It makes a lot of good points about what data is needed to improve models that can guide exit strategies and has a good short discussion on herd immunity and incl. three challenges for even determining the herd immunity threshold:
1. “most of the quantities for calculating the threshold are not known precisely”, for instance how common immunity is or how long it lasts 2. even the value for R0 needs to be refined 3. Disease clustering lowers threshold but to know how much, more info on transmission needed
Also:
"reaching the herd immunity threshold does not mean that the epidemic is over or that there is no risk of further infections. Great care must be taken in communicating this concept to the public to ensure continued adherence to public health measures."
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So what have I learnt about #misinformation research? I tried to condense it into a list of the 5 biggest challenges the field faces.
Second story in my package of stories about misinformation research is up here (and thread to come):
Let me start with the first:
What even is misinformation?
When I started reporting on the field, eager to delve into things I was really frustrated that I kept coming back to this basic question. I told friends it felt like trying to take a deep dive in a puddle, always forced back to the surface.
In retrospect, it seems obvious that this was going to be a thorny problem that I would have to spend a lot of time on. The definition you use really defines the shape of the problem and it also kinda helps to be sure you're talking about the same thing as your interview partner...
I’ve reported on infectious diseases for 15 years, but during the covid-19 pandemic and even more during the global outbreak of mpox clade IIb, I was shocked by the amount of misinformation I was seeing. Misinfo had always been part of any outbreak, but this felt different.
I ended up spending almost a year at MIT as a Knight Science Journalism Fellow (@KSJatMIT) to try and understand misinformation/disinformation better, to - I hope - be a better infectious disease journalist.
It’s been an interesting experience in turns fascinating and frustrating and when I went back to full-time science writing earlier this year I decided to try and put at least some of what I’ve learnt into words.
I'm seeing a lot of confusion already out there about #mpox and the differences between clades and lineages. I will get into this in more detail later, but for now:
We really don't know for sure whether there is any material difference between clade Ia, Ib, IIa and IIb.
The differences we see might have very little to do with the virus and everything to do with it affecting different populations in different places and spreading different ways once it gets into certain contact networks. Real world data is not comparing apples and apples here...
We will learn a lot in the coming weeks and months and things will become much clearer. But for now there is a lot of uncertainty. My advice as always: Don’t trust anyone who pretends that things are clear and obvious.
In May I wrote about researchers' plans to infect cows in high-security labs with avian influenza #H5N1 to better understand the infections and how easily the virus is transmitted. The results from two of these experiments are now out here in a preprint: biorxiv.org/content/10.110…
WHAT DID THEY DO?
In one experiment (at Kansas State University) 6 calves were infected with an #H5N1 isolate from the current outbreak oronasally and then housed together with three uninfected animals ("sentinels") two days later.
In the other experiment (at Friedrich Loeffler Institut) 3 lactating cows were infected through the udder with an #H5N1 isolate from the US outbreak and 3 other lactating cows the same way with a different #H5N1 isolate from a wild bird in Europe.
One question at the heart of the #h5n1 outbreak in US cows has been: Is there something special about this virus? Or is H5N1 generally able to do this and this particular version was just "in the right place at the right time"?
Quick thread, because it seems we have an answer
Researchers in Germany have done an experiment in a high-security lab infecting cows directly with the strain of #H5N1 circulating in cows in the US (B3.13) and infecting others with an #h5n1 strain from a wild bird in Germany.
(I wrote about the plans here: )science.org/content/articl…
In both cases they infected the udders directly through the teats and in both cases the animals got sick. They "showed clear signs of disease such as a sharp drop in milk production, changes in milk consistency and fever." That suggests there is nothing special about B3.13.
The thing that I find most frustrating about the entire mpox/gain-of-function debate is how the uncertainties that lie at the base of it all just become cemented as certainties that are then carried forward.
(If you know anything about me you know I love me some uncertainty...)
Most importantly: The interim report on the investigation into these experiments released on Tuesday numerous times calls clade II "more transmissible" or even "much more transmissible".
But that is a claim that has very little evidence at all.
In fact you can find plenty of literature that argue the exact opposite, that in fact clade I is more transmissible.
Just, as an example, here is Texas HHS:
"Clade I MPXV, which may be more transmissible and cause more severe infection than Clade II..." dshs.texas.gov/news-alerts/he…