When the B.1.1.7 variant of SARS-CoV-2 was first detected in the UK in December 2020 it was accompanied by unsubstantiated claims of increased transmissibility and virulence. The results of a hospital-based study in London reveals no association of the variant with severe disease in this cohort.
In a note published by NERVTAG on 21 January 2021, the panel concluded that ‘there is a realistic possibility that infection with VOC B.1.1.7 is associated with an increased risk of death compared to infection with non-VOC viruses.’ The death risk ratio for VOC infected individuals compared with non-VOC infected individuals was 1.65. This conclusion was based on analysis of COVID-19 related deaths at several hospitals in the UK. The authors noted in this report that ‘The data set used in the LSHTM, Imperial, Exeter and PHE analyses is based on a limited subset of the total deaths. This includes approximately 8% of the total deaths occurring during the study period’.
In the present study, SARS-CoV-2 PCR-positive samples from hospitalized patients were analyzed that had been collected between 9 November and 20 December 2020 in London. Of these, 341 (58%) were infected with B.1.1.7 and 143 (42%) were infected with an ancestral virus. Results of statistical models showed no association between severe disease and death and the B.1.1.7 lineage.
I hope that these results can begin to reverse the disturbing narrative advanced by some that B.1.1.7 is 50% more virulent than its ancestor. This conclusion was never firmly grounded, yet it has been echoed by mainstream media as if it were dogma.
Unfortunately the authors of this paper continue to promote the idea that B.1.1.7 viruses are more transmissible. Their conclusion is based on increased levels of viral RNA in patient samples as determined by RT-PCR (cycle threshold 28.8 in VOC infected patients versus 32.0 in non-VOC infected patients) and genomic reads by sequencing (1280 vs 831). Increased viral load determined by these methods might be an indication of increased viral fitness, but it does not prove increased transmission. It is not known if VOC-infected patients shed more infectious virus, which might be consistent with increased transmission. Until such experiments are done, it can only be speculated that B.1.1.7 and other VOC have increased transmissibility.
That’s good to know! Thanks, Vincent!
I thought the only way a virus could cause more severe disease.
Is by evading different immune system factors.
Otherwise, wouldn’t it continue its pattern of infection.
Since it connects within the same receptor ace2.
And replicates in the lung epithelium.
Why would alter disease pattern?
Unless its tropism has changed.
It would cause same symptoms?
Right??
I get what you’re saying here, but I think this is a situation where policy makers need to take a decision based on very weak evidence.
E.g. The UK government had to decide whether to continue the lockdown over Christmas, balancing (a) people will be upset at not getting to spend Christmas with their families (b) possible increase in deaths if easing lockdown increases transmission; against the background of (c) substantial scientific uncertainty over whether the infectiousness of the virus is increasing or not.
If you treat this as a statistical optimal decision problem, then some quite plausible assumptions about the cost (a), the cost (b), and your Bayesian prior for (c) lead you to extend lockdown on the basis of even fairly weak evidence that infectiousness might be increasing.
On the other hand, if someone wants to publish a journal article saying the variant is more infectious, a higher level of evidence might be called for. Coming back later when you have better evidence is usually an option in scientific publishing. But government planners sometimes need to make an immediate decision based on the evidence they actually have, not on the evidence they’d like to have.
A second take on this: the question about whether the variant is more infectious or not has become irrelevant now that we have some experience of how the epidemic behaves in the presence of the variant.
When the variant is new, the problem for government planners is that it introduces additional uncertainty about how the epidemic might evolve in future. Once you’ve seen how the number of infections and deaths does, in fact, behave in the presence of the variant, then the planners know the answer to the question they were interested in. Hypotheticals such as “would we be in a better position if the variant hadn’t existed†are of no pragmatic value.
British Columbia’s Health Office, Dr. Bonnie Henry, and Dr. Tam (federal equivalent for Canada) have stated that none of the variants in Canada are more virulent. Dr. Henry spoke from real world data: the absolute number of variant related to hospitalizations, ICU admissions, and deaths is growing but this growth in severe cases is proportional to the number or variant positive cases in each age cohort.
When it comes to transmissibility I am disappointed with the world’s response. I think the distinction is between science and applied science is at play; I want to improve things not simply describe them. The Canadian numbers from British Columbia (pdf) and Ontario (pdf) are unambiguous, the B.1.1.7 variant has some characteristic that, possibly combined with some cohort behavioural effects, increases spread in a given population. P.1 and B.1.351 do not beyond founder effects combined with behavioural cohorts.
It is pedantic to argue whether the B.1.1.7 variant is more transmissible or has increased fitness or a new epidemiological characteristic. The early data/anecdata is that the disease course is slightly modified and this gives rise to a different R(t) somehow. The contact tracers are reporting that transmission within households is higher with entire families contracted the variant while only one or two would be infected with the early variant. After five months it is disheartening to only be able to speculate about this important question; it should have been answered by now.
I’m disappointed that the Europeans didn’t focus on answering the mechanism of action for B.1.1.7’s new epidemiological characteristics and I am puzzled that the world is not demanding the same from Canada. Ontario and British Columbia seem to have a live multi-angle slow-motion data capture of this train wreck yet we seem to be content simply waiting for the post-mortem report.
You might like to have a look at our simulations for “70% faster” in medrxiv.org
https://medrxiv.org/cgi/content/short/2021.04.09.21255166v1 which uses the viral temporal dynamics of Xi, He [Nature Medicine Aug 2020] to relate the required increases in velocity of infections to increases in viral loads.
The required increase in viral loads could easily be clinically measured.
On the other hand, it seems that there is little argument for B.1.17 and P.1 VOCs to be more competitive than the “wild” strains, as they have become the dominant strain in many regions.
Sorry, my earlier comment related to a different medrxiv.org simulation study by mistake. The correct link is:
UK and other SARS-CoV-2-Covariants – Simulation Modeling 70% Increase
Ernie Chang, Kenneth A. Moselle
medRxiv 2021.02.05.21251230; doi: https://doi.org/10.1101/2021.02.05.21251230
Thanks
Ernie Chang
Thanks for the information!!
Yeah, because of those new variants we’re in lockdown AND under a curfew, I’m finding it more difficult this time. So, I see few possibilities here: the first test was PCR, then 22 unidentified tests, then 2 PCRs, could the testing methods be trusted consistently? Also, if he got reinected over his natural immunity either it only lasts a few months or the man was particularly fragile or the second variant was different enough for reinfection variants, so many mutations in one shot is rare they say SO if reinfection is possible with natural immunity, what does it say for vaccines? Ohhhhhhh, scary.