- Sweden never went in to full lockdown. Instead, the country imposed a partial lockdown that was almost entirely voluntary.
- The only forcible restriction imposed by the government from the start was a requirement that people not gather in groups of more than 50 at a time.
- People followed the voluntary restrictions pretty well at the beginning, but that they have become increasingly lax as time has gone on.
- After an initial peak that lasted for a month or so, from March to April, visits to the Emergency Room due to covid had been declining continuously, and deaths in Sweden had dropped from over 100 a day at the peak in April, to around five per day in August.
- Dr. Rushworth hasn’t seen a single covid patient in the Emergency Room in over two and a half months.
- COVID has killed under 6,000 people.
- On average, one to two people per day are dying of covid in Sweden at present, and that number continues to drop.
- In the whole of Stockholm, a county with 2,4 million inhabitants, there are currently only 28 people being treated for covid in all the hospitals combined.
- Sweden seemed to be developing herd immunity, in spite of the fact that only a minority had antibodies, was due to T-cells.
- Immunity may be long lasting, and probably explains why there have only been a handful of reported cases of re-infection with covid, even though the virus has spent the last nine months bouncing around the planet infecting many millions of people.
- Almost all cases of reinfection have been completely asymptomatic.
- People develop a functioning immunity after the first infection, which allows them to fight off the second infection without ever developing any symptoms.
- England and Italy have mortality curves that are very similar to Sweden’s.
- Lockdown only makes sense if you are willing to stay in lockdown until there is an effective vaccine.
Dr. Mike Yeadon, former Chief Scientific Advisor, Pfizer:
- The evidence suggests that a substantial number of the positive cases are false positives.
- The government doesn’t know or is not disclosing the false positive rate.
- False positive rate may be as high as 1%, which would mean most or all of the positives are false positives.
- We are finding traces of an ‘old’ virus which can’t possibly make people sick.
- The test looks for a piece of genetic code. A positive test does not mean someone is sick.
- ONS says the prevalence of the virus is less than 0.1%.
- Pillar 2 (community) testing seems to be flawed. Method of processing samples would be inadmissible if this were a forensic case.
- The number of COVID deaths is continuing to stay low and fallen for 6 months. For it to suddenly increase would need a big change in transmission.
- Young people would have been the first who caught COVID-19 because they were not social distancing. The idea that the young people are now getting it is “for the birds.”
- If positive tests are false, they will be distributed evenly in the population. This is what we’re finding.
- Mass testing is not the answer.
- Sweden is not doing mass testing and their society has had 0.06% of their population die from COVID-19. This is the same as the UK.
- We are using a test with an undeclared false-positive rate.
- Are we re-testing the positives? This is unclear.
- A second lockdown is going to amplify the non-COVID deaths.
- UK’s lockdown was too late to prevent the initial spread.
- Mass population immunity is keeping the deaths low. This is the most reasonable explanation for the differences between the models and reality.
As coronavirus cases rise in pretty much all other European countries, leading to fears of a second wave including in the UK, they have been sinking all summer in Sweden. On a per capita basis, they are now 90 per cent below their peak in late June and under Norway’s and Denmark’s for the first time in five months. Tegnell had told me the first time we spoke in the spring that it would be in the autumn when it became more apparent how successful each country had been.
The choice we face is stark. One option is to maintain a general lockdown for an unknown amount of time until herd immunity is reached through a future vaccine or until there is a safe and effective treatment. This must be weighed against the detrimental effects that lockdowns have on other health outcomes. The second option is to minimise the number of deaths until herd immunity is achieved through natural infection. Most places are neither preparing for the former nor considering the latter.
The question is not whether to aim for herd immunity as a strategy, because we will all eventually get there. The question is how to minimise casualties until we get there. Since Covid-19 mortality varies greatly by age, this can only be accomplished through age-specific countermeasures. We need to shield older people and other high-risk groups until they are protected by herd immunity.
Among the individuals exposed to Covid-19, people aged in their 70s have roughly twice the mortality of those in their 60s, 10 times the mortality of those in their 50s, 40 times that of those in their 40s, 100 times that of those in their 30s, and 300 times that of those in their 20s. The over-70s have a mortality that is more than 3,000 times higher than children have. For young people, the risk of death is so low that any reduced levels of mortality during the lockdown might not be due to fewer Covid-19 deaths, but due to fewer traffic accidents.
The Imperial College study published this morning claiming that 3.4 million people ( six per cent of the UK population) have antibodies indicating that they have been exposed to Covid-19 provides no great revelation. The Office of National Statistics (ONS) has already published similar figures suggesting that 6.5 per cent of the population has been infected. Nevertheless, it is yet more confirmation of how irrelevant are the official statistics for Covid 19 cases – and what a nonsense it is to rely on them for policymaking.
