Chat message

Slack / Private Message Drop, p.328 [SLACK_000542] · slack_pm:msg:03450

Date: 2020-12-20 13:10
Type: chat message · slack
recipient: Robert F. Garry, Edward C. Holmes, Andrew Rambaut
speaker: Kristian G. Andersen
Topics: Intelligence community assessments

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Thanks Bob - this is very helpful. One nagging question I have is that it doesn't seem to me that N501Y _alone_ can explain the 'spreader' phenotype, yet, the lineages in the UK and SA are quite distinct - and as far as I can tell, only share N501Y. However, it's entirely plausible that different mutations can lead to similar conformational changes, that might give the virus a 'spreader' phenotype if N501Y pops up on that genetic backbone.We have seen N501Y before (e.g., Australia), but I don't know that any of those are associated with increased spread? With that said, Australia isn't exactly representative when it comes to the question of spread, and I don't believe N501Y has been observed in that many places (I think just random stray sequences here and there)

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Statement	Grade	Attribution	Stance
However, it's entirely plausible that different mutations can lead to similar conformational changes, that might give the virus a 'spreader' phenotype if N501Y pops up on that genetic backbone.We have seen N501Y before (e.g., Australia), but I don't know that any of those are associated with increased spread?	needs context	uncertain explicit hedge	questions

Statement

Grade

Attribution

Stance

However, it's entirely plausible that different mutations can lead to similar conformational changes, that might give the virus a 'spreader' phenotype if N501Y pops up on that genetic backbone.We have seen N501Y before (e.g., Australia), but I don't know that any of those are associated with increased spread?

needs context

uncertain explicit hedge

questions

In context

A single line often inverts meaning once you see what it answers, so neighbouring messages are always shown.

2020-12-20 12:31 Edward C. Holmes open

Thanks Bob, a lot to think about.
2020-12-20 13:10 Kristian G. Andersen

Thanks Bob - this is very helpful. One nagging question I have is that it doesn't seem to me that N501Y _alone_ can explain the 'spreader' phenotype, yet, the lineages in the UK and SA are quite distinct - and as far as I can tell, only share N501Y. However, it's entirely plausible that different mutations can lead to similar conformational changes, that might give the virus a 'spreader' phenotype if N501Y pops up on that genetic backbone.We have seen N501Y before (e.g., Australia), but I don't know that any of those are associated with increased spread? With that said, Australia isn't exactly representative when it comes to the question of spread, and I don't believe N501Y has been observed in that many places (I think just random stray sequences here and there)
2020-12-20 13:16 Andrew Rambaut open

There are actually 2 501Y lineages in the UK - the other one in South Wales (now up to about 500 genomes but associated with a hospital outbreak as well). Again only N501Y in common. As you say - there was a cluster in Australia - 37 genomes from beginning of June to beginning of July.
2020-12-20 13:18 Kristian G. Andersen open

I missed that - I thought same lineage, but two separate emergence events (from a common source, I assumed). ButI see the differences on Emma's Nextstrain build - very interesting.
2020-12-20 13:19 Andrew Rambaut open

There are 5 from Massachusetts with a shit load of mutations
2020-12-20 13:19 Andrew Rambaut open

Spike A1020S, Spike C15del, Spike D614G, Spike G142del, Spike I870V, Spike L18del, Spike L141del, Spike N17del, Spike N440D, Spike N501Y, Spike Q14del, Spike Q183H, Spike Q493K, Spike S12del, Spike S13del, Spike S494P, Spike T478K, Spike V16del, Spike V143del, Spike Y144F, E T30I, M A2V, N A208S, NS3 Q57H, NS7a S83L, NSP2 I21V, NSP2 T85I, NSP4 A307V, NSP12 P323L, NSP13 T115I

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