chickens, and not infection. This enabled asymptomatic spread and provided a breeding ground for avian flu to mutate into more dangerous strains.
We can only hope that there are other immune mechanisms at work that provide immunity to SARS-Cov-2 and that a vaccine will be successful, but assuming things is dangerous.