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One possibility I have not seen discussed much is that B.1.1.7 might appear more transmissible just by having a slightly different susceptibility profile than "wild-type" strains.
A thread on how this theory would fit into the evidence (and how one would falsify it).
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A thread on how this theory would fit into the evidence (and how one would falsify it).
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Although heterogeneity in biological susceptibility is difficult (if not impossible) to quantify directly, we do not generally expect all people have equal susceptibility (in the sense of having equal likelihood of infection at given exposure levels).
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2/14
For example, suppose, as a thought experiment, that 1/3 of the population is 3x as susceptible to infection than the other 2/3 from wild-type strains.
Suppose now that a new variant strain would have the same property but with respect to a *different* third of the population.
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Suppose now that a new variant strain would have the same property but with respect to a *different* third of the population.
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[One might imagine various ways this change in susceptibility profile might be mediated; for example, to the extent that cross-reactive immunity has any effect on susceptibility, a variant strain may not be escaping SARS-CoV-2 immunity but cross-reactive immunity.]
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4/14
In a population in which significant numbers of infections have happened (for wild-type strains), the remaining susceptible population would be more favorable to the variant strain, as a greater fraction of it's most susceptible individuals would remain.
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The consequence would be that the the variant strain would increase in frequency relative to wild-type strains.
This kind of hypothesis is consistent with some of the evidence we have around B.1.1.7, but not all of it. For example:
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This kind of hypothesis is consistent with some of the evidence we have around B.1.1.7, but not all of it. For example:
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It would not explain increased viral loads in B.1.1.7 patients. This would have to be explained some other way (perhaps by epidemic dynamics affecting the timing of PCR tests of different strains, etc).
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7/14
But it would explain why the relative frequency of B.1.1.7 is increasing relative to other strains in the UK.
How would this kind of theory be distinguished from the theory that B.1.1.7 is generally more transmissible?
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How would this kind of theory be distinguished from the theory that B.1.1.7 is generally more transmissible?
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To the extent that B.1.1.7 is growing in relative frequency by admitting a different heterogeneous profile of susceptibility (rather than, e.g., people being generally more susceptible to B.1.1.7) it's advantage over wild-types depends on their being many previous infections.
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As such, this theory would predict that B.1.1.7 would have the greatest advantage in places which have had enough infections that immunity dynamics are affecting the epidemic trajectory.
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10/14
Note this is different from saying that if Country 1 has 2x as many infections as Country 2, then B.1.1.7 has a greater advantage in Country 2, since we should expect immunity effects to matter at different levels in different countries. However:
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11/14
This theory would certainly predict that B.1.1.7 would have less of an advantage in countries which have had very few infections relative to their population size.
For example:
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For example:
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If this were really the only meaningful difference between B.1.1.7 and other strains, then it would not pose a greater threat to countries like Taiwan or New Zealand, though it would certainly pose a greater threat to countries like the United States.
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13/14
In particular, if B.1.1.7 proves to pose a greater risk of outbreaks in places which have so far been spared significant number of infections, that would clearly show that other properties of the variant are in play.
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14/14
Also h/t @javid_lab on the hypothetical example of "cross-reactivity escape".
15/14 https://twitter.com/javid_lab/status/1344856096628830208
15/14 https://twitter.com/javid_lab/status/1344856096628830208
