Spike gene target failure (SGTF) can serve as a proxy for carriage of the VOC (cf.
Section Impact on diagnostic assay below). Classifications of SGTF are preliminary as
case definitions are still being developed. On this basis, we adjusted rates of SGTF for
variable specificity over time and between local authorities and then applied the same
models to estimate the association of VOC frequency and reproduction number. This
analysis shows an increase of Rt of 0.52 [95%CI: 0.39-0.70] when we use a fixed effect
model for each area. We also fitted a similar model but with a random effect model on
the area, giving an estimated additive effect of 0.60 [95%CI:0.48 - 0.73]. Similar
estimates of 0.56 [95%CrI:0.37-0.75] were obtained using a Bayesian regression model
accounting for errors in VUI frequencies and Rt estimates. As an example, under the fixed effect model, an area with an Rt of 0.8 without the new variant would have an Rt of
1.32 [95%CI:1.19-1.50] if only the VOC was present.]/quote]
So does that mean we need a lockdown strong enough to bring the Rt of covid version 1 to about 0.4 to get this one under 1? I can't see how that's possible with schools open.
Spike gene target failure (SGTF) can serve as a proxy for carriage of the VOC (cf.
Section Impact on diagnostic assay below). Classifications of SGTF are preliminary as
case definitions are still being developed. On this basis, we adjusted rates of SGTF for
variable specificity over time and between local authorities and then applied the same
models to estimate the association of VOC frequency and reproduction number. This
analysis shows an increase of Rt of 0.52 [95%CI: 0.39-0.70] when we use a fixed effect
model for each area. We also fitted a similar model but with a random effect model on
the area, giving an estimated additive effect of 0.60 [95%CI:0.48 - 0.73]. Similar
estimates of 0.56 [95%CrI:0.37-0.75] were obtained using a Bayesian regression model
accounting for errors in VUI frequencies and Rt estimates. As an example, under the fixed effect model, an area with an Rt of 0.8 without the new variant would have an Rt of
1.32 [95%CI:1.19-1.50] if only the VOC was present.
So does that mean we need a lockdown strong enough to bring the Rt of covid version 1 to about 0.4 to get this one under 1? I can't see how that's possible with schools open.
Spike gene target failure (SGTF) can serve as a proxy for carriage of the VOC (cf.
Section Impact on diagnostic assay below). Classifications of SGTF are preliminary as
case definitions are still being developed. On this basis, we adjusted rates of SGTF for
variable specificity over time and between local authorities and then applied the same
models to estimate the association of VOC frequency and reproduction number. This
analysis shows an increase of Rt of 0.52 [95%CI: 0.39-0.70] when we use a fixed effect
model for each area. We also fitted a similar model but with a random effect model on
the area, giving an estimated additive effect of 0.60 [95%CI:0.48 - 0.73]. Similar
estimates of 0.56 [95%CrI:0.37-0.75] were obtained using a Bayesian regression model
accounting for errors in VUI frequencies and Rt estimates. As an example, under the fixed effect model, an area with an Rt of 0.8 without the new variant would have an Rt of
1.32 [95%CI:1.19-1.50] if only the VOC was present.
So does that mean we need a lockdown strong enough to bring the Rt of covid version 1 to about 0.4 to get this one under 1? I can't see how that's possible with schools open.
Lets see what happens to cases in Tier 4 areas over the next week or so. If cases don't start leveling off or even decreasing then the only options will be an April style lockdown letting cases rise until everyone is vaccinated.
One issue is that a raised r will also mean that the herd immunity threshold is higher.
I've got a quick question or three based on a facebook discussion. No one seemed to know there.
Some people are calling this a new strain, some a variation or variant. Are these terms well defined in scienceworld? if so, which one should we be using here, and when does a variant become a strain?
So it could just be that the UK isn't doing enouf to prevent the spread?
I think it’s unlikely. The new variant has a specific mutation to the spike protein called N501Y which improves binding to ACE2. That mutation has separately evolved in South Africa and it is associated with increased transmissibility (also rapidly becoming dominant in part of SA).
See:
We found someone in Ancona with the new variant (swabbed due to having a "bad cold"), and they don't have any obvious links to the UK.
having that swing is a necessary but not sufficient condition for it meaning a thing
@shpalman@mastodon.me.uk
@shpalman.bsky.social / bsky.app/profile/chrastina.net
threads.net/@dannychrastina
Bird on a Fire wrote: Wed Dec 23, 2020 1:49 pm
Mutations to become more infectious and less harmful are generally what you'd expect a pathogen or parasite to do after finding a new host population.
