Merged 2019-nCoV / Corona virus

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Planigale said:
In answer to your question the selective pressure to increase virulence is the development of (partial) immunity in the host population. Partially immune hosts will be less likely to be infected, with milder shorter lived disease and less viral shedding. Either mutations that suppress or evade the immune response or increase viral shedding, will favour continued viral circulation.

Back to you, what are the selective pressures to decrease virulence which you claim is what happens.

This paper which looked at a number of viruses suggests virulence should increase during outbreaks.

This paper identifies a specific mechanism in circulating H3N2 to explain its re-emergence as it has gained increased resistance to humoral immunity, thus increasing its virulence and increasing its infectivity. There are other papers documenting similar gains in virulence in circulating strains.
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Go back and see what I actually posted.
http://www.internationalskeptics.com/forums/showthread.php?postid=12984987#post12984987

You continue to ignore the fact there is no one size (or theory) fits all. You seem to think the '80s theory was some big revelation that replaced all past ideas about microorganism evolution that came before it. That is not what happened. Rather a more simplistic theory was replaced with a more complex one. That happened across the board with evolution theory.

Around that same time, inexpensive readily available PCR amplification became available to researchers and practitioners opening the door wide to studying these microorganisms by their genetics and not just by observation and theory.

I went back to review the theory you keep going on about and their idea is a trade-off curve, but not purely a random mutation rate that can go one way or the other. That is very much consistent with what I said:
I did not say selection to milder strains was the only selection pressure. It isn't. If that were true we'd never have incredibly virulent flu epidemics.
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=https://www.ncbi.nlm.nih.gov/pmc/a...he dynamic of acute and persistent infections
An entirely different view on virulence and adaptation emerged in 1980s. A mathematical model predicted the existence of a trade-off between mortality and transmission [2,3]. The hypothesis, introduced by Anderson & May 1982 [4] and Ewald 1983 [5], assumed that host resources that could be used by the virus are limited. Therefore, increasing viral replication -- and thus transmission -- without harming the host is not possible. Transmission increases as a function of pathogenesis.
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"As a function of" does not mean randomly nor does it mean a single direct correlation. Thus the tradeoff model was introduced.

One strategy for a virus to increase the transmission to pathogenesis would be to prolong the virus existence within a host (i.e., minimize α + γ) as illustrated with arboviruses that persist in mosquitoes and HIV in humans. However, since many viruses are unequipped to establish lifelong persistence, they may evolve to maximize their yields within limited time windows (i.e., maximize β). In this connection, while describing possible virus strategies, Alizon at al [3] allude to the Achilles’ dilemma, a choice between a short and bright life (i.e. brief acute infection with high virus loads) versus a long but inglorious one (persistent infection with low virus loads excreted during longer periods). Severe symptoms or even the death of hosts may be evolutionarily beneficial for a virus if they increase the resulting number of infectious particles excreted and transmitted.
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The bolded sentence seems to be what you think happens randomly along with random attenuation.

In contrast to the classical view that prevailed over a century, some highly virulent viruses retain high pathogenicity in the long-term. The trade-off models [3] help to understand this observation. Below we describe several sets of potentially important factors driving benign/virulent infection equilibrium:
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some viruses persist for life while the others are incapable of establishing long-term persistence. In addition some viruses kill rapidly, while the others can hardly cause an apparent disease. These observations imply that different areas on the trade-off chart (Fig 1B–F) are differently accessible to various virus species (at least within the visible evolutionary timeframes), affecting their final choice of the replication strategy.
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IOW, no one size fits all.
And in some cases, like with widespread flu:
A virus strategy that involves fast and severe pathogenesis should be more efficient in very dense populations where the hosts are contacting each other more frequently. Highly pathogenic viruses should also benefit from the high rate of host’s reproduction, as this masks the declines in host’s numbers caused by infection-related death. However, such viruses indirectly limit their own progression by decimating the host population (i.e. by decreasing S), making lethal diseases a poor long-term strategy.
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Regarding your citations, are you incapable of providing links? :mad:
No one should have to look these up for you.

https://royalsocietypublishing.org/doi/full/10.1098/rsif.2009.0384

https://bmcinfectdis.biomedcentral.com/articles/10.1186/s12879-016-1738-1

I'll look at them and get back to you.
 
