Coronavirus antibodies can start to fade away within weeks, according to a new study which puts a 'nail in the coffin' in the idea of herd immunity https://www.businessinsider.com/cor...hows-antibodies-fade-after-three-weeks-2020-7 Coronavirus antibodies start to fade away just weeks after people show symptoms, a new study by UK scientists showed. King's College London research found that the presence of antibodies peaked three weeks after symptoms appeared, before fading away. In some cases, the antibodies were undetectable three months afterwards. It followed a Spanish study last week that also showed antibody protection rapidly declining in many patients. One of the UK study's authors said it put "another nail in the coffin of the dangerous concept of herd immunity." Antibodies to the coronavirus may disappear within months for many patients, according to a major new UK study which found that their presence peaked three weeks after symptoms appeared, before gradually fading away. For some patients, no antibodies were detected after just a few months, throwing doubt on hopes for a long-lasting vaccine. The study, which was carried out by scientists at King's College London and first reported by The Guardian, "puts another nail in the coffin of the dangerous concept of herd immunity," one of its authors said. The study was based on the antibody responses of 90 patients and health workers at Guy's and St. Thomas' NHS Foundation Trust. It showed that 60% of those tested had "potent" antibodies while battling COVID-19, but just 17% had the same level of potency three months later. The potency of the antibodies fell by as much as 23 times over the three months, the study found, and in some cases were undetectable at the end of that period of time. The study, which has not yet been peer-reviewed, found that antibodies were more potent and lasted longer in patients with the most severe cases of the COVID-19 virus. However, the findings suggest that like a common cold, the coronavirus can reinfect people, even if they developed antibodies during their first infection. It is the latest study to pour cold water over so-called herd immunity — the theory that a population will become immune to the virus if at least 60% of people catch it. A similar study in Spain, which was published last week, found that just 5% of people tested maintained coronavirus antibodies. Fourteen percent of people who tested positive for the antibodies in the first round of testing did not test positive in subsequent tests carried out weeks later. Two of the Spanish study's authors, Isabella Eckerle and Benjamin Meyer, said: "In light of these findings, any proposed approach to achieve herd immunity through natural infection is not only highly unethical, but also unachievable." Authors of the new UK report reached similar conclusions. One of the UK study's authors, professor Stuart Neil, said the study showed any immunity generated "doesn't last very long." "One thing we know about these coronaviruses is that people can get reinfected fairly often," he said. "What that must mean is that the protective immunity people generate doesn't last very long. It looks like Sars-Cov-2, the virus that causes Covid-19, might be falling into that pattern as well." The study "puts another nail in the coffin of the dangerous concept of herd immunity," professor Jonathan Heeney, a virologist at the University of Cambridge, said, adding that deliberately trying to get infected in the name of herd immunity created the risk of severe health damage in the future. "I cannot underscore how important it is that the public understands that getting infected by this virus is not a good thing. Some of the public, especially the youth, have become somewhat cavalier about getting infected, thinking that they would contribute to herd immunity," he said. "Not only will they place themselves at risk, and others, by getting infected, and losing immunity, they may even put themselves at greater risk of more severe lung disease if they get infected again in the years to come," he added. (More at above url)
Natural Herd Immunity is a myth! A leading antibody expert says you can get coronaviruses again, so 'there's not much we can do until there's a vaccine' https://www.businessinsider.com/ant...et-coronaviruses-again-we-need-vaccine-2020-7 More and more research is starting to point toward the idea that people could get the novel coronavirus a second time. One leading virus expert said that, for this reason, "there's not much we can do until there's a vaccine" to create herd immunity. Even if and when coronavirus vaccines prove successful, they may require booster shots. Roughly six months into the coronavirus pandemic, emerging evidence is starting to suggest that people who've been infected with this virus could still be susceptible to getting it again. "We know that from other coronaviruses, from regular human, common cold coronaviruses, that you probably get immunity for some time once you're infected," Florian Krammer, a vaccine scientist and virus expert at the Icahn School of Medicine at Mount Sinai in New York, told Business Insider. "But it's not perfect." Krammer says that a person's second coronavirus infection could be milder, or even asymptomatic — where they display no outward signs of sickness at all. But his assertion backs up what new data around the world is also starting to suggest: that the body may, after a few months, start to forget it had the disease caused by the novel coronavirus, COVID-19. This prospect of a potential for waning coronavirus memory in our immune systems may make it more difficult to rid the world of this virus, permanently, especially without a vaccine. Growing evidence immunity may not last Research published in the medical journal The Lancet earlier this month suggests that people who had the coronavirus in Spain, and subsequently developed antibodies to it — producing the proteins thought to possibly help protect against reinfection— are seeing their antibody levels wane, just months after an illness. Likewise, new research out of the UK on Saturday (which has yet to be peer-reviewed) also suggests that a person's coronavirus antibody levels tend to peak a few weeks after an infection, before gradually declining, and in some cases, disappearing entirely. This data suggests that the prospect of herd immunity — the idea that enough people in a given community could develop immune protection against a virus, halting its spread and shielding the vulnerable from infection — is going to require more than just natural-borne illnesses. "There's not much we can do until there's a vaccine," Krammer said. "With a vaccine, you're able to reach herd immunity very quickly." (More at above url)
