Reader Jim Batterson sent me this 25-minute video with the comment:
I know you prefer to read rather than watch a video, but I wanted to make you aware of a 24-minute YouTube video from Vince Racaniello, a virologist at Columbia University who leads a cast of virology geezers and one younger immunologist in a weekly zoomcast production of “This Week in Virology”. He did this standalone presentation to rant a bit on the way that this latest variant in the UK is being hyped to the world. I think he does a pretty good job for any viewer who has had a biology course in the past five or so years.
Racaniello then shows the changes in the new mutant “strain”, noting that only one of the several mutants in the spike protein is even a candidate for a change in spreadability, but there is not an iota of evidence that any of those mutations actually make the strain more spreadable. Nevertheless, all of us are inundated with media scare stories about this “superspreader virus”.
Racaniello’s point is that though there are epidemiological data showing a correlation between the presence of the mutant in some areas and a greater spread of the virus, that’s just a correlation without evidence of causation. And there could be several causes, including accidents. To show this mutant is a “super virus”, you simply have to do lab experiments; epidemiological correlations show nothing.
Racaniello doesn’t rule out that this mutant spreads faster than its ancestors, but he’s not convinced it is, and doesn’t think that we yet have a reason to be concerned. In fact, he suggests that the changes in the new strain may make it less spreadable. Let me add that Racaniello knows what he’s talking about, as he’s co-author on a well known textbook of virology.
Like all good scientists, Racaniello isn’t declaring that this virus is “neutral” compared to its competitors—he’s simply saying that we don’t have any data suggesting it’s more nefarious. In fact, the same story happened earlier with a different mutant that spread widely, but nothing ever came of that. We need experimental cell-culture data from the lab on viral shedding, and that doesn’t exist.
His final comment:
“We should move on from the scary headlines, and get ahead with vaccination programs, which are underway—and that is going to be the way we get away from this pandemic.”
Anyway, this is a good and clear mini-lecture, and listening to it should calm you down a bit if the media have gotten you worried.
Cow viruses are always moootating!
Boooooo🤓
Ps mutations aplenty! As we know – natural selection is so cool!
https://www.bbc.co.uk/news/live/world-55421730
There suddenly was a lot of panic. But then again, Covid-19 has been a disruptive virus.
Heard pretty much the same take from ZDoggMD, who I frequently check with through YouTube. Probably he wouldn’t appeal to everybody with his style, and his videos can go too long. But generally good info. And he has interviewed some excellent folks.
To understand the spike region or reactive binding domain to better understand Vince’s talk, readers might view britt glaunsingers talk, lecture 2 in the free mit series of one-hour video lectures on sars/covid19…a generally excellent set of lectures geared to a general (but educated) audience at url.
https://biology.mit.edu/undergraduate/current-students/subject-offerings/covid-19-sars-cov-2-and-the-pandemic/
I think our current infection rate numbers are good enough evidence for me to be convinced that the new virus spreads more easily. Infections are increasing dramatically in London and the South East in spite of our current strict precautions.
Even if it is not more virulent than other strains of the virus, there is still cause for worry due to the effects of panic.
For example, France closed its border with the UK leading to Kent being turned into an enormous lorry park. There are thousands of lorry drivers there now without adequate facilities for hygiene and food, many of whom will not make it home for Christmas. They’re angry. The locals are angry and tension is high.
Some of the information about the 1918 flu seemed to show super fast transmissions when the flu returned later after having gone down. Of course they had no science on this at the time but it caused lots of panic.
Test
You passed the test, but that does not mean you are virus free!
My small friend who is 22 months old had it in March, & just tested positive again 😥
First time he was in hospital anyway & ran a fever but was OK.
Racaniello’s 2020 Columbia U virology course in on YouTube. It is very good.
‘..the variant may not have any effect on spreadability itself but can increase in frequency as a byproduct of “superspreader events”—’
But that’s precisely why the British medical advisers are alarmed . All the other variants came to prominence during periods of low prevalence, when a single superspreader event can have a large influence.
But this variant came to prominence in a period of high prevalence (when a superspreader event doesn’t have much of an impact) and it showed exponential growth during semi-lockdown conditions in November.
I’d call this high evidence of higher spreadability.
