Coronavirus (No Politics)

Correct. Mutations are random, and there's no guarantee, considering how quickly the virus mutates that we won't see a more dangerous variant.

After all two of it's sieblings, the original SARS and the MERS virus have a lethality of correspondingly 10% and up to 30%. Fortunately, they did/does not spread as easily as the bugger harassing us now. Yet.

pibbur who is a bit troubled by this

You are of course correct in that a more dangerous variant could arise by chance. This could, for example, happen if a mutation that increases lethality happens to coincide with another one that increases transmissibility. However, that would be a coincidental effect, while off the top of my head I cannot think of many mechanisms that would actively select for greater lethality. Any more lethal strain arising by chance would also need an edge to transmissibility in order to outcompete all its brethren.

I'm just speculating here, but I'd guess that being able to reproduce more rapidly in the upper airways immediately after infection would be what would have the biggest effect on transmissibility, but at the same time, this would probably increase the chance of triggering the immune response before the virus gains a foothold in the lung, which might help reduce the severity in most cases. Such a mechanism, if it is more than speculation, would actually favor an anticorrelation of transmissibility and lethality.

So while a more aggressive strain that also has enhanced transmissibility is something that's certainly in the realm of the possible, I'm not seeing any active selection mechanism that would make me expect such a combination beyond the pure coincidence of two traits acquired by unrelated mutations.

But of course, the more of the buggers there are in the world, the higher the chance of a such a coincidental mutation becomes, so it's in the best of our own interest not just to get vaccinated ourselves, but also make sure that developing countries get sufficient vaccine supplies and logistical support.
 
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Correct. Mutations are random, and there's no guarantee, considering how quickly the virus mutates that we won't see a more dangerous variant.

After all two of it's sieblings, the original SARS and the MERS virus have a lethality of correspondingly 10% and up to 30%. Fortunately, they did/does not spread as easily as the bugger harassing us now. Yet.

pibbur who is a bit troubled by this

I am not sure that mutation are always random anymore. There are a couple of books on stress induced mutations. Like when something is having trouble surviving that it has some effect on mutations. Those books are quite expensive so i never bought them.
 
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It doesn't have to develop both more transmissibility and lethality. A mutation of the omikron strain which already seems to be more transmissible into a more lethal variant would be a real problem. And it doesn't have to replace current strains to make real havoc. For many infections, like for instance influenza several strains are at work all the time, some more dangerous than others.

It has been said that a less lethal variant of a virus would outcompete a more deadly one and therefore the virus will become less dangerous over time. That's not entirely true. First it's relevant only if there is a limited number of hosts, which clearly is not the case now, meaning, there are at the moment few selection mechanisms that would prevent development and establishment of a more deadly variant. Secondly, we have lots of examples of highly infections diseases remaining deadly, like smallpox which killed around 25% of it's victims to the end of it's days. Or diseases becoming more significantly deadly like the influenza strain causing the Spanish flu.

As for what affects transmissibility, yes, the number of viruses is important. But also several other factors, like how it spreads: droplets vs airborne, and how easily virus is able to infect a vicitim (which may be due to how easily it binds to the cells). Higher proliferation of viruses in the airways, won't necessarily induce a stronger immune response. Anyhow, it takes time from infection to developing an immune response, thus the patient may be contagious for a long time before that happens.

pibbur

PS. About droplet vs. airborne transmission, consider measles which transmits via airborne aerosols. For measles, 1 m distance is not enough, and the virus may remain airborne for hours, which means you can be infected after the source of infection has left the room. This is also illustrated by the R number of the measles virus which is around 15. Covid 19, who AFAIk mostly transmits via droplets, would without any restrictions have an R-number of around 3, far less, but still enough to infect a lot of people when there's little immunity. DS.

PPS. There is also another mechanism that is relevant for some viruses. Sometimes, if a host is infected by two related virus strains at the same time, a combination of the two may arise. This is why we are afraid of coinfections with bird flu (dangerous, but not very contagious in humans) and swine flu (less dangerous, but highly contagious). I don't know if that is a problem with coronaviruses, but as I've said earlier, there are very deadly coronaviruses (especially MERS) which would be a significant problem if they could combine with the COVID virus. Fortunately, at the moment this is speculation. DS

EDIT: There are hints that the omikron strain may be at least partially a result of coinfection with common cold, resulting in a virus with properties of both viruses, and that this may be responsible for the omikron infecting vaccinated people and people formerly infected with covid. It's not as far-fetched as one might think, after all there are many coronaviruses causing the common cold. Fortunately it's supposed to be easy to "edit" the current vaccines (at least the mRNA types) to protect against the new variant.

I found some references yesterday, but can't find them now (possibly they're listed on the second page of Google reults, which no one visits) DS.
 
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I am not sure that mutation are always random anymore. There are a couple of books on stress induced mutations. Like when something is having trouble surviving that it has some effect on mutations. Those books are quite expensive so i never bought them.

Interesting. Could you give me some examples of books.

pibbur, who as a filthy rich Norwegian, might want to take a look at them. DS.
 
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I am not sure that mutation are always random anymore. There are a couple of books on stress induced mutations. Like when something is having trouble surviving that it has some effect on mutations. Those books are quite expensive so i never bought them.

