Discover and read the best of Twitter Threads about #SARS2

Most recents (24)

I got zero feedback when claiming that #SARS2 is effective climate policy - obvious to anyone who looked in early 2020 but undeniable since Omicron (#SARS3). Here BOE confirms it. Transmission must be stopped (#ZeroCovid).

Read @DonEford’s LongCovid article if you don’t see why.
China shows #zerocovid works. This was always clear for #SARS2 - the West has failed catastrophically in allowing uncontrolled spread & evolution. Since Omicron (#SARS3) we have no choice. “Let it rip” will end society. China scholars, where is your voice?
Where is everyone’s critical voice? Who is organizing meaningful policy advice? h/t China and global governance scholars - @AMFChina @thorstenbenner etc.

Rates of learning are far too slow. Our time to act is running out - not only on climate change policy.
Read 6 tweets
The two of the best economic blogs I've been reading for years are written by brilliant, independent individuals: by Bill McBride @calculatedrisk, and by the anonymous blogger called New Deal Democrat.
The recent post by NDD about #SARSCoV2 illustrates the prevalent reasoning that led to the current policy blind alley.
"A year ago I thought that between nearly universal vaccinations & an increasing percentage of the population already infected...
the virus would wane into a BACKGROUND NUISANCE BY NOW.
No more. I am now thoroughly convinced that there will be an UNENDING SERIES of VARIANTS that will create CONTINUING WAVES of new infections and, increasingly importantly, RE-infections."
Read 13 tweets
🤖 Good evening humans. I'm making an exception to my @fitterhappieraj-only rule and have translated this important thread by @VirusesImmunity. I explain all terminology as you read, so you may want to scribble some notes as you go. It's a long thread:
The study looks at how #SARS2 variants of concern (VOCs) suppress the genes (MHC I) that help killer T cells recognise the virus on cell surfaces. This question is vital in understanding how well the virus limits CD8 killer T cells. 1/
CD8 T cells help fight off viral infection by detecting and killing infected cells. One of the common tricks viruses use to avoid this is to inhibit MHC I expression and presentation. 2/
Read 17 tweets
#SARS2 has so many possible ways of evading human immunity. Even Dr Aj didn’t expect so many. He explains why your T cells are at such a disadvantage. 1/
Dr Aj thought #Alpha evaded the killer & suppressor T cells (CD8) because of its immune-evading protein (ORF8). It's more sinister: #SARS2 has a “Negative Factor” like HIV, which elevates viral concentration. He explains why this is grim news... 2/
... it’s not just evading killer & suppressor T cells (CD8), #SARS2 can also escape the T Cells that enable your body to detect viral presence (CD4). Dr Aj believes this also helps the virus establish a reservoir in your body. 3/
Read 4 tweets
It felt vindicating to read this paper "Disentangling the relative importance of T cell responses in #COVID19: LEADING ACTORS OR SUPPORTING CAST?" & to see the same conclusions I independently came about from my layman/trader perspective by using mathematics & logical deduction.
Oh, how many times have I written this to "experts" overselling T cells as a team of superheroes:
"These factors highlight the difficulty in establishing a role for T cells in protective immunity to #SARS2 infection beyond a general assumption that they are likely to be helpful."
"However, it is easy to make the discussion a binary one between ‘all antibodies’ and ‘all T cells’ contributing to protection, whereas the IMMUNE SYSTEM typically DEFIES such SIMPLIFIED DICHOTOMIES...
Read 5 tweets
Finally, some reason & common sense in the official immunology.
"We describe several lines of evidence that argue AGAINST a direct impact of vaccine-induced memory T cells in PREVENTING symptomatic #SARSCoV2 INFECTION...
The contribution of T cell immunity in REDUCING the SEVERITY of infection, particularly with #SARS2 variants, REMAINS TO BE DETERMINED.
In reality protective immunity to most pathogens does not refer to a binary outcome (susceptible vs protected) but instead REFLECTS a SPECTRUM."
1) "To address the role of T cells in protection from #SARS2 infection is to identify contexts where T cell & nAb responses at least partially ‘decoupled’.
There is relatively little loss of T cell cross-reactivity to VoCs, including #Omicron. Thus, exposure of...
Read 16 tweets
"The effectiveness of 3 doses vs. hospital admission due to #Delta... fall from 89% <3 months to 71% from 3 months+...
After 3 doses, VE of BNT162b2 against hospital admission due to the #Omicron variant was 85% at <3 months but fell to 55% at 3 months+."…
I'm very interested in the virologists' explanation of why would VE vs. hospitalization wane this much over time if, for severity, T-cells are exclusively more important than antibodies. It seems to me real-life data doesn't support currently presumed dogma. Novelty=severity, no?
"Our study is one of the 1st to report long-term follow-up outcomes after receipt of a booster dose, stratified by age. Similar to a recent CDC report showing waning effectiveness of mRNA #COVID19 vaccines after a 3rd dose, we also detected early SIGNS of WANING against SEVERE...
Read 11 tweets
#Monocytes at the Center of #SARS2 triggered inflammation & severe #Covid19

