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Browse the articles related to this topic below.
YouTube has removed interview so we have archived the video in the above location. It is currently available on Unlocked Facebook page:
https://www.facebook.com/unlockedunitedkingdom/videos/vb.112364983833705/409747283542470/
https://sebastianrushworth.com/2020/09/19/covid-19-does-sweden-have-herd-immunity/
https://medicalxpress.com/news/2020-08-exposure-common-cold-coronaviruses-immune.html
Original source: https://sebastianrushworth.com/2020/08/04/how-bad-is-covid-really-a-swedish-doctors-perspective/
“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.
https://www.biorxiv.org/content/10.1101/2020.06.29.174888v1.full
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[9] 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.
https://www.spectator.co.uk/article/science-doubt-and-the-second-wave-of-covid
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.