30 ms·
As discussed on TWiV yesterday, B.1.1.7 isn't a "strain," which has demonstrably different biological properties, but is still considered a "variant." https://
by sigil 6y ago
As discussed on TWiV yesterday, B.1.1.7 isn't a "strain," which has demonstrably different biological properties, but is still considered a "variant."
https://www.microbe.tv/twiv/twiv-697/ https://www.microbe.tv/twiv/twiv-697/
Any biological differences are theorized solely from the genome at this point. In the episode, Racaniello is at pains to point out that genomic differences alone don't imply biological differences in say transmission, and things like founder effects might also explain the variant's prevalance. We simply don't know yet.
There's a neat cautionary example at 35:10 which I'll try to summarize here. Polio was endemic, with low incidence, for thousands of years. Around 1900 it went from endemic to epidemic. Why? Did it suddenly mutate into a deadlier or more transmissable strain? While we don't have polio sequences from before and after 1900 to compare, we do know that rapid improvements in sanitation delayed exposure to the polio virus. Babies were now encountering the virus after maternal antibodies to it had waned! And it turns out this adequately explains the spike in polio a century ago.
Goes to show how complex the dynamics of these systems can be!
- trebligdivad 6y ago[edited to add newer doc] The UK NERVTAG had other measures of transmissability that got them to the conclusion it did have higher transmissability; https://khub.net/documents/135939561/338928724/SARS-CoV-2+variant+under+investigation%2C+meeting+minutes.pdf/962e866b-161f-2fd5-1030-32b6ab467896?t=1608470511452 https://khub.net/documents/135939561/338928724/SARS-CoV-2+va... and have a newer one where they're more confident: https://app.box.com/s/3lkcbxepqixkg4mv640dpvvg978ixjtf/file/756964987830 https://app.box.com/s/3lkcbxepqixkg4mv640dpvvg978ixjtf/file/...
- sigil 6y agoThey discuss these in that TWiV episode as well!
- randomsearch 6y agoWorth noting that you can’t test a hypothesis from the data you used to formulate it. I haven’t seen any work on this variant that doesn’t fall into that trap.
- disgruntledphd2 6y agoI would really, really hope that they are using a good cross-validation strategy (as they'll definitely need it).
- randomsearch 6y agocross validation won't save you in this situation. it's a subtle point, but you can't say "omg this strain is increasing and it must therefore be more contagious" and then show that it is more contagious by showing it is increasing... this is counter-intuitive even to most scientists, in my experience. I remember when I learnt this during my PhD. I suspect many people high up in academia don't understand this point.
- randomsearch 6y agoan observation that may help: as your stats at time t+1 are dependent on stats at time t, you cannot separate your validation set from the set you used to perform exploratory data analysis - they are highly interdependent.
- jsnell 6y agoTWIW has kind of painted themselves into the corner by insisting that anything except biological evidence is irrelevant. The evidence for B.1.1.7 being more transmissive is quite solid, and seems to be getting more so as time goes on. But no matter how strong the statistical data is, it could never be good enough for them. So their policy recommendation ends up as "do nothing at all until there is 100% certain non-circumstantial evidence". The problem is that action now is way more valuable than action in 1-2 months. Mass vaccination is right around the corner, we just need to buy time to get there. If there is a substantially more transmissive variant around, that will make it much harder to buy that time. You need to be able to act on the balance of probabilities, not wait for perfect information. (And their claim that there's nothing we can do differently is just total bunk.) And because they run a popular podcast, their view gets massively amplified by being parroted in internet discussion.
- SomeoneFromCA 6y agoThere is some other point I heard recently on Twitter - the appearance of new variants with increasingly faster speed of spread (BTW, if anyone remembers, there was a mutation in Australia, which had shorter incubation - 8 HOURS), may quite soon cause rise of true strains, and, it might potentially lead to the ADE, when suboptimal vaccines will make disease much worth instead of easing it.
- endgame 6y agoYou're not thinking of the pizza worker in SA who told porkies, are you? https://www.theguardian.com/world/2020/nov/21/south-australia-makes-young-pizza-worker-scapegoat-for-covid-19-failures https://www.theguardian.com/world/2020/nov/21/south-australi...
- SomeoneFromCA 6y agoNot sure, just read about it somewhere.
- bonzini 6y ago> 8 hours That seems weird, to be kind. Source?
- skybrian 6y agoIt would be more accurate to say that we don't know yet whether it should be considered a new strain or not. Any adjective like "strain" implies a binary distinction, but that doesn't mean you should round off "don't know" to false.
- didibus 6y agoOkay, but from your own explanation, this is only a hypothesis and it's possible that sanitation had nothing to do with it either. So I'm not sure what this really shows us except that we can make up any justification for anything after the fact. Correlation is easy to show, causation is hard.
- jpster 6y agoI’m a big fan of TWiV podcast (This Week in Virology) and I understand Racaniello’s point of view. However, this thread and other info I’ve read lead me to believe that this is an important new development. https://twitter.com/billhanage/status/1341857733633581063?s=21 https://twitter.com/billhanage/status/1341857733633581063?s=...
- deleted 6y ago[deleted]
- tailspin2019 6y agoThanks for this link, a lot of valuable insight in those 17 tweets! I share your opinion.
- mssundaram 6y ago> Polio was endemic, with low incidence, for thousands of years. Around 1900 it went from endemic to epidemic. Why? Did it suddenly mutate into a deadlier or more transmissable strain? While we don't have polio sequences from before and after 1900 to compare, we do know that rapid improvements in sanitation delayed exposure to the polio virus. Babies were now encountering the virus after maternal antibodies to it had waned! What is the source for this? I've read another explanation: the overuse of pesticides like Paris Green, DDT (see pictures of kids literally sprayed with it on their clothing), and the use of "medical metals" to treat any kinds of diseases - giving mercury, arsenic etc. All of these (pesticides, metals) can weaken the bowels and allow the polio virus (which resides in the bowels) to enter into the spine where it then causes paralysis. Maternal transfer of antibodies is one of my favorite immunity topics - it is far overlooked in usefulness lately, largely seen as impractical due to changes in lifestyle (not many mothers breastfeed) Dear downvoters: what do you find does not contribute to conversation about sharing this theory?
- suifbwish 6y agoWell if it isn’t a different strain then the vaccine should still work on it.