#SARS2 can cause acute respiratory distress & death in some patients. Although severe #COVID19 disease is linked to exuberant inflammation, how #SARS2 triggers inflammation is not understood. 1/
Monocytes & macrophages are the key sentinel cells that sense invasive infection to form inflammasomes that activate inflammatory cascade by secreting caspase-1 and gasdermin D, leading to inflammatory death (pyroptosis) & release of potent inflammatory mediators. 2/
~6% of monocytes in COVID patients are infected w/ SARS2

Monocyte infection depends on uptake of Ab-opsonized virus by Fcγ receptors

SARS2 begins to replicate in monocytes, but infection is aborted & infectious virus is not detected in infected monocyte culture supernatants. 3/
Read 5 tweets
#Omicron though the mildest avatar of #SARS2, but is the most transmissible VOC of the SARS2. The original WT variant had an Ro of ~2.5 & the currently dominant variant BA.2 has 12.5! So, there is marked variability in both transmissibility & severity of these VOCs. 1/
Will the next #VOC, whenever it emerges, be the mildest of all variants? A new #Scottish study concludes that it may not be the case, & severity associated with future SARS2 variants is inherently unpredictable. 2/
The principal findings of this study of the relative severity of #COVID19 cases caused by successive SARS2 variant waves in #Scotland was that, #Alpha was associated w/ more severe disease than B.1.177, #Delta was associated with more severe disease than Alpha…….3/
Read 6 tweets
#Retinal involvement in #Covid19 and possibly also in Long-Covid

There is more to #SARS2 than meets the eye:

1-Coronavirus not only infects the human retina, but can also replicate in it!

2-The so-called ‘long-Covid’ symptoms may include degenerative retinal disease. 1/ Image
Which cells in the retinal organoids are affected?

The researchers analyzed the organoids under a fluorescence microscope. 2/
With the help of different immune markers for the different cell types of the retina & with a #fluorescent antibody against the #nucleoprotein (N-protein) of #SARS2, it was shown that mainly two cell layers of the retinal organoids were infected. 3/ Image
Read 7 tweets
#Covid becomes much more dreaded disease in company with other respiratory viruses!!

Clinical outcomes of co-infection with influenza viruses, respiratory syncytial virus, or adenoviruses in 212 466 adults with #SARS2 infection. 1/
Viral co-infection was detected in 583 (8·4%) patients: 227 patients had influenza viruses, 220 patients had RSV, and 136 patients had adenoviruses. 2/
Co-infection with influenaza viruses was associated with increased odds of receiving invasive mechanical ventilation compared with SARS2 monoinfection
SARS2 co-infections with influenza viruses & adenoviruses were each significantly associated with increased odds of death. 3/ Image
Read 4 tweets
Antibody & Memory B-cell immunity in a heterogeneously #SARS2 infected & vaccinated population from #Mexico where five different vaccines have been deployed to populations with high SARS2 incidence. 1/
Levels of antibodies that bound a stabilized prefusion spike trimer, neutralizing antibody titers & memory B-cell expansion correlated with each other across vaccine platforms. 2/
Neutralizing antibody titers against SARS-CoV-2 variants vary between different vaccines: different vaccines elicited variable levels of B-cell immunity, & the majority of recipients had undetectable neutralizing activity against the recently emergent omicron variant. 3/
Read 5 tweets
The rise of #SARS2 variants & evidence of immunological interference (like OAS & weakened T-cell immunity) underscore the need for preemptive, next-gen vaccines that confer broad protection ag Covid