According to the Government’s Covid “dashboard”, updated at 4pm on Wednesday, 313,798 people in Britain have had the disease. This is less than one tenth of the number suggested by the Imperial study. In other words, for all Matt Hancock’s efforts to ramp up testing, the vast majority of cases have not been detected.
- Exposure to Covid-19 is similar in Stockholm and London, based on antibody tests, despite different lockdown strategies.
- The research, published in the Journal of the Royal Society of Medicine, found that 17% of people tested in April in Stockholm had developed antibodies.
- This compares with 17% of Londoners tested in April and May, and 5%-10% of people living in Geneva.
- Official data from NHS England points to a huge drop in the number of coronavirus patients being treated in hospitals today compared to mid-April, during the height of the pandemic.
- Dr Daniels: Britain is “almost reaching herd immunity”.
- Increase in hospital admissions nor a second wave to hit the UK.
- “I think that’s highly unlikely because the pubs have been open for over a month, people have been socially interacting heavily during that time, and the natural history of this disease is that if you contract the virus and you’re going to end up in hospital, you’re pretty much in hospital within 15 days of contracting it.”
Humans have never been particularly good at eradicating entire viruses, and COVID-19 might not be any different.
More than 19 million people have tested positive for the coronavirus globally, and at least 722,000 have died. In the U.S., nearly 5 million people have tested positive and more than 160,000 have died. While scientists are racing to find a cure for the virus, there’s a chance COVID-19 will never fully go away — with or without a vaccine.
Vineet Menachery, a coronavirus researcher at the University of Texas Medical Branch, told NPR’s Weekend Edition that one of the more likely scenarios is that the spread of COVID-19 will eventually be slowed as a result of herd immunity. He said that he’d be surprised “if we’re still wearing masks and 6-feet distancing in two or three years” and that in time, the virus could become no more serious than the common cold.
The first thing to remember is that we haven’t been successful at eradicating many viruses at all. Really the lone exception is smallpox, but many of these viruses exist not only in the human population but in animal populations. So coronaviruses may be removed from the human population, like SARS coronavirus in 2002, but we know that those viruses or viruses that are similar to it still exist in nature and at any time they may gain the tools to reemerge in humans again.
Fatalities are down 99% and some hospitals have no coronavirus patients, sparking hope that ‘herd immunity’ may be near
The number of people in hospital with Covid-19 has fallen 96% since the peak of the pandemic, official data reveals.
Hospital staff are now treating just 700 coronavirus patients a day in England, compared to about 17,000 a day during the middle of April, according to NHS England.
Last week, some hospitals did not have a single coronavirus patient on their wards, with one top doctor suggesting that Britain is “almost reaching herd immunity”.
Swedish health experts say struggle against pandemic is ‘marathon not a sprint’
The country has one of the highest death rates from coronavirus in the world
Anders Tegnell’s refusal to impose lockdown is held up by critics as a warning
But is it possible the Scandinavian nation made the right call in the long-term?
- Article based on experience working as a doctor in the emergency room of one of the big hospitals in Stockholm, Sweden, and of living as a citizen in Sweden.
- Unlike other countries, Sweden never went in to complete lockdown. Non-essential businesses have remained open, people have continues to go to cafés and restaurants, children have remained in school, and very few people have bothered with face masks in public.
- COVID hit Stockholm like a storm in mid-March. One day I was seeing people with appendicitis and kidney stones, the usual things you see in the emergency room. The next day all those patients were gone and the only thing coming in to the hospital was COVID. Practically everyone who was tested had COVID, regardless of what the presenting symptom was. People came in with a nose bleed and they had COVID. They came in with stomach pain and they had COVID.
- Then, after a few months, all the COVID patients disappeared.
- At the peak three months back, a hundred people were dying a day of COVID in Sweden, a country with a population of ten million. We are now down to around five people dying per day in the whole country, and that number continues to drop. Since people generally die around three weeks after infection, that means virtually no-one is getting infected any more.
- The risk of dying is at the very most 1 in 200 if you actually do get infected.
- In total COVID has killed under 6,000 people in a country of ten million.
- Sweden has an annual death rate of around 100,000 people. Considering that 70% of those who have died of COVID are over 80 years old, quite a few of those 6,000 would have died this year anyway.
- COVID will never even come close to major pandemic numbers like 1918 flu.
- If herd immunity hasn’t developed, where are all the sick people? Why has the rate of infection dropped so precipitously?
