The biology of coronavirus COVID-19 - including research and treatments

Sasha said:
What exactly is it (or could it be) about this virus that would make it more transmissible? That is, what's the biology?

I suddenly realise that I don't know what makes any virus more transmissible than another.
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A very good question. It matters whether the variant survives longer in droplets or on surfaces or is produced more profusely by presymptomatic individuals or infects at lower dose number or... whatever.

I am not sure anyone has any idea yet.

I am pretty sure that the surge in cases in the South East of England is not due to this variant. The variant cases do not account in any way for the sudden rise, which looks to be entirely consistent with inadequate social distancing policy. On the other hand it must be better at transmitting to be increasing in terms of the proportion of cases with this variant over the last few weeks.
 
Sasha said:
What exactly is it (or could it be) about this virus that would make it more transmissible? That is, what's the biology?

I suddenly realise that I don't know what makes any virus more transmissible than another.
Click to expand...

This is from July, but the same caveat applies. (lack of sufficient evidence for the claims)
https://www.virology.ws/2020/07/09/no-evidence-for-increased-human-transmission-of-sars-cov-2/



To answer the question about increased (population) infectivity, think about the mechanisms of spread at different scales.

At the intracellular scale, more efficient or effective replication (eg better at delivering the viral genes to be transcribed (DNA) or translated (RNA)), due to higher stability or more effective hijacking of cellular machinery, more effective virion reassembly or more effective exit from the cell.

At the extracellular level, more effective cell entry receptor binding or membrane fusion and entry. Greater capsid stability (in the given conditions) such that the virus can transit circulation/lymph for longer, less immunogenic cell-surface receptors.

At the host level, milder symptoms, or a higher viral load/longer infectious asymptomatic period, so that the host is more likely to come in contact with others and spread the virus.

Outside the host, greater capsid or envelope (if it has one) stability, so it can survive for longer outside a host.

At a population level, if there is pre-existing immunity in the population, then variation the viral surface receptors to evade this immunity.

Edit - I just noticed the post above. I agree with Jonathan that the most likely explanation is due to a difference in behaviour in the population, rather than the small number of differences in the spike protein that has been characterised as an important new variant by the media.
 
Jonathan Edwards said:
A very good question. It matters whether the variant survives longer in droplets or on surfaces or is produced more profusely by presymptomatic individuals or infects at lower dose number or... whatever.

I am not sure anyone has any idea yet.

I am pretty sure that the surge in cases in the South East of England is not due to this variant. The variant cases do not account in any way for the sudden rise, which looks to be entirely consistent with inadequate social distancing policy. On the other hand it must be better at transmitting to be increasing in terms of the proportion of cases with this variant over the last few weeks.
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This report talks about it I think
https://virological.org/t/prelimina...defined-by-a-novel-set-of-spike-mutations/563
Several aspects of this cluster are noteworthy for epidemiological and biological reasons and we report preliminary findings below. In summary:
The B.1.1.7 lineage accounts for an increasing proportion of cases in parts of England. The number of B.1.1.7 cases, and the number of regions reporting B.1.1.7 infections, are growing.
B.1.1.7 has an unusually large number of genetic changes, particularly in the spike protein.
Three of these mutations have potential biological effects that have been described previously to varying extents:

  • Mutation N501Y is one of six key contact residues within the receptor-binding domain (RBD) and has been identified as increasing binding affinity to human and murine ACE2.
  • The spike deletion 69-70del has been described in the context of evasion to the human immune response but has also occurred a number of times in association with other RBD changes.
  • Mutation P681H is immediately adjacent to the furin cleavage site, a known location of biological significance.
The rapid growth of this lineage indicates the need for enhanced genomic and epidemiological surveillance worldwide and laboratory investigations of antigenicity and infectivity.
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One virologist talks about cell infectivity but that it is unclear how this relates to transmission

 
Snow Leopard said:
At the host level, milder symptoms, or a higher viral load/longer infectious asymptomatic period, so that the host is more likely to come in contact with others and spread the virus.
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isn't this the way virus' are supposed to 'work'? I'm thinking of the 1918 pandemic where presumably the virus eventually mutated and stopped killing most of its hosts. (not sure of the timeline but wasn't it within 2-3 years).
I'm curious as to whether the introduction of vaccines in this instance (am not being anti-vaxxer here)
actually inhibits this 'natural' progression?
 
This is how I understand it:
The virus can't change the way it mutates. Mutations are random events, and most either have no effect on its function, or make it non functional. Sometimes variations arise that enable it to spread more easily, or are more or less virulent. So I guess what you are meaning is, what effect does vaccination have on which sorts of variants become more dominant.
 
I don't think there is any benign mechanism whereby viruses tend to get less virulent. It is the other way around, as Trish says. If they get less virulent they are more likely to be tolerated and become endemic. Smallpox never got less virulent, nor did measles.

Another way to look at it is that a vaccine is the perfect 'benign mutant' so just the thing. There is no reason to want to let a virus carry on spreading and get less dangerous. Flu does exactly the opposite. It has been allowed to become endemic and every now and again it throws up lethal strains, not benign ones. The only reason those strains do not take over is that measures are taken to limit their spread.

So allowing spread isn't a good idea.
 
BurnA said:
Is there a point where a variant becomes a strain or is there a hierarchy of mutations?
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I think terms are being thrown around ambiguously in the media.

