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Saved by @jay_millerjay

Brief thread to debunk the repeated claims we hear about transmission not happening 'within school walls', infection in school children being 'a reflection of infection from the community', and 'primary school children less likely to get infected and contribute to transmission'.

 I've heard a lot of scientists claim these three - including most recently the chief advisor to the CDC, where the claim that most transmission doesn't happen within the walls of schools. There is strong evidence to rebut this claim. Let's look at this.

https://t.co/NiNHZV6TDO
Let's look at the trends of infection in different age groups in England first- as reported by the ONS. Being a random survey of infection in the community, this doesn't suffer from the biases of symptom-based testing, particularly important in children who are often asymptomatic
A few things to note:
1. The infection rates among primary & secondary school children closely follow school openings, closures & levels of attendance. E.g. We see a dip in infections following Oct half-term, followed by a rise after school reopening.
We see steep drops in both primary & secondary school groups after end of term (18th December), but these drops plateau out in primary school children, where attendance has been >20% after re-opening in January (by contrast with 2ndary schools where this is ~5%).
Concerningly, the REACT-1 study data released today show that prevalence of infection across England is now highest in primary school children & young adults, with the drops being less steep in primary school children compared to other age groups.
These data are consistent with outbreak data from PHE surveillance, showing that outbreaks in primary schools & pre-school settings continue to occur (albeit at a lower rate than before in primaries), but much more than in secondary schools- in line with higher attendance.
This evidence also feeds into the second myth we hear about - that primary school children don't contribute substantively to transmission. This simply doesn't hold up to scrutiny. The plot from the PHE shows that the number of clusters of cases has been very similar in both.
We also see from the ONS data that primary and secondary school children had the highest prevalence of infection in the community compared to all age groups in December, prior to school closures -prevalence was 2% among primary school children and 3% in 2ndary school children.
All this evidence strongly suggests that infection among children is not simply 'a reflection of infection in the community'. It makes no sense to think that children are getting infected in their households and not within schools.
It's clear that infection in children closely tracks school openings, closure, & the level of attendance. We've seen this in England time and time again. And it's not just secondary schools. It's clear that primary schools play an important role. What about global evidence?
This comprehensive study in Nature Human Behaviour that looked at thousands of interventions implemented at different time points in >200 countries showed that closure of educational institutions was one of the most effective interventions in reducing R.
https://t.co/ANWt3OiiZv
But what about the impact of closure of preschool vs primary vs secondary schools. There was no difference- all of them were similarly effective in reducing R- and closure of any setting had a substantial impact on reducing R.
We also have evidence from the UK from our last lockdown in November, when schools were open, and regions where the new variant was dominant (as it is across the UK now) were showing increases in cases (R>1). R in these regions dropped to below 1 only after schools were closed.
This real-world evidence is reflected in recent modelling by LSHTM that also suggests that in almost all scenarios opening primary or secondary schools would lead to rises of R above 1 in England.
https://t.co/opkso4Nx2S
It's astonishing that despite all this evidence, the need for mitigatory measures in schools in England has been ignored, and we still promote the myth that primary school settings don't contribute significantly to transmission, and that transmission doesn't happen within schools
We don't have to even look to the 8th of March when the govt is planning to reopen schools. We're having outbreaks in schools now - in preschool & primary school settings. Primary school children have the highest prevalence of infection along with young adults. When will we act?
Want to end on the ONS data on school transmission from last year that showed that primary school children were 2x more likely than adults to be the first case in the household, and once infected, 2x more likely to infect contacts than adults.

https://t.co/suNOYlSYgy
This is some of the least biased evidence we have - as it's based on random surveys of children so not dependent on them being symptomatic, and tested. Why are we ignoring this breadth of evidence to the detriment of children, teachers, and communities?

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This is the exact problem with our government's thinking & response- despite this strategy of 'tolerating deaths' and half-way measures having spectacularly failed, it's quite amazing that our govt still hasn't learned anything, & continues to promote a policy of death. Thread


Had we adopted an elimination strategy early on, rather than one of tolerating a certain level of infection, we wouldn't be here now. The reason we're here is because the govt never committed to elimination.

We eased lockdown in May when infection levels were much higher than when other countries in Europe did this. The govt was warned about this, but did this to 'help the economy'. Not only did this lead us into the 2nd wave, the need for further lockdowns harmed the economy further

It's very clear from global evidence that we cannot 'tolerate a level of community transmission' and maintain 'R at or just below 1', which has been our governments policy for a long time. This isn't sustainable & very rapidly gets out of control, leading to exponential rises

Coupled with late action to contain these surges, not only does this lead to many more deaths, and much more morbidity with Long COVID, it also creates a fertile ground for viral mutations to accumulate with a greater risk of adaptation, which is exactly what happened in the UK
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I'm honestly at a loss as to understanding what our government is thinking & what evidence they're considering in enacting gravely negligent policies that will almost certainly lead to tens of thousands of deaths in the coming weeks. Thread.