Areas of New York have up to 68% antibodies... Imagine how many have killer T cells and helper t cells and b cells Parts of NY may have herd immunity right now. https://www.nytimes.com/2020/07/09/nyregion/nyc-coronavirus-antibodies.html
your "experts" models have nothing to do with the real world of a virus like this. ===== "It doesn’t make intuitive sense, Gomes admits, but “the homogenous models just don’t make curves that match the current data,” she said. Dynamic systems develop in complex and unpredictable ways, and she believes that the best we can do is continually update models based on what is happening in the real world. She can’t say why the threshold in her models is consistently at or below 20 percent, but it is. “If heterogeneity isn’t the cause,” she said, “then I’d like for someone to explain what is.”" “We just keep running the models, and it keeps coming back at less than 20 percent,” Gomes said. “It’s very striking.” A New Understanding of Herd Immunity The portion of the population that needs to get sick is not fixed. We can change it. https://www.theatlantic.com/health/archive/2020/07/herd-immunity-coronavirus/614035/ Warning... the above reading is not for morons that think that herd immunity is a myth and can only be reached when 70 percent of the population has antibodies. Here... is a sample... In the absolute simplest, linear model, if 70 percent of the world were to get infected, that would mean more than 54 million deaths. But the effects of the coronavirus are not linear. The virus affects individuals and populations in very different ways. The case-fatality rate varies drastically between adults under 40 and the elderly. This same characteristic variability of the virus—what makes it so dangerous in early stages of outbreaks—also gives a clue as to why those outbreaks could burn out earlier than initially expected. In countries with uncontained spread of the virus, such as the U.S., exactly what the herd-immunity threshold turns out to be could make a dramatic difference in how many people fall ill and die. Without a better plan, this threshold—the percentage of people who have been infected that would constitute herd immunity—seems to have become central to our fates. Some mathematicians believe that it’s much lower than initially imagined. At least, it could be, if we choose the right future. .... here is another paragraph later... much more at link.... This is not the case when a virus is spreading in the real world. Instead, the complexities of real life create what modelers refer to as heterogeneity. People are exposed to different amounts of the virus, in different contexts, via different routes. A virus that is new to the species creates more variety in immune responses. Some of us are more susceptible to being infected, and some are more likely to transmit the virus once infected. Even small differences in individual susceptibility and transmission can, as with any chaos phenomenon, lead to very different outcomes as the effects compound over time, on the scale of a pandemic. As Gomes explains, “There doesn’t need to be a lot of variation in a population for epidemics to slow down quite drastically.” more at the link...
Essentially, at present, New York City—where I live—might be said to be at a version of herd immunity, or at least safe equilibrium. Our case counts are very low. They have been low for weeks. Our antibody counts mean that a not-insignificant number of people are effectively removed from the chain of transmission. Many more can be effectively excluded because they’re staying isolated and distanced, wearing masks, and being hygienically vigilant. If we keep living just as we are, another big wave of disease seems unlikely. https://www.theatlantic.com/health/archive/2020/07/herd-immunity-coronavirus/614035/ Also note.... At Stockholm University, Tom Britton, the dean of mathematics and physics, thinks that a 20 percent threshold is unlikely, but not impossible. His lab has also been building epidemiological models based on data from around the globe. He believes that variation in susceptibility and exposure to the virus clearly seems to be reducing estimates for herd immunity. Britton and his colleagues recently published their model, demonstrating the effect, in Science. “If there is a large variability of susceptibility among humans, then herd immunity could be as low as 20 percent,” Britton told me. But there’s reason to suspect that people do not have such dramatically disparate susceptibility to the coronavirus. High degrees of variability are more common in things such as sexually transmitted infections, where a person with 100 partners a year is far more susceptible than someone celibate. Respiratory viruses tend to be more equal-opportunity invaders. “I don’t think it will happen at 20 percent,” Britton said. “Between 35 and 45 percent—I think that would be a level where spreading drops drastically.” Models like Britton’s and Gomes’s also assume that, after infection, people obtain immunity. This is a clear caveat that all the researchers make. COVID-19 is a new disease, so no one can be sure that infected people become immune reliably, or how long immunity lasts. But Britton noted that there are no clear instances of double infections so far, which suggests that this virus creates immunity for at least some meaningful length of time, as most viruses do.