I'm sure I read predictions that this would happen back in the spring/summer.
having that swing is a necessary but not sufficient condition for it meaning a thing
@shpalman@mastodon.me.uk
@shpalman.bsky.social / bsky.app/profile/chrastina.net
threads.net/@dannychrastina
Bird on a Fire wrote: Wed Dec 23, 2020 1:49 pm
Mutations to become more infectious and less harmful are generally what you'd expect a pathogen or parasite to do after finding a new host population.
I'm sure I read predictions that this would happen back in the spring/summer.
True, though it doesn't yet seem to be less harmful.
Social distancing will have exerted strong evolutionary pressure, and mutations to make it more infectious are the result.
So it could just be that the UK isn't doing enouf to prevent the spread?
I think it’s unlikely. The new variant has a specific mutation to the spike protein called N501Y which improves binding to ACE2. That mutation has separately evolved in South Africa and it is associated with increased transmissibility (also rapidly becoming dominant in part of SA).
See:
Bird on a Fire wrote: Wed Dec 23, 2020 1:49 pm
Mutations to become more infectious and less harmful are generally what you'd expect a pathogen or parasite to do after finding a new host population.
I'm sure I read predictions that this would happen back in the spring/summer.
True, though it doesn't yet seem to be less harmful.
Social distancing will have exerted strong evolutionary pressure, and mutations to make it more infectious are the result.
I was wondering what to read into the fact that the viral loads are higher but the proportion needing hospitalisation doesn't seem to have changed. Could that be a pointer on a turn towards "less harmful"? Probably too early to say, I suspect, but something to watch.
I think it’s unlikely. The new variant has a specific mutation to the spike protein called N501Y which improves binding to ACE2. That mutation has separately evolved in South Africa and it is associated with increased transmissibility (also rapidly becoming dominant in part of SA).
See:
I think it’s unlikely. The new variant has a specific mutation to the spike protein called N501Y which improves binding to ACE2. That mutation has separately evolved in South Africa and it is associated with increased transmissibility (also rapidly becoming dominant in part of SA).
See:
UK brings in extra restrictions on travel from South Africa after cases of the SA variant found in Britain.
having that swing is a necessary but not sufficient condition for it meaning a thing
@shpalman@mastodon.me.uk
@shpalman.bsky.social / bsky.app/profile/chrastina.net
threads.net/@dannychrastina
We estimate that VOC 202012/01 is 56% more transmissible (95% credible interval across three regions 50-74%) than preexisting variants of SARS-CoV-2. We were unable to find clear evidence that VOC 202012/01 results in greater or lesser severity of disease than preexisting variants. Nevertheless, the increase in transmissibility is likely to lead to a large increase in incidence, with COVID-19 hospitalisations and deaths projected to reach higher levels in 2021 than were observed in 2020, even if regional tiered restrictions implemented before 19 December are maintained. Our estimates suggest that control measures of a similar stringency to the national lockdown implemented in England in November 2020 are unlikely to reduce the effective reproduction number Rt to less than 1, unless primary schools, secondary schools, and universities are also closed. We project that large resurgences of the virus are likely to occur following easing of control measures. It may be necessary to greatly accelerate vaccine roll-out to have an appreciable impact in suppressing the resulting disease burden.
SARS-CoV-2 Spike amino acid replacements in the receptor binding domain (RBD) occur relatively frequently and some have a consequence for immune recognition. Here we report recurrent emergence and significant onward transmission of a six-nucleotide deletion in the S gene, which results in loss of two amino acids: H69 and V70. Of particular note this deletion, H69/V70, often co-occurs with the receptor binding motif amino acid replacements N501Y, N439K and Y453F. One of the delH69/V70+ N501Y lineages, B.1.1.7, is comprised of over 1400 SARS-CoV-2 genome sequences from the UK and includes eight S gene mutations: RBD (N501Y and A570D), S1 (delH69/V70 and del144/145) and S2 (P681H, T716I, S982A and D1118H). Some of these mutations have possibly arisen as a result of the virus evolving from immune selection pressure in infected individuals and possibly only one chronic infection in the case of lineage B.1.1.7. We find the delH69/V70 enhances viral infectivity, indicating its effect on virus fitness is independent to the N501Y RBM change. Enhanced surveillance for the delH69/V70 deletion with and without RBD mutations should be considered as a priority. Such mutations have the potential to enhance the ability of SARS-CoV-2 to generate vaccine escape variants that would have otherwise significantly reduced viral fitness.
