Naked Science Forum
Life Sciences => Physiology & Medicine => COVID-19 => Topic started by: set fair on 20/12/2020 06:58:13
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I'm sick and tired of "there's no evidencs it leads to more serious illness". We paid for (or more accurately we will pay for) the bally research - any chance of us seeing it? For example, are the 17 mutations cumulative from 17 different events, I haven't even been able to find the answer to that.
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"there's no evidencs it leads to more serious illness" is a political statement. They could just as easily say "there's no evidencs it doesn't leads to more serious illness". Basically, no one knows yet and they are trying to put a good spin on things.
Even where there are known mutations (and there are a lot) it is difficult to tell whether they are responsible for increased transmission, illness or death in different countries. At the moment this increased transmission is a correlation not a known causation, but there are a lot of resources, including Porton Down being thrown at it so we maight see results soon.
If you are interested in worldwide mutations, this is an interesting overview https://www.frontiersin.org/articles/10.3389/fmicb.2020.01800/full
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We'll publish a podcast on this shortly, but for now here's a summary of what we know about VUI-202012/01, the catchy name given to the new "variant under investigation" dubbed the "new variant".
The variant was first detected in September by the Covid-19 Genomics UK consortium (COG-UK), which has so far analysed over 140,000 genomes from UK covid patients. Their role is to track genetic changes in the circulating viruses in order to spot the emergence of changes that might alter the pattern of disease activity.
When it was first highlighted, the new variant, which carries a constellation of 17 changes, was present in only a small proportion of positive tests. It was present across the country but concentrated chiefly in the east, southeast and parts of Greater London.
By November, the fraction of positive tests attributable to this variant had grown to about a quarter, and by mid December it was accounting for up to 60% of cases in some places.
Because these detections map onto the same parts of the country where the rates of change of coronavirus cases are growing most rapidly, scientists suspect that the new variant might be up to 70% more transmissible than existing Covid-19 strains. This, modelers suggest, has the potential to increase the value of R (the reproductive number) by 0.4.
Increased transmissibility is not surprising; all viruses evolve to optimise their spread through their hosts, and Covid-19 has done this already earlier in the year through the emergence of the D614G mutant that appears to be "spikier" and hence "stickier" making it more infectious.
The changes carried by the new variant have been documented in a pre-print paper (https://www.biorxiv.org/content/10.1101/2020.12.14.422555v2); they show that the new viral strain includes changes to the gene that encodes the viral "spike" that is used to infect cells. Changes here might confer enhanced infectivity. But because the spike is not involved in how the virus physically replicates once it's inside cells, the actual virulence or severity of infection is not likely to be impacted.
The spike protein is also the target of neutralising immune responses to the virus and is the element represented in the vaccine. This makes us concerned that the agent might therefore be evolving to sidestep immunity conferred by the vaccine, but for the moment, there is no evidence that this is case. Porton Down are actively pursuing this and I would expect to hear answers quite rapidly since these experiments are extremely easy to carry out.
As more information emerges, I'll report on it here.
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are the 17 mutations cumulative from 17 different events
People who watch these things suggest that there is a new mutation (RNA base-pair change) about every 2-4 weeks.
- This is a fairly low rate of mutations for an RNA virus. It is due to a copy-auditing gene in SARS-COV2, which validates each copy (although sometimes, the audit process overlooks a mutation).
The mutation is additive to virus which spawned the mutation.
- However, there are thousands of strains circulating around the world, so the new mutation is not additive to all of the thousands of previous mutations; it is only additive to the mutations in it's ancestors, back to it's first human "Patient Zero".
You can see a "family tree" of SARS-COV2 strains here (wait a minute for it to load):
https://nextstrain.org/ncov/global
You can zoom into your region, or just strains found in your country.
The actual viral sequences are available on the GISAID website:
https://www.gisaid.org/
Here is what GISAID says about the latest virus from the UK (and how it relates to previous 24,746 virus strains sampled from the UK):
UK reports new variant, termed VUI 202012/01
The United Kingdom reported a new variant, termed VUI 202012/01 (Variant Under Investigation, year 2020, month 12, variant 01). It was defined by multiple spike protein mutations (deletion 69-70, deletion 144-145, N501Y, A570D, D614G, P681H, T716I, S982A, D1118H). There are currently 24,746 viruses from the UK in GISAID EpiCoV with a collection date since 1. November. A small fraction of them, about 6% (all from clade GR) share several of these mutations.
As seen on many occasions before, mutations are naturally expected for viruses and are most often simply neutral regional markers useful for contact tracing. The mutations seen have rarely been affecting viral fitness and almost never affect clinical outcome but the detailed effects of these mutations remain to be determined fully.
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I'm sick and tired of "there's no evidencs it leads to more serious illness".
Would you prefer the scientists to lie, and tell you that there is evidence?
Perhaps you would prefer less a less "formal" approach like "FFS! It's new we haven't found out yet."
It seems that you problem is that you are asking scientists, rather than someone who will look into a crystal ball for you- provided that you cross their palm with silver.We paid for (or more accurately we will pay for) the bally research - any chance of us seeing it?