Dr.Sid said:
Well Earth could do with few % of humans gone. Thing is, it won't be so easy. After crisis there is war. And these days, after war there is nothing.
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That wouldn't be a good result.

Giordano said:
I would like to think that it is possible to appropriately recognize a danger and respond to it as intelligently, effectively, and forcefully as possible and necessary.
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That's exactly my point - I've both best and worst-case scenarios, as well as the middle ground.

Skeptic Ginger said:
Belz is right, TA, your posts read like a panic attack.
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Only if the reader is a moron and misses the If at the start of the post.
 
Guess I shouldn't be surprised.

India's Leaders Claim Drinking Cow Urine Will Cure the Coronavirus
India’s Prime Minister Narendra Modi and his extreme Hindu backers are making some amazing claims about science.
Indian nationalists peddle something worse than snake oil. It's the The Cow Dung Cure for Coronavirus.

Swami Chakrapani Maharaj, president of the Hindu Mahasabha—a century-old organization that advocates Hindutva (or “Hinduness”)—declared that “consuming cow urine and cow dung will stop the effect of infectious coronavirus.” The swami added that a “person who chants ‘om namah shivay’ and applies cow dung” on his body “will be saved.” The Sanskrit chant is a salutation to Shiva, a Hindu deity.

The swami is a prominent figure in hard-line Hindu circles and has an ideological affinity with Mr. Modi.
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Just when I thought India was moving forward toward the modern world.
 
Just this week at the VA Hospital I had to make some effort to move my wheelchair away from the people who, two times, came into my personal space with some hacking nonsense, not even using the standard "Cover your cough" techniques. The third time I couldn't move too far because it was the receptionist who was scheduling my next appointment. I couldn't fathom why she was even allowed to work with the public that day.
 
alfaniner said:
Just this week at the VA Hospital I had to make some effort to move my wheelchair away from the people who, two times, came into my personal space with some hacking nonsense, not even using the standard "Cover your cough" techniques. The third time I couldn't move too far because it was the receptionist who was scheduling my next appointment. I couldn't fathom why she was even allowed to work with the public that day.
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I have stories you wouldn't believe.
 
The Atheist said:
I get paid a lot of money for writing plain English, so I'm pretty happy with my skills.







Good - I hope the leaders all do that, along with taking the homeopathic remedies their ministry recommends.
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But of course they won't. Yeah they might swallow a homoeopathic pill or two, whilst accessing the best possible modern medical care that is out of reach of most of their constituency.
 
Darat said:
But of course they won't. Yeah they might swallow a homoeopathic pill or two, whilst accessing the best possible modern medical care that is out of reach of most of their constituency.
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Oh, you can bet the rent on that.
____________________________________

Meanwhile, the cruise ship in Japan is proving it's not a hard disease to catch, with 39 new cases for a total of 175, so the chances of it getting out of control just got a bit higher.

The number of serious cases outside China is still low, but the vast majority of cases are less than a week since diagnosis, so it's too early to say how many will become severe.
 
More on the classification:
Viral serotypes — Coronaviruses are widespread among birds and mammals, with bats being host to the largest variety of genotypes [12]. Animal and human coronaviruses fall into four distinct genera (figure 1) [1,2]. There are five non-SARS coronavirus serotypes that have been associated with disease in humans: HCoV-229E, HCoV-NL63, HCoV-OC43, HCoV-HKU1, and a novel coronavirus (MERS-CoV) that emerged in 2012.

The alphacoronavirus genus includes two human virus species, HCoV-229E and HCoV-NL63. HCoV-229E, like several animal alphacoronaviruses, utilizes aminopeptidase N (APN) as its major receptor [13]. In contrast, HCoV-NL63, like the SARS-CoV (a betacoronavirus), uses angiotensin-converting enzyme-2 (ACE-2) [14]. Important animal alphacoronaviruses are transmissible gastroenteritis virus of pigs and feline infectious peritonitis virus. There are also several related bat coronaviruses among the alphacoronaviruses.
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Skeptic Ginger said:
Go back and see what I actually posted.
http://www.internationalskeptics.com/forums/showthread.php?postid=12984987#post12984987

You continue to ignore the fact there is no one size (or theory) fits all. You seem to think the '80s theory was some big revelation that replaced all past ideas about microorganism evolution that came before it. That is not what happened. Rather a more simplistic theory was replaced with a more complex one. That happened across the board with evolution theory.

