When the vaccine drops to ~50% efficacy, what does it mean in practice? This is how I interpret it.

when a vaccine is ~50% effective it does not mean "breakthrough" infection will be 50% less severe.

No, it means that out of 100 vaccinated, 50 will be protected & 50 will not The problem with such efficacy is that one cannot know in which "50" group one is: protected group or unprotected group.

In practice, it means that when one is vaccinated but the vaccine drops to ~50% efficacy, a given individual can be 100% protected or 0% protected.

I see people are still debating what is the level of protection from 2-dose vaccine against symptomatic #covid19.Enough studies now show at ~6 months post vaccination it is <50% efficacy and frequently close 0%,meaning without masks rate of infection is the same for vax/unvax 1/

https://twitter.com/Mike_aka_Logiqx/status/1436982536039772161

but protection against severe/death is still good at 6 months (~70% efficacy).

But due to the uncertain nature of the level of Ab titers and its waning speed, immune priming or failing, and underlying conditions, is it better to wear the masks pretty much constantly outside 2/

immunologically speaking, there no rhyme or reason to believe that if 2-dose vaccine-induced neut Abs hang around for 6 months, somehow they will hang around much longer after 3rd dose. 1/ in general, it is quite unexpected that after such robust 2-dose antigen priming, as mRNA vaccine does (based on Ab titers immediately after 2nd dose), we should see such a precipitous drop in vaccine efficacy within 6 months. 2/

Recently, we published the concluding part III of the #SPIRAL model, which we were working on since 2016.

Pathological T Helper Polarization Requires Pre-existing Cross-Reactive Memory T Cells

I'm going to explain the significance of this model.

preprints.org/manuscript/202… In part I published in 2018, we introduced the SPIRAL model. It proposes that cross-reactivity is the basic unit that drives the evolution of adaptive immune system and it is thymus-derived regulatory T cells, Tregs, that rely on cross-reactive epitopes to control other T cells

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/

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.

https://twitter.com/DrEricDing/status/1354899824370462722

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.

In this opinion paper @RMedzhitov went back to drawing board to update his views on #allergy and how it could develop.

#immunology

I read this paper and here is my take on it

1/

https://twitter.com/RMedzhitov/status/1349815141982986242

@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/

let's talk about #CytokineStorm in #COVID19.

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

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.

#immunology

bit.ly/2RAMe8L 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.

bit.ly/2RAMe8L

#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.

A new paper in @sciencemagazine from #Belkaid lab at #NIH described an #alternative differentiation #pathway for #commensal-specific T cells in presence of inflammation. Do the data presented support conclusions? Let's dive in.

science.sciencemag.org/content/363/64… 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.