Different flu strains have different hemagglutinins and neuraminidases and these are classified differently as they have substantial differences in structure. (often due to the viral reservoir being different species).

As such, I'd suggest this article is still true:
https://www.virology.ws/2020/05/07/there-is-one-and-only-one-strain-of-sars-cov-2/
 
On 8 December, during a regular Tuesday meeting about the spread of the pandemic coronavirus in the United Kingdom, scientists and public health experts saw a diagram that made them sit up straight. Kent, in the southeast of England, was experiencing a surge in cases, and a phylogenetic tree showing viral sequences from the county looked very strange, says Nick Loman, a microbial genomicist at the University of Birmingham. Not only were half the cases caused by one specific variant of SARS-CoV-2, but that variant was sitting on a branch of the tree that literally stuck out from the rest of the data. “I've not seen a part of the tree that looks like this before,” Loman says.

Less than two weeks later, that variant is causing mayhem in the United Kingdom and elsewhere in Europe. Yesterday, U.K. prime minister Boris Johnson announced stricter lockdown measures, saying the strain, which goes by the name B.1.1.7, appears to be better at spreading between people. The news led many Londoners to leave the city today, before the new rules take effect, causing overcrowded railway stations. Also today, the Netherlands, Belgium, and Italy announced they were temporarily halting passenger flights from the United Kingdom. The Eurostar train between Brussels and the British capital will stop running at midnight tonight for at least 24 hours.
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https://www.sciencemag.org/news/202...om-sets-alarms-its-importance-remains-unclear
 
As a German virologist points out in a Guardian quote, the extra spreadability of this variant is actually very hard to be sure of. I now realise that the massive increase in proportion of cases being this variant in SE England could just be a super spreader effect. If restrictions are favouring local superseder mini-epidemics the fact that one of those is anew variant may be of no consequence. There may be more to it than that but the German gave the impression that he did not see anything concrete so far.

The good news might be that a brisk reaction to this story might just get the necessary restrictions put in place to make next year tolerable.
 
BBC News - New coronavirus variant: What do we know?
https://www.bbc.co.uk/news/health-55388846

In this BBC article it states
"Studies by the same group suggest the deletion makes antibodies from the blood of survivors less effective at attacking the virus", with a link to paper they released.

Later in the article they ask will the vaccines work against the new variant and the answer is "almost certainly yes, at least for now" and then they conclude with:

A presentation by Prof David Robertson, from the University of Glasgow on Friday, concluded: "The virus will probably be able to generate vaccine escape mutants."

So it's not very clear to me what effect this variant will have on vaccines. Is it fair to say they just don't know yet?
 
Latest from BBC:

The government's New and Emerging Respiratory Virus Threats Advisory Group (Nervtag) has upgraded its confidence that the new variant spreads more easily, the group's chair has said.

Prof Peter Horby told a Science Media Centre briefing: "We now have high confidence that this variant does have a transmission advantage over other virus variants that are currently in the UK."

Minutes from a meeting on Friday said the group, which advises the UK government, had "moderate confidence" in this.

Another Nervtag member, Prof Neil Ferguson, from Imperial College London, told the briefing there was strong evidence the new variant is 50% more transmissible than the previous virus.

He also said there was a "hint" the new variant infects children more.

"There are other epidemiologically interesting trends with the virus, there is a hint that it has a higher propensity to infect children... but we haven't established any sort of causality on that, but we can see that in the data," he said.
 
Snow Leopard said:
Edit - I just noticed the post above. I agree with Jonathan that the most likely explanation is due to a difference in behaviour in the population, rather than the small number of differences in the spike protein that has been characterised as an important new variant by the media.
Click to expand...

So, effectively saying that the chaos we're currently going through in the UK - ports blocked, unable to travel internationally, virtually everything shut down again, inability to leave one's local area and see family at Christmas, etc. - is probably down to a false alarm?

Oh well, I suppose if it gets people to behave more responsibly and stop being complete idiots ...
 
Vincent Rancaniello, the virologist on Twiv microbe tv, said
here:



that this variant is due to probably a founder effect and then some superspreaders. He said it does not qualify by any evidence as a strain, because it has no proven clinical effect different from those we already have studied. He said sure, it is possible, but that the data are not showing that.
 
shak8 said:
that this variant is due to probably a founder effect and then some superspreaders. He said it does not qualify by any evidence as a strain, because it has no proven clinical effect different from those we already have studied. He said sure, it is possible, but that the data are not showing that.
Click to expand...

For what it's worth (not much), I strongly agree with Vincent's analysis and conclusion.
 
BioNtech CEO confident vaccine will work:

"German pharmaceutical company BioNTech is confident that its coronavirus vaccine works against the new UK variant, but further studies are need to be completely sure, its chief executive said Tuesday.

“We don’t know at the moment if our vaccine is also able to provide protection against this new variant,” CEO Ugur Sahin told a news conference the day after the vaccine was approved for use in the European Union. “But scientifically, it is highly likely that the immune response by this vaccine also can deal with the new virus variants.”

On the new strain :

"A leading German virologist who was initially skeptical about reports that the strain was much more contagious voiced concern after seeing further data. Christian Drosten, a professor of virology at Berlin’s Charite hospital, tweeted that “unfortunately it doesn’t look good.”But Drosten added: “What is positive is that cases with the mutation so far only increased in areas where the overall incidence was high or rising. So contact reduction also works against the spread of the mutation.”"
 
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