These two graphs tells the story about 3rd wave with #DeltaVariant.
daily cases vs. daily death. Based on data from 2nd wave,we should have expected already ~ 500-2000 death daily but so far the UK only reported ~ 100 daily death. Does it mean vaccine worked? No. why not?
1/
Why cannot I say with certainty that 10-20 fold lower daily deaths in the 3rd wave indicate that the vaccine is effective?
Simply because the authority consistently say that >90% of those who are diagnosed with #COVID19 are non-vaccinated.
2/
So, >90% with #COVID19 are non-vaccinated and still there is 10-20 fold fewer daily death?
This makes no sense unless #COVID19 positive population in 3rd wave is completely different from those in the 1st and 2nd waves.
3/
As I said earlier vaccine cannot explain the drop in daily death in 3rd wave as >90% of those with #Covid19 ar non-vaccinated.
Only reasonable explanation is 3rd wave population is somehow different. One reasonable argument is that it is much younger, healthier group.
4/
So, what does it all mean?
it means, in my view, that we cannot say that the current vaccine is reducing the daily death rate as it is reduced without a vaccine.
younger, non-vaccinated group is the main target of the 3rd wave because older population is still practicing NPI.
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We are entering a new, endemic stage of #COVID19 spread. Drop in efficacy (50% or less) against new SA variants is a classical example of vaccine efficacy against #influenza virus.
It is clear from all available data that both @BioNTech_Group and @moderna_tx mRNA vaccines will be less effective against SA variant and there will be many more like this.
@RMedzhitov Why focus on allergy? b/c allergy is a paradox. The allergy we recognize is a completely maladaptive response and has no protective role whatsoever. It is not clear why do we even need IgE
2/
@RMedzhitov So, some 10 years ago or so, @RMedzhitov started to suggest that #allergy is an intrinsic property of a certain type of #antigens, many of them with enzymatic function (enzymes). 3/
1st, there is no standard threshold above which something is called #CytokineStorm.
Mechanistically, the simplest form of #CytokineStorm we can understand is when anti-CD19 #CART cells are infused in tumor-bearing recipients.
in this scenario, we have large numbers of antigen-specific T cells (anti-CD19) and large numbers of antigen-bearing cells (CD19+ tumor cells). When too many T cells engage with too many antigens simultaneously in a short period of time we get #CytokineStorm
Why is that? This is because naturally developing an adaptive immune system (T cells) ordinarily doesn't work that way. 1st, for a given antigen we have very few antigen-specific T cells (~ 50 cells/antigen, unlike anti-CD19 CAR-T cells that are in millions).
a removal of a subset of #Tregs called T follicular regulatory cells (Tfr) from the immune system in #Foxp3-cre Bcl6-fl/fl mice #paradoxically reduces, rather than increases, #peanut-specific #IgE responses.
And if you think maybe their knockout mice are some kind of weirdos, not really. Their model also shows that total IgE is increasing as expected. So, the system the authors are using is within acceptable norms.
The authors then went on to show that IL-10 derived from Tfr cells are important for promoting peanut allergy-producing IgE production. (IL-10 is lesser understood cytokine but it is generally accepted as an immunosuppressant.) #immunology
#Antibody response usually protects against infection/re-infection but #Tcells could protect against clinical signs of disease. #COVID19
The paper from #1990 analyzed the antibody response and clinical symptoms of the common cold #coronavirus#229E. Neutralizing antibody titers declined within 1 year after 1st challenge, and 70% from the "immunized" cohort got re-infected but none showed clinical symptoms.
This most likely explanation is that clinical symptoms were controlled by virus-specific T cells. There is an assumption here that a protective level of antibody would have prevented re-infection in the first plays
1. #Commnesal S. epidermidis–specific -#MIIINA:H2-M3+ CD8+ T cells ordinarily differentiate into Tc1 or Tc17 subsets. However, when co-exposed to chitin or sand fly (source of #inflammation), Tc17 subset also produce type II cytokines.
2. In such condition, type II #cytokines such as IL-5 or IL-13 are produced by CCR6+ Tc17 cells (out of which 30% are IL-17+). However, there is no overlap between IL-17+ and IL-5+/IL-13+ CD8+ T cells. So, the authors conclusion about "paradoxical phenotype" is unsubstantiated.