Something can be growing at an “R” equivalent to 1.00000001 (or a doubling time of 1000 years) and still be undergoing exponential growth. “Exponential” has a very specific meaning, and it is not “rapid”. (See also exponential decay, etc.) Sorry, that’s just a pet peeve. Rapid exponential growth with a case doubling time of a week or two is something to worry about.
It is certainly concerning, but the evidence you cite is also not incompatible with, for example, people deliberately spreading the virus by distributing secretions from a “farm” (Petri dish? Nursing home?) of patients onto public transport doors, handrails, etc. I know of no evidence for this proposition, but that is why we test hypotheses with experiments.
No, I wouldn’t put such behaviour past any one of several groups of humans – and they’re not all religious lunatics. For someone who saw financial profit in such a move, they could even call it “rational”, and probably attract venture capital funding.
“..“R” equivalent to 1.00000001 (or a doubling time of 1000 years..”
To give a time, as you did, you need to know how often the ‘splitting’ takes place.
If, with R=1.01, then 100 cases gives 101 cases, but only once a year, it’s not the same as if it happens once every 3 seconds.
Talking heads on TV are not statistical geniuses usually, but like to babble slogans.
I just came across new (to me) evidence which supports Ruth’s point. The increase of proportion of this new strain has been going on for many weeks, in addition to the fact that the virus is already widespread. See Figure 3 in this report.
A few superspreader events coinciding is not a very likely explanation of these data, as far as I can see. (I am not an epidemiologist.) Furthermore they give the new variant “an estimated potential to increase the reproductive number (R) by 0.4 “. That’s huge. That means if your region currently has an R of 0.6 – meaning doing great at reducing the infection rate – and the new variant takes over and the people’s behavior doesn’t change, now your region is just treading water.
Carl Zimmer and Benedict Carey did a reasonable treatment of the new strain and it’s impact in today’s NYT.
(sorry if this is a double posting, there was a problem while sending the comment)
‘..the variant may not have any effect on spreadability itself but can increase in frequency as a byproduct of “superspreader events”—’
But that’s precisely why the British medical advisers are alarmed . All the other variants came to prominence during periods of low prevalence, when a single superspreader event can have a large influence.
But this variant came to prominence in a period of high prevalence (when a superspreader event doesn’t have much of an impact) and it showed exponential growth during semi-lockdown conditions in November.
I’d call this high evidence of higher spreadability.
Shouldn’t have written high evidence here, but good enough evidence..
For another view of the new variant, see this article just published by the British Medical Journal: https://tinyurl.com/ybzedwma. Footnote 1 includes a link to the the UK’s New and Emerging Respiratory Virus Threats Advisory Group’s initial analysis of the variant.
This is not a different view from the one in the video. As the article says:
That’s based on epidemiology, which–and I agree with Racaniello here–epidemiology cannot by itself determine whether there are innate genetic differences between strains that affect spreadability. You need experiments to do that.
The NERVTAG analysis appears to have been based on four converging factors:
“Four analytic approaches were reviewed regarding the transmissibility of VUI-202012/01
o Growth rate from genomic data: which suggest a growth rate of VUI-202012/01 that
that is 71% (95%CI: 67%-75%) higher than other variants.
o Studies of correlation between R-values and detection of the variant: which
suggest an absolute increase in the R-value of between 0.39 to 0.93.
o PCR ct values: which suggest a decrease of ct value of around 2 associated with
the new variant.
o Viral load inferred from number of unique genome reads: which suggests 0.5
increase in median log10 inferred viral load in Y501 versus N501.”
On this occasion, I disagree with Vincent. He’s taking a purist scientific view of this issue, and is (technically/scientifically) correct. The problem is that if we wait until we have the perfect data, it’ll be too late to do anything about it. No-one is saying it’s proven, what they are saying is that we have enough data to say we should take some action ‘just in case’. All we really have is the rate of increase in this particular variant, but that increase really is very striking – all the more so because it’s happening in the background of fairly high transmission levels, where founder effects should be less of an issue. So I think it’s appropriate to be alarmed, albeit that we accept it isn’t proven, and might turn out to be unwarranted. Can you imagine if we didn’t take action, and it really does spread 70% better than the old strain?!
Agree. Better err on the side of caution. If Europe/US had acted on that principle when Covid first emerged, we would have had far less morbidity and death up to now.