To recap - NHS capacity is critical in many places. Hospitals have reported oxygen shortages, and doctors are talking about having to choose who to put on ventilatory support. We have rapidly rising case numbers, >50,000 daily reported cases & 981 deaths reported yesterday.

Let's remember that the impact of socialising over christmas hasn't even begun to show in our numbers yet. And that hospitalisations are indicative of infections that happened ~2-3 wks ago (since then we have been seeing exponential rises in cases).

This means even if we act today, and bring R to below 1 right now, hospitalisations will continue to rise for another 2 wks or so - in line with exponential rises in cases over the past 2 weeks. And deaths will continue to rise for 2-4 wks after we act.

Given current doubling periods, this means very conservatively, 20-30,000 deaths over the next 4 weeks or so, which we sadly can't do anything about now, because most of those who will die during this period have already been infected.
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@dgurdasani1
I've been seeing a lot of discussion around the dosage gaps recommended by government for the Astra/Oxford & Pfizer/BioNTech vaccines. My thoughts on the potential benefits & risks of such an approach, and the need for much greater transparency around these decisions. Thread.


The UK govt announced recently that both the Oxford & BioNTech vaccines would be now administered with a gap of between 4-12 weeks (so prioritise administration of first dose, given limited resources).

What is the basis of this?

The basis that's been discussed seems to be that
1) the first dose is likely to confer some degree of protection against disease, so better to roll this out as fast as possible, and
2) that for Oxford/Astra efficacy may be higher when the gap between doses is greater.

I discuss some of the technical details around the Oxford trial below for those interested in these. If you'd just like a summary of this, please skip to the summary tweet titled 'SUMMARY'.

What does published evidence show? The Astra/Oxford data are a bit messy because of protocol changes during the trial. This is because the trial was originally planned as a single dose trial, but a booster dose was added when developers realised that this would likely help.
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Deepti Gurdasani
Deepti Gurdasani
@dgurdasani1
My thoughts on the govt announcement yesterday regarding a new viral strain potentially driving an increase in cases in London. The claim, at least from listening to the daily briefing seems to be based on the strain increasing in frequency more recently. 1/N

Cases have been rising exponentially in England- much of the increase being attributed to the South, although declines have slowed even in the North following easing of lockdown. Much of this is anticipated, and expected, given the behaviour of the virus. 2/N

SARS-CoV-2, like any other viruses mutates as it multiplies (albeit slower than influenza). Mutations occur randomly and most are 'neutral' - i.e. have little to no effect on transmission, ability to evade the natural or vaccine-related immune response

Having said that, few mutations have been shown to be less likely to be neutralised by plasma from patients infected by the usual (wild-type) virus. Whether this translates to a lower response to vaccines or higher risk of re-infection is unclear at the moment.

Also worth noting that just because a variant becomes more frequent in a region doesn't necessarily mean it offers a fitness advantage to the virus. Many mutations rise to different frequencies in different regions due to random processes. The frequency of strains varies globally
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Deepti Gurdasani
Deepti Gurdasani
@dgurdasani1
Thread on the recent report on the possible risk of increased death associated with the new UK variant (B117)- with a discussion of the evidence around this, and what this means.

First, there is strong evidence to support increased transmissibility of B117 - current estimates of increased transmissibility range between 30-70% - from epidemiological evidence examining the differential rate of growth of B117 with respect to other variants & increase in R

There is also evidence from PHE contact studies that the risk of transmission from those carrying the B117 variant is ~50% greater than with other non-B117 variants.

Increased transmissibility, even if a variant has the same fatality rate can increase deaths substantially, because the rate of growth of cases is higher- & more cases means more deaths.

Increased fatality rates also increase deaths- but do so


So how was risk of death with the variant studied?
We don't routinely sequence all samples for the virus. We've found that the variant has a particular deletion which means that some PCR tests on samples with the variant give a different read-out when the variant is present.
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1/OK, I should really write another thread about university-centric regional development, because I think people often make some (very understandable) mistakes when thinking about this issue.

2/The biggest myth, I think, is that universities help regions by educating locals as undergraduates.

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Another example of #FactCheckBait. This sanghi wants you to identify them while pointing out the very obvious flaws in their logic. This sanghi is counting on it to improve their visibility. Don't give them that oxygen. Call them out like this, without IDs, if you must.


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