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- We have experience of SARS in 2003 and MERS in 2012, while in the UK there are at least four known strains of coronavirus which cause the common cold.
- Many individuals who’ve been infected by other coronaviruses have immunity to closely related ones such as the Covid-19 virus.
- Multiple research groups in Europe and the US have shown that around 30 per cent of the population was likely already immune to Covid-19 before the virus arrived – something which Sage continues to ignore.
- Prof. John Ioannidis, professor of epidemiology at Stanford University in California, have concluded that the mortality rate is closer to 0.2 per cent – 1 in 500 infected die.
- Around 45,000 Covid deaths in the UK
- Approximately 22.5million people have been infected – 33.5 per cent of our population – not Sage’s 7 per cent calculation.
- Not every infected individual produces antibodies.
- The human immune system has several lines of defence:
- Innate immunity which is comprised of the body’s physical barriers to infection and protective secretions (the skin and its oils, the cough reflex, tears etc);
- Inflammatory response (to localise and minimise infection and injury), and the production of non-specific cells (phagocytes) that target an invading virus/bacterium.
- Antibodies that protect against a specific virus or bacterium (and confer immunity) and T-cells (a type of white blood cell) that are also specific.
- T-cells that are crucial in our body’s response to respiratory viruses such as Covid-19.
- World Health Organisation says 750million people have been infected by the virus as of October and almost none have been reinfected.
- Mortality in 2020 so far ranks eighth out of the last 27 years.
- The death rate at present is also normal for the time of year – the number of respiratory deaths is actually low for late October.
- Not only is the virus less dangerous than we are being led to believe, with almost three quarters of the population at no risk of infection.
- I am convinced this so-called second wave of rising infections and, sadly, deaths will fizzle out without overwhelming the NHS.
- 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.
- Your immune system’s ‘memory’ T cells keep track of the viruses they have seen before.
- New study led by scientists at La Jolla Institute for Immunology (LJI) shows that memory helper T cells that recognize common cold coronaviruses also recognize matching sites on SARS-CoV-2, the virus that causes COVID-19.
- Having a strong T cell response, or a better T cell response may give you the opportunity to mount a much quicker and stronger response.
- 40%-60% of people never exposed to SARS-CoV-2 had T cells that reacted to the virus showing that their immune systems recognized the virus.
- This finding turned out to be a global phenomenon and was reported in people from the Netherlands, Germany, the United Kingdom and Singapore.
- This discovery suggests that fighting off a common cold coronavirus can induce cross-reactive T cell memory against SARS-CoV-2.
- 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.
“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.
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.
One of the key things about science – obvious to its practitioners, but often obscure to outsiders – is that it is fuelled by doubt, not certainty. When the ‘facts’ change (as they often do), and when original assumptions are qualified or overturned, then any scientist worth their salt re-examines and, if necessary, alters their conclusions. The presence of cross-reactive helper cells in maybe half the population means that ideas about a possible second wave must be rewritten. This finding must make a second wave less likely, probably much less likely. And the fact that there has been no ‘second wave’ (as opposed to isolated outbreaks) anywhere where lockdown has been released also fits this hypothesis. It may well also explain why the first wave didn’t infect much higher proportions of the population.
Exposure to microbes during early childhood is associated with protection from immune-mediated diseases such as inflammatory bowel disease (IBD) and asthma. Here, we show that in germ-free (GF) mice, invariant natural killer T (iNKT) cells accumulate in the colonic lamina propria and lung, resulting in increased morbidity in models of IBD and allergic asthma as compared with that of specific pathogen-free mice. This was associated with increased intestinal and pulmonary expression of the chemokine ligand CXCL16, which was associated with increased mucosal iNKT cells. Colonization of neonatal—but not adult—GF mice with a conventional microbiota protected the animals from mucosal iNKT accumulation and related pathology. These results indicate that age-sensitive contact with commensal microbes is critical for establishing mucosal iNKT cell tolerance to later environmental exposures.