But that would have cost our government’s cronies and (literal) neighbours the opportunity to snout at the public trough to the tune of literally billions of quid. And that is definitely an unacceptable outcome.
I think the same.
Ok, but one can’t have it both ways. It’s no good saying to the anti-mask idiots that they should ‘trust the science”, then turn around and say we don’t trust the science when an actual virologist says there’s no evidence yet of higher transmission of a specific new strain.
This argument doesn’t really work – I’m an ‘actual virologist’, as are many of the people on NERVTag, and we’re all saying ‘there’s enough evidence here to make it worth acting as a precaution’. It’s not black and white, of course – that’s why I tried to make clear in my post which aspects of Vincent’s post I disagreed with, and why. But no-one is saying we shouldn’t trust the science – we’re saying that the science isn’t yet settled, but sometimes we have to act on imperfect science, because not doing so would be really bad.
I think that vince would also say (since i hear him say these things every week on his TWiW-cast) in addition to getting on with the vaccination program, that we MUST (everyone) practice universal public health precautions of distancing, mask wearing, frequet hand washing, staying away as much as possible from indoor public places. These are not yet 100% habits in the U.S. even with the strain or strains that are currently taking in excess of 3000 lives a day…every day. Universal precautions are appropriate regardless of the strain.
Look, in 2002 we got SARs-1 and now in 2019 SARs-2, aka Covid-19. The first seems to have come from a civet and the second a hammerhead bat, perhaps via pangolins raised or captured for human consumption. Don’t tell me this category of virus doesn’t or can’t dangerously mutate; it can and did, twice in the past 20 years. Covid-19 started in very modest source, many many times smaller that the virus population breeding at present. The rational path is to aim to eradicate Covid-19, like was done with smallpox, and to force societies to suppress practices that favor new viruses like these to enter human populations. The next time we humans may not be so lucky, as lucky as we have been up until now.
Testing. . . . . 1,2,3
As it happens, the fifth edition of Principles of Virology has just become available.
Damn your principles!
😁
I just watched Admiral Brett Giroir interviewed about this strain from England. Regardless of what anyone thinks of him as Assistant Director of Health appointed by Donald Trump, he is a 4 Star Admiral in the U.S. Public Health Service and he was very forthcoming in the interview. Anyway, he said that it seems the strain may be more spreadable or contagious (I forget which word he used) and if it is, it’s undoubtedly already in the U.S., but there is every reason to believe that the vaccines already being given to Americans are effective against this strain the same way it is against others. The only way to know though is to test it, he went on, and we will know definitively within a few days but not in the next 24 hours.
That’s more than I’ve heard from anyone else on the subject. He didn’t appear to be trying to reassure anyone, but I found him reassuring anyway. He answered each question in a straightforward manner as thoughtfully as he could. It seemed that way to me.
I once decadently binged hour after hour on This Week in Virology and This Week in Parasitology. This was back in 2011 when I did a cross-country drive. Very pleased to see this video by Vincent Racaniello. Thanks for posting it, Ceiling Cat.
His Lectures in Virology, available via YouTube, are excellent, too.
A new preliminary analysis by a team at London School of Hygiene and Tropical Medicine offers a summary of some molecular evidence that supports the hypothesis that the new variant is more infectious:
“VOC 202012/01 is defined by 17 mutations (14 non-synonymous mutations and 3 deletions), among which eight are located in the spike protein. At least three mutations have a potential biological significance. Mutation N501Y is one of the key contact residues in the receptor binding domain and has been shown to enhance binding affinity to human ACE2 (2, 3). The function of mutation P681H is unclear, but it is located immediately adjacent to the furin cleavage site in spike, a known region of importance for infection and transmission (4, 5). The deletion of two amino acids at positions 69-70 in spike has arisen in multiple independent circulating lineages of SARS-CoV-2, is linked to immune escape in immunocompromised patients and enhances viral infectivity in vitro (6, 7). This deletion is also responsible for certain commercial diagnostic assays failing to detect the spike glycoprotein gene (S gene drop-out), with genomic data confirming these S gene target failures are primarily due to the new variant (1). Accordingly, molecular evidence is consistent with a potentially altered infectiousness phenotype for this variant.”
See here: https://tinyurl.com/yc9c3uk2.