- The reason we test for antibodies is because it is easy and cheap. Antibodies are in fact not the body’s main defence against virus infections. T-cells are. But T-cells are harder to measure than antibodies, so we don’t really do it clinically.
- Sweden ripped the metaphorical band-aid off quickly and got the epidemic over and done with in a short amount of time, while the rest of the world has chosen to try to peel the band-aid off slowly.
- I am willing to bet that the countries that have shut down completely will see rates spike when they open up. If that is the case, then there won’t have been any point in shutting down in the first place, because all those countries are going to end up with the same number of dead at the end of the day anyway. Shutting down completely in order to decrease the total number of deaths only makes sense if you are willing to stay shut down until a vaccine is available. That could take years.
- COVID has at present killed less than 6000 in Sweden. It is very unlikely that the number of dead will go above 7,000. An average influenza year in Sweden, 700 people die of influenza. Does that mean COVID is ten times worse than influenza? No, because influenza has been around for centuries while COVID is completely new.
- So it is quite possible, in fact likely, that the case fatality rate for COVID is the same as for influenza, or only slightly higher, and the entire difference we have seen is due to the complete lack of any immunity in the population at the start of this pandemic.
But with no sign of a second summer wave nor an autumn eruption reminiscent of 1918, the commentariat has amended the definition. Suddenly, a “second wave” meant Covid’s seasonal return, in winter, a year on. Widespread adoption of a new phrase in the Covid lexicology – “winter wave” – has academically formalised the idea.
But instead of looking us square in the eye, the Tories have chosen Big Brother’s panopticon; No 10’s new Joint Biosecurity Centre, which will drive “whack-a-mole” local lockdowns, is slickness posing as strategy – and, as it happens, reporting into track-and-trace app failure Dido Harding. When the public twigs that the infection is unlikely to be controlled in this way, the sheer panic could send us back into national lockdown. Three scenarios might help avoid the latter: a vaccine comes along; the Government gets its act together with a plan to protect the vulnerable; or we put in place safety valves against mass hysteria.
Imperial College’s research needs to be particularly scrutinised, as its international influence grows. Dr Seth Flaxman – the first author in the paper that notoriously claimed lockdowns may have prevented over 3 million deaths in Europe – this week won fresh funding to model the pandemic across several countries.
Revelations that disrupt the narrative also need to find a stronger voice: within 24 hours, the scandal of PHE’s inflated daily death figures was running out of mileage. This week’s London School of Hygiene and Tropical Medicine modelling on the impact of the pandemic on cancer deaths never gathered steam. So too a paper by Oxford’s Prof Sunetra Gupta, which elegantly combined those uneasy epidemiological bedfellows – theory and evidence – to find some parts of the UK may already have reached herd immunity.
“Intensive care units are getting empty, the wards are getting empty, we are really seeing a decrease — and that despite that people are really loosening up. The beaches are crowded, social distancing is not kept very well … but still the numbers are really decreasing. That means that something else is happening – we are actually getting closer to herd immunity. I can’t really see another reason.”
“I can’t say if the Swedish approach was right or wrong – I think we can say that in one or two years when we are looking back. You have to look at the mortality over the whole period.”
“I don’t think that we have more new cases, I think we are just detecting more cases”
“We found that if you have a mild case you can be negative for antibodies afterwards … in those almost all of them had strong T-cell activity. This study says that there are cases that you can have a strong T-cell response even though you have not had antibodies, meaning that you have encountered the virus and built up immunity.”
“[R]oughly twice as many people have developed T-cell immunity compared with those who we can detect antibodies in.“
SARS-CoV-2-specific memory T cells will likely prove critical for long-term immune protection against COVID-19. We systematically mapped the functional and phenotypic landscape of SARS-CoV-2-specific T cell responses in a large cohort of unexposed individuals as well as exposed family members and individuals with acute or convalescent COVID-19. Acute phase SARS-CoV-2-specific T cells displayed a highly activated cytotoxic phenotype that correlated with various clinical markers of disease severity, whereas convalescent phase SARS-CoV-2-specific T cells were polyfunctional and displayed a stem-like memory phenotype. Importantly, SARS-CoV-2-specific T cells were detectable in antibody-seronegative family members and individuals with a history of asymptomatic or mild COVID-19. Our collective dataset shows that SARS-CoV-2 elicits robust memory T cell responses akin to those observed in the context of successful vaccines, suggesting that natural exposure or infection may prevent recurrent episodes of severe COVID-19 also in seronegative individuals.
- We have already developed herd immunity to COVID-19 and will continue to manage it through herd immunity.
- Flu is much more dangerous than COVID-19.
- COVID-19 will settle into an endemic state just like flu.
- Hopefully vaccines will be important in protecting the vulnerable.