Interesting indeed. Are you sure they were not merely talking about selection pressure on populations in general, but about mechanisms applying to individual specimen?

They might also have been referring to epigenetics, but I'd presume that this wouldn't apply to vira, seeing as they don't have a metabolism nor mechanism for gene expression of their own, or do they?

pibbuR said:
It doesn't have to develop both more transmissibility and lethality. A mutation of the omikron strain which already seems to be more transmissible into a more lethal variant would be a real problem. And it doesn't have to replace current strains to make real havoc.

It probably depends on how you define havoc. There are probably already around ~100.000 people in the world with the Omicron strain. So if one of them mutated into killer-Omicron, statistically you still wouldn't expect more than 1/100000 of the world's population to ever be affected by the killer variant at any later point, would you? That would only be a blip in total mortality rates.

Of course, it's always possible that an unlucky coincidence or a coincidental mutation might give that particular substrain an edge. But that's the very question that I'm trying to get at for the purposes of risk evaluation: Is the scenario of a "killer mutation" spreading far and wide just dependent on coincidence, or are there any active biological mechanisms that might enhance that probability?

Or, more precisely, is p(strain becomes dominant | strain is more lethal) <,= or > p(strain becomes dominant)?
 
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I think you misunderstand several things here. However, to be sure (and give a sensible response) I have to check a few things. I will come back to you, but it will take a couple of days.

pibbuR who admits he is a bit rusy on a couple of (many?) things
 
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My brother-in-law did survive his bout with covid, first he was downgraded and moved out of ICU, and two days later he was home. He's still a bit under the weather yet able to sleep in a normal bed again, and most of the respiratory issues have cleared up. We're all super grateful for this outcome!
 
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My brother-in-law did survive his bout with covid, first he was downgraded and moved out of ICU, and two days later he was home. He's still a bit under the weather yet able to sleep in a normal bed again, and most of the respiratory issues have cleared up. We're all super grateful for this outcome!

Good to hear. Wishing him a full recovery.
 
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Interesting. Could you give me some examples of books.

pibbur, who as a filthy rich Norwegian, might want to take a look at them. DS.

Interesting indeed. Are you sure they were not merely talking about selection pressure on populations in general, but about mechanisms applying to individual specimen?

They might also have been referring to epigenetics, but I'd presume that this wouldn't apply to vira, seeing as they don't have a metabolism nor mechanism for gene expression of their own, or do they?

Its been a while since i saw the books on it. But here is one such paper on it:
https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC3319127/

This isnt one of the books i saw but a new one:
https://books.google.com.au/books/a...ion_and_Evol.html?id=qczzBwAAQBAJ&redir_esc=y


The books i saw prior were written by professors in the field but i have forgotten their names so i cant seem to find them. Apologies for that.
 
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On a more boring note - got my booster yesterday evening (4:30pm GMT). Have a slight ache when reaching for things that are high up. Slept ok. Drinking lots of tea (is this a side-effect?). Otherwise ok.
 
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Its been a while since i saw the books on it. But here is one such paper on it:
https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC3319127/

The books i saw prior were written by professors in the field but i have forgotten their names so i cant seem to find them. Apologies for that.

That's fascinating reading, thanks for sharing! This mechanism probably doesn't apply to a virus, but still - nature never fails to amaze, always one more layer of complexity to discover.

And fortunately, one doesn't even have to be Norwegian to read this. Nor filthy rich.
 
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Hope so.

From the BBC site:

"Almost 70 medics who attended a large Christmas party in southern Spain have since tested positive for Covid-19, authorities say.

Most of the 68 infected are doctors and nurses working in the intensive care unit at Mailaga's regional hospital.

Health authorities said they were all at a party attended by about 170 people last Wednesday.

All guests returned negative antigen tests before the event but more than half are now isolating."


Not sure what to draw from this. About 74% of the total population in Spain have been fully vaccinated and 9% have had booster shots, according to the latest data. I suppose it just requires a false test result or some-one not taking the test but being infected to give these kinds of results.
 
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I also live in the NE of the US and seen similar things in many grocery stores. Not as bad as that shot but there are plenty of holes and empty areas spread out in certain places where they used to be full.
 
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Not here in The Netherlands. Why is it like that? Is it because of people hoarding, or is it a supply chain issue?
Although I suppose the latter could cause people to do the first.
 
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Not here in The Netherlands. Why is it like that? Is it because of people hoarding, or is it a supply chain issue?
Although I suppose the latter could cause people to do the first.
Hoarding plays a factor but based on data available it's mostly due to supply chain issues. The lock-downs and quarantines around the world messed up supply.

As once the lock-downs ended citizens wanted more supply and the makers are finding they can't keep up due to shortages of components. Especially electronics.

Then we have various ports just sitting full of merchandise that's not getting shipped at all. Mostly on the western side. So the trailers keep backing up more and more.

It also doesn't help that China is part of the problem with the freighters being stalled. You also have to factor in renting and shipping those containers has tripled or more.

In the end it's thousands of little bottlenecks ruining the supply system/chain globally.
 
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Not here in The Netherlands. Why is it like that? Is it because of people hoarding, or is it a supply chain issue?
Although I suppose the latter could cause people to do the first.

I live in a very seasonal area where a lot of people come for just the winter months, so that might also be a factor.
 
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