Around that same time, inexpensive readily available PCR amplification became available to researchers and practitioners opening the door wide to studying these microorganisms by their genetics and not just by observation and theory.

I went back to review the theory you keep going on about and their idea is a trade-off curve, but not purely a random mutation rate that can go one way or the other. That is very much consistent with what I said:

=https://www.ncbi.nlm.nih.gov/pmc/a...he dynamic of acute and persistent infections
"As a function of" does not mean randomly nor does it mean a single direct correlation. Thus the tradeoff model was introduced.

The bolded sentence seems to be what you think happens randomly along with random attenuation.

IOW, no one size fits all.
And in some cases, like with widespread flu:



Regarding your citations, are you incapable of providing links? :mad:
No one should have to look these up for you.

https://royalsocietypublishing.org/doi/full/10.1098/rsif.2009.0384

https://bmcinfectdis.biomedcentral.com/articles/10.1186/s12879-016-1738-1

I'll look at them and get back to you.
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Thank you for taking my comments seriously rather than dismissing them with 'I know better'.

I am sorry for not providing links, but my links would be behind a password protected commercial database and so would be no use to most, but for the lazy reader the abstracts are probably easier than having to click on links.

I was just trying to counter the narrative that viral infections especially flu become 'attenuated' with time. This implies if we just sit back and do nothing Sars-CoV-2 will naturally become less virulent. Whilst mutations are random, there is no reason to think less virulent strains would become dominant and some evidence to think the opposite is the case. The reason that morbidity and mortality falls with endemic flu is more to do with changes in the host population and the development of immunity than circulating flu strains losing virulence. You asked for and I provided a reference to show how a circulating flu strain mutated to gain virulence, and that mutation and increased virulence was possibly the cause of that strain becoming a dominant circulating strain.

Diseases are a bit like dating. Some pathogens are looking for a long term relationship, they will be with you for life like retroviruses, herpes viruses or leprosy. Some are just looking for a hook-up like flu or Sars-CoV-2. The former with a lifetime to transmit may be associated with relatively low transmissibility and low morbidity and mortality, some may even be principally spread vertically rather than horizontally. These are the group where evolutionary pressures may select for decreased virulence. The latter are just after a big bang, and especially when they have an infectious prodrome as we see with Covid 19, what happens after they have already moved on is irrelevant, these viruses especially in an epidemic situation may be more likely to increase in virulence as this will be associated with increased viral shedding. But as the model says there are a series of trade offs and each host / pathogen / environment will result in its own equilibrium. Some like Ebola may even be significantly transmitted by the death of the individual. Funeral practices were thought to be an important factor in the spread of Ebola, so one might even expect in that situation a selection towards killing the host.
 
Planigale said:
I was just trying to counter the narrative that viral infections especially flu become 'attenuated' with time.
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It seems that a big factor is the novel nature of the virus, as in the case of SARS:

Normally a mutation that leads to a loss of viral fitness will disappear from the population, because viral lineages with the mutation cannot compete with more fit viruses circulating in humans. Surprisingly, during the SARS outbreak, a less fit virus remained. The authors suggest that this unusual event occurred because there was no competition – SARS-CoV had just spilled over from bats and was unique to humans. It didn’t matter that the virus was somewhat wimpy – there were no other similar viruses to outcompete it.
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http://www.virology.ws/2020/01/23/a-lesson-from-sars-cov-for-2019-ncov/

With the death rate dropping from Covid-19, it might be the same kind of mutation happening there. Keep watching...
 
The Atheist said:
Jesus H Christ, if you read the thread, you'd see that all the way through I've been hopeful it is kept under control, but facts are facts
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But it's not the facts I was addressing; it's your constant fan-fiction where hundreds of millions die. Those aren't facts, they're speculation, and it always points in the same direction: catastrophe.

You can cuss all you want but the fact remains that this is what you've been doing all thread long.
 
Belz... said:
But it's not the facts I was addressing; it's your constant fan-fiction where hundreds of millions die. Those aren't facts, they're speculation, and it always points in the same direction: catastrophe.

You can cuss all you want but the fact remains that this is what you've been doing all thread long.
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It's a possibility, which can't be ruled out at the moment, and he isn't saying it's anything else.
 
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