- Another way to protect the vulnerable sector is to allow the population to develop natural immunity.
- There’s no reason to think the virus will mutate into a lower level of virulence.
- During the 1918 flu because of a large number of ‘immunologically naive’ individuals but this is not the case with COVID-19.
- Most of us have some degree of coronavirus immunity and therefore some protection to COVID-19.
- The current H1 influenza strain is antigenically identical to the 1918 flu. H1 flu doesn’t kill as many people as the 1918 flu because most people already have cross immunity.
Antibody tests on random samples of the population have so far shown much lower levels of general infection than the government’s scientific advisers claimed would be necessary to attain ‘herd immunity’. In London, for example, tests have shown that 17 per cent of the population have antibodies to Sars-CoV-2, the virus that causes Covid-19. In New York, the figure is 21 per cent. At the beginning of this crisis, on the other hand, Sir Patrick Vallance, the chief scientific adviser, suggested that at least 60 per cent of the population would have to be infected in order to achieve herd immunity.
Naturally acquired herd immunity to COVID-19 combined with earnest protection of the vulnerable elderly – especially nursing home and assisted living facility residents — is an eminently reasonable and practical alternative to the dubious panacea of mass compulsory vaccination against the virus.
This strategy was successfully implemented in Malmo, Sweden, which had few COVID-19 deaths by assiduously protecting its elder care homes, while “schools remained open, residents carried on drinking in bars and cafes, and the doors of hairdressers and gyms were open throughout.
Stockholm is the best population to test Covid theory whereby it was hit hard early and did not have lockdowns. Nobel Prize winner Dr Michael Levitt postulated that the virus burns out when it has infected 15-20% of the population. According to this, he’s right.
So what does this mean? Lockdowns were a waste of time and resources. Minimizing deaths just delays the inevitable. Those countries which were not hit are most likely to see continued spikes and outbreaks. Maybe less during the summer but a second wave later this year.
Up to 81% of of the population can mount a strong response to COVID-19 without ever having been exposed to it before:
Cross-reactive SARS-CoV-2 T-cell epitopes revealed preexisting T-cell responses in 81% of unexposed individuals, and validation of similarity to common cold human coronaviruses provided a functional basis for postulated heterologous immunity
The SARS-CoV-2 pandemic calls for the rapid development of diagnostic, preventive, and therapeutic approaches. CD4+ and CD8+ T cell-mediated immunity is central for control of and protection from viral infections[1-3]. A prerequisite to characterize T-cell immunity, but also for the development of vaccines and immunotherapies, is the identification of the exact viral T-cell epitopes presented on human leukocyte antigens (HLA)[2-8]. This is the first work identifying and characterizing SARS-CoV-2-specific and cross-reactive HLA class I and HLA-DR T-cell epitopes in SARS-CoV-2 convalescents (n = 180) as well as unexposed individuals (n = 185) and confirming their relevance for immunity and COVID-19 disease course. SARS-CoV-2-specific T-cell epitopes enabled detection of post-infectious T-cell immunity, even in seronegative convalescents. Cross-reactive SARS-CoV-2 T-cell epitopes revealed preexisting T-cell responses in 81% of unexposed individuals, and validation of similarity to common cold human coronaviruses provided a functional basis for postulated heterologous immunity in SARS-CoV-2 infection[10,11]. Intensity of T-cell responses and recognition rate of T-cell epitopes was significantly higher in the convalescent donors compared to unexposed individuals, suggesting that not only expansion, but also diversity spread of SARS-CoV-2 T-cell responses occur upon active infection. Whereas anti-SARS-CoV-2 antibody levels were associated with severity of symptoms in our SARS-CoV-2 donors, intensity of T-cell responses did not negatively affect COVID-19 severity. Rather, diversity of SARS-CoV-2 T-cell responses was increased in case of mild symptoms of COVID-19, providing evidence that development of immunity requires recognition of multiple SARS-CoV-2 epitopes. Together, the specific and cross-reactive SARS-CoV-2 T-cell epitopes identified in this work enable the identification of heterologous and post-infectious T-cell immunity and facilitate the development of diagnostic, preventive, and therapeutic measures for COVID-19.
All through the Covid-19 pandemic we have been hampered by a lack of data on just how many people have had the disease. Given that several studies have indicated that as many as 80 per cent of people who are infected show no symptoms whatsoever, it is extremely difficult to estimate this crucial figure – which determines the mortality rate of Covid-19 and also how far away we might be from achieving a position of herd immunity.
Today, however, comes some very substantial data. The Medical Research Council’s Biostatistics Unit has published estimates of infections derived from serological studies on samples collected from the NHS Blood Transfusion Service.