A single line often inverts meaning once you see what it
answers, so neighbouring messages are always shown.
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B.1.1.7 just looks different to me - again, mutations fixed intrahost in the first place, then near-fixation in the population because of being inherently more transmissible. I think partial immune escape adds to its success aswell.
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But overall, yes, I agree with the hypothesis and think the distinction of different waves being due to differentmitigation efforts is a good one - but as you say, massively politically charged.The fourth wave will likely be driven almost entirely by vaccine escape.
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Makes a lot of sense to me.
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(this ain't the flu, btw). Bob, I'll look at the document today!
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2021-02-20 09:18
Andrew Rambaut
@Kristian Andersen I generally agree - I am 100% convinced that B.1.1.7 is different from everything in its origin story but has converged on the same peak.
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I guess the first question to demonstrate is that has there been a shift in the adaptive landscape (rather than just alot more unusual stuff happening because there are shed loads of cases - although that too). Possible reasons for awide-spread shift in the population level landscapes are 1) NPI, 2) deployment of anti-viral treatments, 3) increasing seroprevalence 4) ? anything else? Then there is the possibility of a shift in within host landscapes - more chronic infections, possibly inimmuno-compromised, possibly treated. Here it is a numbers game - more infections mean more of these and more chance some of them hit this population-fit fitness peak and then transmit onwards.
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Yeah, these are good - I think very likely #1 (broadly defined) and #3 - not sure about #2.
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? anything else? Perhaps something about the demographics shifted too - no data just an impression that a lot more young adults started to get infected in the second wave. That may be because US sucked at testing early on and young adults were getting infected just not counted. Young adults also more likely not to adhere to NPI. In terms ofthe "numbers game" the fact that SubSaharan Africa remains largely devoid of massive outbreaks til you get downto South Africa tells me they are different (which makes the Uganda variant all the more important) - my bias basedon some serology that we are ~sitting on~ trying to get out tells me differences in exposure to seasonal coronaviruses (known and perhaps unknown) could be driving the difference btwn Africa nd the rest of the world.
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Worth adding to the same speculations - what might we expect the future to look like? I have little doubt that the virus will escape our vaccines relatively quickly, meaning we will still continue to see cases - there's no herd immunity here. That scenario may seem like doom, however, it's possible that via vaccination and (re)infections there will beenough immunity to protect against severe disease. I think most virologists believe this is the likely outcome - i.e.,SC2 becomes the common cold. However, I am very concerned this is wishful thinking. SC2 does not appear to be another ccCoV to me. It can infecta huge range of animals and a huge range of tissues. It can infect not just the upper airways (like ccCoVs), but alsolungs, hearts, and other major organs (in fact, pretty much all of them). Some of the reinfections have been severe and have organ involvement (I believe?). To my knowledge, that has never been described with ccCoVs, unless patients have been immunocompromised. So while I'm sure _some_ immunity will _almost_ always be better than none, I am not convinced that this will simply fade into the background like ccCoVs, as I think many scientists believe. It's a very attractive scenario creating a huge confirmation bias. But do we honestly and seriously believe that once most people have gotten that one shot - or been infected - this will become just another ccCoV?I certainly hope so, but I have a hard time convincing myself the data support such a scenario being the most likely outcome.