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.
The big "blackout" zones, especially in the East are largely because the Cambridge Lighthouse lab does not use the relevant assay, and that's where most of the pillar 2 tests in that region go. Don't be fooled: from genome data we know the new variant is very common there!
Here's where the news gets good. The PHE team took ~1800 new variant cases and created a 1:1 cohort of "Covid classique" matched on age, sex, date of + test and location. They then studied hospital admissions and deaths. The two groups had reassuringly similar rates of both.
Updated analyses in coming weeks with more samples will be definitive, but for now we can firmly say that the new variant does not cause dramatically worse illness. That's a big relief.
Next analysis is on re-infection, and again no difference: 2 in the new variant group, 3 in the old variant group. Small numbers, but it pretty much rules out hypothesis that the new variant is spreading so fast by re-infecting tons of people who previously had the old variant.
Final analysis is "secondary attack rate". When you find a case and trace contacts, how many get infected? 15% for new variant vs 9% for old. There's no p-value on this finding, but my guess is that's a significant difference, and consistent with increased transmissibility.
So: the new variant is spreading fast, more easily among close contacts. But doesn't seem any better at reinfection, nor does it cause much more severe disease or death. Massive kudos to the PHE team for getting this out so fast over🎄!
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)
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.