Coronavirus: Levels of herd immunity in UK may already be high enough to prevent second wave, study suggests https://www.independent.co.uk/news/...wave-oxford-study-boris-johnson-a9623791.html Levels of herd immunity within the UK may already be high enough to prevent a second wave of coronavirus, a new study by Oxford University scientists suggests. The researchers posit that some of the population may already have a high level of immunity to Covid-19 without ever having caught it. In a paper yet to be peer-reviewed, they point to evidence suggesting exposure to seasonal coronaviruses, such as the common cold, may have already provided some with a degree of immunity, and note that others may be more naturally resistant to infection. Modelling how differing levels of pre-existing immunity between individuals could affect the overall “threshold” needed to prevent a resurgence of the virus, they found that this could be as low as 20 per cent. “It is widely believed that the herd immunity threshold (HIT) required to prevent a resurgence of SARS-CoV-2 is in excess of 50 per cent for any epidemiological setting,” wrote Jose Lourenco, Francesco Pinotti, Craig Thompson, and Sunetra Gupta, all of Oxford University. “Here, we demonstrate that HIT may be greatly reduced if a fraction of the population is unable to transmit the virus due to innate resistance or cross-protection from exposure to seasonal coronaviruses.” They added: “These results help to explain the large degree of regional variation observed in seroprevalence and cumulative deaths and suggest that sufficient herd immunity may already be in place to substantially mitigate a potential second wave.” Calculations along a similar line by Gabriela Gomes, a professor of mathematics and statistics at Strathclyde University, have also placed the threshold needed for herd immunity at below 20 per cent. For diseases where a vaccine is available, herd immunity is often calculated with the assumption that everybody has the same level of immunity – known as a homogenous model. But, as with the Oxford researchers, Dr Gomes has been studying what are known as heterogeneous models – which operate on the basis that there are vastly differing levels of immunity within the population. The two models can have vastly different results. “There doesn’t need to be a lot of variation in a population for epidemics to slow down quite drastically,” Dr Gomes told The Atlantic this week. “The outbreaks look similar at the beginning. But in the heterogeneous population, individuals are not infected at random. “The highly susceptible people are more likely to get infected first. As a result, the average susceptibility gets lower and lower over time.” She added: “We just keep running the models, and it keeps coming back at less than 20 percent. It’s very striking.” the article then reviews the doomer side reviewing the recent findings that antibodies seem to disappear
Coronavirus could be burning out after 20% of local population is infected. https://theconversation.com/coronav...t-after-20-of-a-population-is-infected-141584 More than half a million people have died from COVID-19 globally. It is a major tragedy, but perhaps not on the scale some initially feared. And there are finally signs that the pandemic is shuddering in places, as if its engine is running out of fuel. This has encouraged many governments to relinquish lockdowns and allow everyday life to restart, albeit gingerly. The spread of SARS-CoV-2 has been difficult to predict and understand. On the Diamond Princess cruise ship, for example, where the virus is likely to have spread relatively freely through the air-conditioning system linking cabins, only 20% of passengers and crew were infected. Data from military ships and cities such as Stockholm, New York and London also suggest that infections have been around 20% – much lower than earlier mathematical models suggested. This has led to speculation about whether a population can achieve some sort of immunity to the virus with as little as 20% infected – a proportion well below the widely accepted herd immunity threshold (60-70%). The Swedish public health authority announced in late April that the capital city, Stockholm, was “showing signs of herd immunity” – estimating that about half its population had been infected. The authority had to backtrack two weeks later, however, when the results of their own antibody study revealed just 7.3% had been infected. But the number of deaths and infections in Stockholm is falling rather than increasing – despite the fact that Sweden hasn’t enforced a lockdown. Hopes that the COVID-19 pandemic may end sooner than initially feared have been fuelled by speculation about “immunological dark matter”, a type of pre-existing immunity that can’t be detected with SARS-CoV-2 antibody tests. Antibodies are produced by the body’s B-cells in response to a specific virus. Dark matter, however, involves a feature of the innate immune system termed “T-cell mediated immunity”. T-cells are produced by the thymus and when they encounter the