Out today: two academic publications (not yet peer reviewed) that formally test whether the new B.1.1.7 variant is more transmissible. Both conclude yes, about 50% more. 🧵
First, a pre-print led by @erikmvolz and @neil_ferguson at Imperial, which applied a variety of different models using both genome sequence data and the S-gene dropout data I've mentioned before. imperial.ac.uk/mrc-global-inf…
Comparing genomes (sparse and lagged) and S-gene dropout (dense and up-to-date) shows the same rapid expansion we all know about in London, the East and the Southeast.
Using different models (lots more detail in the paper), spatial resolutions, and either the genomes or S-gene dropout to track B.1.1.7, the conclusion is very consistent: about a 0.5 additive increase to R.
Second, a preliminary report led by @MoritzGerstung and
@harald_voeh, who adapted a hierarchical Bayesian model they made to study the rate of positive tests around England to consider separately B.1.1.7 and other lineages. virological.org/t/lineage-spec…
We estimate proportion of B.1.1.7 in each region of England week-by-week from ~random genome sequences from the past few month. It rose early in the SE (e.g. Medway), later elsewhere (Milton Keynes), or is just arriving (Manchester).
Then we use those estimates to split the observed positive test rates each day into B.1.1.7 and other lineages, so we can study their different growth patterns over time.
Finally, as in the other paper, we can model the R number. If > 1 the epidemic is growing, < 1 shrinking. And consistently (a) B.1.1.7 is 50% higher than others and (b) it was often > 1 during the November lockdown in England.
In both papers, if we look across all English regions, in the overwhelming majority B.1.1.7 expands during lockdown while other lineages contract. We almost never see the reverse. Conditions during lockdown were usually enough to suppress older variants, but not B.1.1.7.
When you get consistent answers from different statistical models, that's usually a good sign that the findings are robust. As B.1.1.7 is detected around the world, I hope these analyses will be useful for countries confronting this more rapidly spreading variant.

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More from @jcbarret

30 Dec 20
MHRA approval document has some information on the basis for approving Oxford/AZ vaccine. Efficacy numbers are the same (pooled) as from the Lancet paper. assets.publishing.service.gov.uk/government/upl…
There's no mention of 1/2 doses, but what's interesting is this table on antibody titres after doses 1 & 2. First of all, some effect after 1 dose, secondly way higher antibodies if second dose is >12 weeks after 1st.
Of course will be key to see if that translates into better clinical efficacy (presumably trials ongoing or starting), but I can now see rationale behind UK gov't's apparent plan: get first jab into tons of people, and space out second jab.
Read 4 tweets
29 Dec 20
Big update posted last night by @PHE_uk on the new UK variant of #SARS-CoV-2 (aka B.1.1.7 or VOC 202012/01), including first solid evidence that it does not cause more severe clinical disease. Highlights in the 🧵...
We can now see that the S-gene target failure (SGTF) in the Thermofisher TaqPath assay I've discussed before is a very good proxy for the new variant almost everywhere in England.
So we can use SGTF as a near-real-time proxy for spread of the new variant. It is present at some level everywhere in England, and has almost replaced all other variants in London and the Southeast.
Read 10 tweets
20 Dec 20
One of the key questions about the new variant (B.1.1.7) is whether there is conclusive evidence that it is more transmissible. I don't think we are absolutely certain yet, but I am pretty confident that it is more transmissible. (1/N)
First, what's the alternative hypothesis? A lineage can get "lucky" and increase in frequency because it happened to be present in local circumstances that favour growth (e.g. poor compliance with social distancing). (2/N)
A good example of this is 20A.EU1 that spread widely throughout Europe after the summer (see excellent @firefoxx66 paper: medrxiv.org/content/10.110…). So far, evidence seems to suggest that was just a "lucky" case, rather than a biological change in the virus. (3/N)
Read 9 tweets
19 Dec 20
One of the lines of evidence on transmission is in this tweet. One of the mutations in the new variant (deletion of amino acids 69 & 70 in spike) by coincidence causes 1 of the 3 channels of a widely used PCR test to drop out, giving us a way to track it in real time. (thread)
First, an important note: this assay has probes in two other parts of the SARS-CoV-2 genome, and they are not affected by the new lineage. Since not all three channels have to "light up" to declare a positive, this doesn't significantly affect test sensitivity.
Our sequencing data lags by about 2 weeks, but this read-out at test sites only lags by 24 hours, so we can see how fast the variant spreads in real time. Figuring this relationship out in the past few days was one thing that clarified the seriousness of the situation.
Read 4 tweets

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