My piece in @theWireScience👇 @fitterhappierAJ…
What is common between Denmark, Israel, Austria, France, Switzerland, the UK, and the US? They all suffered an unprecedented severe wave of Omicron despite having some of the highest vaccination rates in the world. 2/ @1amnerd @thewire_in
@1amnerd @thewire_in Most of the Covid19 vaccines are based on spike-protein of SARS2. They have worked reasonably well so far. However, with the advent of #Omicron, one of the most mutated variants has exposed the limitations of these vaccines, particularly their ability to prevent infections 3/
Read 34 tweets
A new study from #Austria:

The researchers analyzed samples from BA.1 (Omicron) convalescent patients with different constellations of prior #SARS2 immunity regarding vaccination & previous infection with a non-Omicron variant & determined titers of NAbs against diff VOCs 1/
What did they find?

1-For vaccinated individuals, high NAb titers against all variants after BA.1 breakthrough infection & also for individuals after infection with a pre-omicron variant followed by BA.1 infection. 2/ Image
2-In contrast, samples from naive unvaccinated individuals after BA.1 infection mainly contained NAbs against BA.1 but only occasionally against the other variants. 3/
Read 4 tweets
#Exponentiële #Explosie #Omicron & #BA_2:
M'n #Prognose staat nog steeds.
#RIVM: >½ #Miljoen positieve tests +45% vorige week.
>115.000 gisteren, achterstand van 81.000. Ziekenhuisbezetting stijgt, ondanks
veel #Thuis-#Patiënten met #Zuurstof:

👉👈via @NOS
#Exponentiële #Explosie #Omicron & #BA_2:
100.000 nwe besmettingen per dag.
Werkelijk aantal: ~150.000 +achterstand+testweigeraars.
Totaal in isolatie: 1,3 miljoen
in quarantaine: ~1,5 miljoen.
Nog te gaan: 17 miljoen. Dat is 113 dagen.
Herstelbewijs 180 dagen geldig.
Genieten maar...

Europe #Endless.......
Kraftwerk cover:
via @YouTube
Read 6 tweets
The most burning 🔥 Questions right now:

Will #SARS2 continue to mutate to escape antibody protection? Do we need another booster? If so, what’s the next formula? For example, do we need an Omicron-specific vaccine?
By the time an Omicron-specific vaccine is tested, we won’t have an Omicron wave anymore. So, is there still value in rolling it out? 2/
It all depends on how the SARS2 keep on evolving? The problem is it’s not following a fixed pattern. We know about evolutionary features of two viruses namely #flu and #measles. 3/
Read 18 tweets
An interesting study!

Researchers investigated whether antibodies stimulated by mRNA vaccination (BNT162b2), including 3rd dose boosting, differ from those generated by infection or adenoviral (ChAdOx1-S & Gam-COVID-Vac) or inactivated viral (BBIBP-CorV) vaccines. 1/
They analyzed human lymph nodes after infection or mRNA vaccination for correlates of serological differences. 2/
Antibody breadth against viral variants is less after infection compared to all vaccines evaluated, but improves over several months. 3/
Read 16 tweets
A lot of people around the world are feeling elated & treating emergence of #Omicron as a signal of the end of the pandemic! Most believe it will bring “endemicity".