molecules that combat viruses, known as antigens, they become programmed to fight the same or similar viruses in the future. Studies show that people infected with SARS-CoV-2 indeed have T-cells that are programmed to fight this virus. Surprisingly, people never infected also harbour protective T-cells, probably because they have been exposed to other coronaviruses. This may lead to some level of protection against the virus – potentially explaining why some outbreaks seem to burn out well below the anticipated herd immunity threshold. Young people and those with mild infections are more likely to have a T-cell response than old people – we know that the reservoir of programmable T-cells declines with age. In many countries and regions that have had very few COVID-19 cases, hotspots are now cropping up. Take Germany, which quickly and efficiently battled the virus and has had one of the lowest death rates among the large northern European countries. Here, the R number – reflecting the average transmission rate – has risen again, below 1 until June 18, but rocketing to 2.88 just days later, only to drop again a few days later. It may be tempting to argue that this could be because the hotspots never got close to the 20% infection that was seen in other regions. But there are counter examples, albeit particularly in older and immunocompromised populations. In the Italian COVID-19 epicenter in Bergamo, a town where one in four residents are pensioners, 60% of the population had antibodies by early June. 60% of people in Bergamo have antibodies. angellodeco/Shutterstock The same is true in some prisons: at the Trousdale Turner Correctional Center in Hartsville, US, 54% of inmates had tested positive for COVID-19 by early May. And more than half of the residents in some long-term care facilities have also been infected. Genes and environment So how do we explain this? Could people in places with higher rates of positive antibodies have a different genetic make-up? Early in the pandemic, there was much speculation about whether specific genetic receptors affected susceptibility to the SARS-CoV-2 virus. Geneticists thought that DNA variation in the ACE2 and TMPRSS2 genes might affect susceptibility to, and severity of, infection. But studies so far have shown no compelling evidence supporting this hypothesis. Early reports from China also suggested that blood types may play a role, with blood type A raising risk. This was recently confirmed in studies of Spanish and Italian patients, which also discovered a new genetic risk marker termed “3p21.31”. While genetics may be important, the environment also matters. It is well known that airborne transmission of droplets is enhanced in colder climates. Super-spreading events in several meat production facilities where the indoor climate is cold suggest this has enhanced contagion. People also tend to spend more time indoors and in close proximity during inclement weather. Warm weather, however, brings people together, albeit outdoors. Indeed, June has been uncharacteristically hot and sunny in many northern European countries, causing parks and beaches to be overrun and social distancing rules flouted. This will likely drive contagion and cause new COVID-19 outbreaks in the weeks to come. Yet another factor is how interpersonal interactions affect contagion. Some previous models have assumed that people interact in the same way regardless of age, well-being, social status and so forth. But this isn’t likely to be the case – young people, for example, are likely to have more acquaintances than the elderly. Accounting for this reduces the herd immunity threshold to around 40%. Will COVID-19 disappear? The lockdowns enforced far and wide, combined with the responsible actions of many citizens, have undoubtedly mitigated the spread of SARS-CoV-2 and saved lives. Indeed, in cases such as Sweden – where lockdown was eschewed and social distancing rules were relatively relaxed – the virus has claimed an order of magnitude more lives than in its pro-lockdown neighbours, Norway and Finland. Stockholm on June 24, 2020. Stina Stjernkvist/TT/EPA But it is unlikely that lockdowns alone can explain the fact that infections have fallen in many regions after 20% of a population has been infected – something that, after all, happened in Stockholm and on cruise ships. That said, the fact that more than 20% of people have been infected in other places means that the T-cell hypothesis is unlikely to be the sole explanation either. Indeed, if a 20% threshold does exist, it applies to only some communities, depending on interactions between many genetic, immunological, behavioural and environmental factors, as well as the prevalence of pre-existing diseases. Understanding these complex interactions is going to be necessary if one is to meaningfully estimate when SARS-CoV-2 will burn itself out. Ascribing any apparent public health successes or failures to a single factor is appealing – but it is unlikely to provide sufficient insight into how COVID-19, or whatever comes next, can be defeated.