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Slack / Private Message Drop, p.386 [SLACK_000600] · slack_pm:msg:04023

Page text: p.386 · original PDF

Date
2021-01-12 07:31
Type
chat message · slack
recipient
Robert F. Garry, Edward C. Holmes, Andrew Rambaut
speaker
Kristian G. Andersen

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If we weigh being 'successful' in a population due to inherently being (a) inherently more transmissible vs (b) being able to escape immunity, an important consideration is what the immune selection pressure is. Is it the oneexperienced within a single (chronically) infected individual or is it standing immunity as a virus is spreading througha population? Given that we're seeing the same sets of mutations in independent lineages in different areas, clearly there must be a strong and directed selection pressure (immune or otherwise). I'm starting to think that it's probably the former - rare events happening in individual people (or a zoonotic host -probably not likely, but has to be considered) that may or may not be immunocompromised and may and may not have received treatments. The increased transmission effects (probably high for UK lineage) and population immune evasion (probably higher in RSA/Brazil lineages) are just side-effects of the intrahost selection pressures that fixed the mutations in the first place - I don't necessarily think they _are_ the selection pressures. The transmission phenotype may be a side-effect of "better binding" and population immune evasion a side-effect of intrahost immune evasion. The reason why we're (a) observing these now, and (b) they pop up in areas of high previous attack rates, might bemore down to chance than selection. Chronic infections are probably rare events, take time to fix a large number of(onwards successfully) mutations, and therefore more likely to pop up in areas of high previous attack rates. Ifthey're then able to escape _some_ immunity in the population, they're also more likely to successfully propagate insuch a population.

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  1. 2021-01-12 07:31 Kristian G. Andersen
    If we weigh being 'successful' in a population due to inherently being (a) inherently more transmissible vs (b) being able to escape immunity, an important consideration is what the immune selection pressure is. Is it the oneexperienced within a single (chronically) infected individual or is it standing immunity as a virus is spreading througha population? Given that we're seeing the same sets of mutations in independent lineages in different areas, clearly there must be a strong and directed selection pressure (immune or otherwise). I'm starting to think that it's probably the former - rare events happening in individual people (or a zoonotic host -probably not likely, but has to be considered) that may or may not be immunocompromised and may and may not have received treatments. The increased transmission effects (probably high for UK lineage) and population immune evasion (probably higher in RSA/Brazil lineages) are just side-effects of the intrahost selection pressures that fixed the mutations in the first place - I don't necessarily think they _are_ the selection pressures. The transmission phenotype may be a side-effect of "better binding" and population immune evasion a side-effect of intrahost immune evasion. The reason why we're (a) observing these now, and (b) they pop up in areas of high previous attack rates, might bemore down to chance than selection. Chronic infections are probably rare events, take time to fix a large number of(onwards successfully) mutations, and therefore more likely to pop up in areas of high previous attack rates. Ifthey're then able to escape _some_ immunity in the population, they're also more likely to successfully propagate insuch a population.

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