1/ There is absolutely no discussion that if you have a disease that doubles its size every 3-4 days and 2% of those infected requires hospitalization you are going to have a quite difficult situation to deal with. Not even a newbie modeler would disagree with @neil_ferguson
2/ But as @gidmk told me once in one of our initial exchanges (and respectful disagreements): "Everyone comes into epidemiology for the uncertainty and stay for the nuance" (if I recall it correctly, corrections please). The entire response rest on those nuances, let's dissect.
3/ At least in my mind there is no doubt that the Ro of SARS-Cov-2 is very high (we estimated 3.3) and if we account for the UK variant we are probably 30% up from there. So, we can say we agree probably up to the decimals level.
4/ The second assertion is at the very least weak. 2% is a HUGE number. If that would be true we should be watching hundreds of young adults and kids hospitalized. I know there are some, but that ain't happening to the number that would be required to accept that number.
5/ Then it is difficult to accept the dismissal of the whole issue based on that fact. I read also @derekwinton opinion piece, and being a software developer I can agree the code is a bit of a mess, and I write code that is run to this date on several 10000s of machines daily.
6/ But while it is interesting to see that such piece of complex simulation software has almost no test code; that to me is a moot argument, if the software work, it works.
7/ What it is interesting though is he mentioned all 4 models agree. Well let's say that it would be a thing if they didn't, they are modeling the same underlying process. If your model is not capturing a key piece of the process, then it does not work.
8/ @neil_ferguson talks about the specifics about the response or how the UK hasn't been using it to inform, now that begs the question; what the is optimal response those 4 models gives to minimize deaths? Because, our own work suggest that uniform suppression is not the answer.
9/ So, either their models are not capturing a key part of the process which is age stratification or they should be showing how mitigating uniformly actually increases the death toll. Given their model style is based on agents I don't have much confidence they could know either.
10/ The reason is that those types of models are highly sensitive to stochasticity and also to underlying assumptions. What if instead of 1 bus per block, you have 2? What if the length of the trip is 5 blocks or 10 blocks?
11/ Mobility for example is key to those types of models where you simulate a whole city or country by cells, and those parametrizations rest on assumptions, those assumptions will throw you off the mark pretty fast when left unchecked. That's why we decided to go classic.
12/ And going classic (ODE style) you win the ability to explore easily and cheaply the space of solutions and parameters. That's why you discover 'strange' behaviors (for the epidemiologists at least) like that many viral parameters do not influence immunity.
13/ Assumptions, Assumptions, Assumptions. All good modelers should be able to show how their assumptions modify the behavior and make them explicit in their model. You should not take a model at face value without understanding them. They are ALL.
14/ So my question for all of SAGE researchers like @neil_ferguson, @mlipsitch, etc is: "Back in march, what is the set of policies that ensure that we would minimize deaths?" And remember that we know already (and we knew back then) that this is a age risk stratified disease.

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More from @federicolois

23 Feb
1/ When we wrote this paragraph back in October I wouldn't know how close to home it would hit. Back in October my mother-in-law (65+) fainted in the bathroom while having diarrhea. It was quite a scare as she got hit very hard.

Ref: medrxiv.org/content/10.110…
2/ Not long after my father-in-law (80+) was diagnosed with anorexia nervousa. Doctors presume that loneliness caused by the lockdown, plus the scare of the episode would have been more than enough to cause it.
3/ Back then I immediately told my wife that those were signs of COVID, being health personnel and working on the lab at the hospital knew very well the evidence. On her account, the evidence was definitely not anywhere near what they thought were signs of the disease.
Read 9 tweets
20 Feb
Let's play a game. I will ask a few things about SARS-Cov-2 and you respond in a poll. Let's see how many points do you get.

#1: Is there a non-human reservoir or vectors (or both)?
#2: Is the disease geographically restricted?
#3: Is there a 'sterilizing' vaccine or any other transmission-disrupting alternative?
Read 14 tweets
17 Feb
1/ By popular demand I was going to do a deep dive into the European CDC Face Mask recommendation study. Well, it may end but be a bit shallow. There is not much depth to be diving into. ecdc.europa.eu/en/publication…
2/ The study follows a usual form with clear inclusion and exclusion criteria (which is good). It uses the GRADE framework to ascertain the evidence and generate a recommendation. That is among the best we got in the evidence based land.
3/ The number of studies included is 'interesting'. With a n=118 we would expect to get a nice body of clear cut evidence to support the recommendation. Image
Read 17 tweets
11 Feb
1/ What does this mean for research? For example, while my twitter followed has increased absurdly since early last year because of my work on data analysis on SARS-Cov-2, I was mostly known for my work in performance analysis.
2/ What performance analysis teaches you is that you run experiments of the type 'If P then Q' every single day, several times a day.
For ex. "If I change this data structure then I will be able to obtain better performance by accessing memory contiguously"
3/ Now, when you enter into the realm of 'how the physical CPU is working' then becomes far more difficult. The reason behind that is that with that many moving parts noise is very difficult to separate from the signal.
Read 8 tweets
7 Feb
1/ Let's look at this paper: "Influenza Virus Aerosols in the Air and Their Infectiousness" from 2014 (we cannot claim this was unknown). We know now that we have a new kid on the block now, ready to challenge Influenza for supremacy in the transmissibility metric.
2/ So there were these guys that actually infected people with Influenza to measure how infectious it was. That is a 'challenge study', this is no 'model' this is actual humans. And they found, that with as much as 3000 copies you get it.
3/ Another study actually measured how many particles an adult would inhale in 1 hour given the concentrations found on a health center, a day-care center, and airplanes.
Read 19 tweets
6 Feb
1/ I was sent this paper. You know I have disregard it before because the filtering mechanic was really not significative for the type of airflow conditions imposed by masks. How wrong I was on not looking deeper.
2/ I have been told by @Kevin_McKernan that you always have to look for "Where is Waldo?" in this type of studies. The first interesting fact comes from Table 1. Each experiment has different experimental setups, that is good enough to disqualify in my book.
3/ But then I skipped to Table 4. Mind you, almost none were statistically significative. But remember Table 1. So you see a correlation there?
Read 6 tweets

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