There was a scary story published today in the LA Times about the "California variant" of coronavirus, but the data behind the claims are not yet published. So here's a 🧵about this variant that does have some data in it. 1/N
What's claimed in the newspaper? Well, it sounds pretty bad: "it not only spreads more readily than its predecessors, but also evades antibodies generated by COVID-19 vaccines or prior infection and is associated with severe illness and death" 2/N
That's in the first of six paragraphs of terrifying conclusions, but we then learn the study is, "currently under review by the public health departments of San Francisco County and the state...It is expected to post late this week to MedRxiv" 3/N
I look forward to reading the pre-print when it lands. While we wait, what data do we have? Well, first of all, it is Pango lineages B.1.427 and B.1.429, which share 3 spike mutations (S13I, W152C, L452R), plus a couple other mutations that may or may not be functional. 4/N
L452R has garnered most attention, because it's in the ACE2 receptor binding domain. A quick lit search turns up a mention of resistance to some monoclonal antibodies (…) . 5/N
But there are lots of papers out now scanning for mutations that affect immune escape (e.g. @jbloom_lab's lovely papers), and L452R is not one of the famous mutations that comes up repeatedly (e.g. E484K). 6/N
More importantly (IMHO), L452R has popped up in various places without growing rapidly, e.g. in California as early as September 2020:
And in various little sparks elsewhere in the US: 7/N
And over 150 times in the UK between October and now: 7 are B.1.427 or B.1.429, with the rest spanning 19 different lineages. This is a boring picture that shows we have seen this mutation several times but it has not grown. 8/N
Of course, the UK has been in lockdown for the second half of that graph, to suppress B.1.1.7, but it was either open, or in "lockdown lite" in the first half, which I think puts some upper limit on increased transmissibility of L452R on its own. 9/N
It may be that something about the combination of mutations in B.1.427 and B.1.429 have different properties, and it may be that the upcoming pre-print has compelling data, but I don't think any conclusions can be drawn at present about this lineage based on press reports. 10/10

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More from @jcbarret

8 Jan
In the latest @PHE_uk Technical Briefing we see the #b117 variant of concern continues to spread throughout England, get bigger numbers on the secondary attack rate analysis, and see a glimpse of planned virology experiments to come. 🧵…
Using the S-gene target failure (SGTF) as a proxy (details in previous reports, updated in this report) we can see that as of January, #b117 is more than half of new infections almost everywhere in England. Of all TaqPath tests in the UK in the past few days >75% are #b117.
The SGTF data allows analysis of 2ndary attack rate in about half a million contacts of infected people. It is consistently 40% higher for #b117. This isn't a fully matched cohort, but is pretty compelling that the new variant transmits more readily in typical contact situations.
Read 5 tweets
31 Dec 20
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.…
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.
Read 10 tweets
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.…
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:…). 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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