You may be aware that we now have a choice of vaccines for this virus which was unknown to science a year ago. The scientists (and others of course) have been rather busy.
Stop whingeing; you sound like a kin in a car asking "are we nearly there yet"
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But you have to admit it is politically convenient.
Having blown any possibility of controlling the epidemic by "saving Christmas", HMGovt was rapidly acquiring egg on face as the hospitals began to fill up.
You can't admit to being wrong if you are a politician (it's the career of choice for sociopaths) so you have to wait for a new reason to change the rules. Just in time, a sort-of-scientific justification for finally doing the right and obvious thing, only 10 months too late to avert a disaster.
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I wondered if this mutation was real or just an excuse for politicians to U turn after making a crazy decision to get everyone infected over Xmas.
A bit of both I think.
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I wondered if this mutation was real or just an excuse for politicians to U turn after making a crazy decision to get everyone infected over Xmas.
A bit of both I think.
When the data isn't published, I'm sure lotd of people will wonder. One of the future hurdles is going to be % vaccine uptake. A serious obstacle is conspiracy theories and not being open and telling us all the facts stokes these theories.
I had thought that mutations were one neucleotide at a time for corona viruses. Here we have double deletions - are these thought to have been one at a time (coincident birthdays theorem) or together? I also thought deletions led to frameshift which would render the mutant unviable.
Are we to expect that 'spreads more quickly' means a lower innoculum is needed for illness?
Thanks for the replies.
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A serious obstacle is conspiracy theories and not being open and telling us all the facts stokes these theories.
LOL
Someone telling everyone there's a G where there should be an A at the thousandth base pair is going to stop conspiracy theories.
What stokes the conspiracy nuts is when we start saying " we don't know, but we think it's probably X"
And then we get some more data and say "No, sorry, it turns out it was Y; we did say we weren't sure."
And all the covidiots say "They don't know what they are talking about: why should we wear masks?"
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Are we to expect that 'spreads more quickly' means a lower innoculum is needed for illness?
Which part of
"FFS! It's new we haven't found out yet."
didn't you understand?
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On a scale of one to ten, how convenient is it for Boris to be able to blame cross channel delays and difficulties in early January on quarantine rules rather than Brexit's abject failure?
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One of the future hurdles is going to be % vaccine uptake.
The BBC were filming at Danbury surgery in Essex last week. One of the staff said that they were having quite a few people refusing the vaccine, not because of safety worries, or even Bill Gates' microchips, but because it's made by them forriners, and not British.
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And within 24 hours, the French have noticed that closing the channel ports severely inconveniences the wine and cheese trade at this time of year. Intriguingly, the queue of trucks on the roads today seem to be mostly empties trying to get back to Europe.
The sick joke is that the new beast has spread from Kent, suggesting its origin is actually France.
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One of the staff said that they were having quite a few people refusing the vaccine, not because of safety worries, or even Bill Gates' microchips, but because it's made by them forriners, and not British.
Nice to know there are still people willing to die for their country
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I had thought that mutations were one neucleotide at a time for corona viruses. Here we have double deletions
Yes, the vast majority of mutations occur one nucleotide at a time.
- The average number of mutations since the original Wuhan RNA sequence is around 7 or 8, although some variants have been seen with twice this number
The fact that this variant has suddenly turned up with multiple changes affecting multiple nucleotides has led some to suggest that perhaps the virus infected another host (which encourages more radical mutations), circulating in the other host for some time (accumulating more mutations) before jumping back into humans.
- This recent variant is known to be distinct from the outbreaks seen on mink farms in Europe
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........, circulating in the other host for some time (accumulating more mutations) before jumping back into humans.
There is also a suggestion that the host may have been a human who has been ill for some time allowing multiple mutations. We also know that some familiar animals such as dogs and cats can take in the virus.
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UPDATE 23/12/20
The mutations identified in the new variant have been documented in this paper: https://virological.org/t/preliminary-genomic-characterisation-of-an-emergent-sars-cov-2-lineage-in-the-uk-defined-by-a-novel-set-of-spike-mutations/563
This is a screenshot of the reported changes:
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Current questions surround the suggestion, made by epidemiologist Professor Niall Ferguson, that the agent might be better at infecting children. This is speculation at this time and requires further analysis and biological confirmation. I'll address this question, and the argument that an immunocompromised patient with Covid-19 might have been the origin of this new variant, in my next post.
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Vincent Racaniello, who should know if anybody does, says that the evidence isn't strong enough to say that the new variant is more infective, on the other hand a virologist might not like being told by epidemeologists
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Vincent Racaniello, who should know if anybody does, says that the evidence isn't strong enough to say that the new variant is more infective, on the other hand a virologist might like being told by epidemeologists
This article in Scientific American gives a perhaps more balanced view:
https://www.scientificamerican.com/article/the-u-k-coronavirus-mutation-is-worrying-but-not-terrifying/
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Perhaps in the UK (and some other countries) there was some immunity to the previous variant (eg cross-immunity from the most recent common coronavirus outbreak here) and the new variant spread so fast, not because it was much more infectious but because that partial immunity didn't extend to the new variant - ie we as a population are more susceptoble to the new variant. The new variant doesn't seem to be surplanting older variants everywhere.