Does it make sense? 1/
How can anyone think we’ve got this under control when a new #variant suddenly pops up, nearly completely evades immunity & then sweeps the world in a few weeks?
Further, we must know “mutations have no schedule.” Could be 4-6 months, could be next week. 2/
“to what extent will #Omicron-like emergence events characterize "endemic" circulation of #SARS2? Given it occurred once, having it occur again would not be at all surprising,…whether to expect this every year or every ten.” 3/

Read 5 tweets
A new study from #Thailand

#COVID19 breakthrough infection after #CoronaVac inactivated vaccine induced robust antibody responses & cross-neutralization of #SARS2 variants, but less immunity against #Omicron

Binding antibody levels in sera from patients with breakthrough infection (BI) were significantly higher than those in individuals who had received AstraZeneca Vaccine as a third vaccination. 2:
However, neutralizing activities against wild-type and variants including Alpha, Beta, & Delta were comparable in patients with BI & individuals who received a 3rd vaccination with AZ vax, which activities are exceeding 90%. 3/
Read 4 tweets
What would be the future scenario w/ #SARS2 variants?

1. Displacement of Delta by Omicron
2. Long-term co-circulation
3. Omicron wave followed by resurgence of Delta & extinction of Omicron
4-Alternate outbreaks of Omicron & Delta
5-An entirely new VOC may displace the two 1/
We know an Omicron infection protects well against reinfection by Delta in previously vaccinated people, but not so well in those that have not been previously vaccinated. In unvaccinated people an Omicron infection only protects well against Omicron reinfection. 2/
This gives advantage Omicron in a highly vaxxed world. But epidemiology of the two VOC in coming weeks should tell us how efficiently Omicron is displacing Delta 3/
Read 12 tweets
How can you deal with a virus that has the capability of even switching its entry route?

Laboratory experiments demonstrate that #Omicron has switched its route of entry in to human cells. 1/
This is likely to influence #Omicron spread and the types of cells it can hijack. 2/
#SARS2 can enter cells via two routes, both routes require spike activation by proteases.

Route 1: Cell surface fusion, triggered by #TMPRRS2.

Route 2: endosomal fusion, triggered by cathepsins.

So far SARS2 has favoured Route 1.
Read 15 tweets
There’s a new COVID19 variant that has people worried. Let’s talk about “omicron.” This assessment must necessarily be very preliminary, since we are in very early days (partly thanks to South Africa generously sounding the alarm!). 1/
Three key issues are whether omicron is 1) more transmissible, 2) more deadly, and 3) more capable of evading current vaccines (or, somewhat analogously, whether it evades current antibody treatments or immunity conferred by prior natural infection, aka “immune escape”). 2/
Based on currently available technical data and on news reports from around the world, here is a *preliminary* opinion about these three issues, along with my level of confidence in these guesses. 3/
Read 47 tweets
What happens if we allow #SARS2 to become endemic? What’s going to happen to us & what’s going to happen to the virus?

If we allow it to become endemic—and some would argue that it is already endemic—this does not mean that it is going to attenuate, not whatsoever. 1/
It is not true that more transmissible versions of #SARS2 will be more benign. What we are seeing is more aggressive, more transmissible versions which are creating more severe illness. And the virus is still adapting to our physiology. It’s doing it at a fantastic rate 2/
What we’re going to see is that it will continue to work against our immune systems, meaning become more immune evasive. It’s going to become more chronic as an infection. 3/
Read 14 tweets
Natural immunity post-#SARS2 infection may not be perfect agains #Delta variant!!

A new study from #Australia:

“The duration & magnitude of #SARS2 immunity after infection, especially wrt the emergence of new VOCs”

At 12 months after mild-COVID19:

1->90% of convalescents remained seropositive for RBD-IgG & 88.9% had circulating RBD-specific memory B cells.

2-Despite this, only 51.2% convalescents had serum neutralising activity against homologous live-SARS2 virus

3-The neutralising activity decreased to 44.2% against live Alpha, 4.6% against Beta, 11.6% against Gamma & 16.2%, against Delta

4-Spike & non-Spike-specific T cells were detected in >50% of convalescents

Read 7 tweets

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