Is Wuflu bound to evolve to become milder? No. That does not always happen. For example, smallpox remained highly lethal for thousands of years. Falciparum malaria remained dangerous over thousands of years, as did sleeping sickness.
Consider myxomatosis, introduced to Australia in an attempt to exterminate those wascally wabbits. Originally, it kill > 99% of infected rabbits. But after a while, rabbits were evolving greater resistance, and the virus changed as well. It only killed 75% of them, or even as low as 50% in some cases. Utterly harmless !
It has continued to evolve: it now has some capability to shut down the immune system, more effectively in lab rabbits than in wild rabbits, that have been co-evolving.
Is this coronavirus being selected for lower virulence? Understand first that it already has fairly low virulence – it only kills a few percent of those infected. It is already mild, as such things go.
Myxomatosis virulence was near 100% – it had nowhere to go but down. You could certainly imagine tradeoffs that reduced virulence and increased transmission. Not the same story for Wuflu: at most it could only gain a few percent of fitness by becoming milder, and if that entailed lower viral production and less transmission, becoming milder might well reduce viral fitness. Indeed, since it seems to be transmitted efficiently in hospitals (a significant percent of all Italian medicos are now infected), higher virulence might be favored.
Consider the American elm, or the American chestnut. How are they doing nowadays?
West Hunter 
Here’s an interesting report: 99% of Those Who Died From Virus Had Other Illness, Italy Says
“The Rome-based institute has examined medical records of about 18% of the country’s coronavirus fatalities, finding that just three victims, or 0.8% of the total, had no previous pathology. Almost half of the victims suffered from at least three prior conditions and about a fourth had either one or two previous conditions.
More than 75% had high blood pressure, about 35% had diabetes and a third suffered from heart disease.”
https://www.msn.com/en-us/news/world/99-25-of-those-who-died-from-virus-had-other-illness-italy-says/ar-BB11mr4X
The actual study is in Italian, so I can’t look at it, but, it seems like very good news for older people who are healthy. The reason more older people are dying at a higher rate is probably just because older people have a higher rate of heart disease, high blood pressure, and (type II) diabetes. Hard to know if there are real medical reasons why having those conditions make people more vulnerable to the corona virus. It may be that having those conditions are just a marker of how robust your immune system is. But it seems people who are healthy aren’t dying at an elevated rate regardless of their age.
1/3 of American adults have high blood pressure. More than half over 50. Some are misinterpreting “co-morbidities” to mean “at death’s door”.
Do American and Italian doctors use the same definition of high BP?
Good question. I sure don’t know.
High blood pressure seems to be way out in front of everything else as a risk factor. Is this significant, or just some random piece of noise?
(I have no competing interests; my blood pressure tends to be low.)
The previous SARS-CoV induced acute hyperglycemia, and the extent of hyperglycemia was an independent predictor of mortality (https://link.springer.com/article/10.1007/s00592-009-0109-4) (https://sci-hub.tw/https://onlinelibrary.wiley.com/doi/full/10.1111/j.1464-5491.2006.01861.x).
Hyperglycemia inhibits thioredoxin ROS-scavenging, which results in inflammation, and its very presence implies that serum glucose would be getting uptaken and likely catabolized by a more insulin-sensitive organism.
Being that glycolysis is our main way of getting ATP without oxygen, who wants to leave sugar on the table while they’re hypoxic? Who wants runaway inflammation while they’re atherosclerotic?
We need to seriously consider insulin therapy for COVID-19 patients, especially with pre-existing conditions. It could be as simple as upping their dose. I’d want to see it done in macaques, but nobody at the national primate research centers would want to infect monkeys with SARS-CoV-2 — not unless they had sold the monkeys to another facility, far away from their colonies. I don’t know if it could get past an IRB without animal trials, however.
Dr. Cochran, where could I take this?
Consider the Spanish flu.
It broke out in two waves, and the second was far deadlier than the first. Apparently, the first outbreak was among civilians, where selection favored mild symptoms (the virus “wanted” people walking around infecting each other).
The second outbreak hit soldiers in trenches. If you became extremely sick you were sent to crowded field hospitals, or discharged from the armed services. Here selection favors bad symptoms: only severely ill soldiers got to spread the disease outside the trenches.
Much depends on the circumstances. We certainly shouldn’t assume that viruses invariably mutate into less dangerous forms like it’s some kind of natural law.
Just heard an interview live-streamed on Youtube . A healthy young man was a named contact of a couple who returned from Italy to New York. He tested positive.
He lives alone in his own house. He arranged for food to be left outside his door.
He felt ill for several days but said he’d had worse flus. He recovered no problem.. Still in self quarantine.
How exactly does virulence affect how well the virus can infiect new gosts? Obviously, a dead host compromise virus chances to infect new hosts, so this is a negative relation between virulence and transmission.
And visibly sick people are also automatically avoided by many potential hosts, so that’s another.
But this one is double-edged: sick people have more contact with health professionals, and maybe family, sore more chance of infecting them. That’s what Greg implied when speaking about transmission within hospital I guess…
Some symptoms are net benefits, like coughing, but that’s an easy one and I would not count that as increased virulence..
Are there other positive relations, like higher virulence is just a symptom of the virus hijacking the cellular machinery to copy himself faster/stronger, hence diffusing more copies of itself in the environment, quicker? something else?
Yes, but there are also factors that tend towards higher virulence. Certainly within each sick person there is evolutionary pressure towards faster viral reproduction. And a virus that makes you sicker generally makes you more contagious (basically spewing more of the virus).
I think I would get get a clearer picture if I knew how viruses kill/make you sick. Is it because, after a while, they make the cell so busy manufacturing viruses that either it dies, or does not perform it’s other cell duties anymore, or both? Or is it something else entirely?
Yes this virus makes the epithelial cells that line your alveoli die and/or fuse together. They lose their barrier function and start to leak interstitial fluid into your airways. Also there are tons of immune cells that come into your lungs, further packing the airways and spitting out inflammatory mediators. The net result is if your immune system doesn’t clear out the infected cells (with T cells) and soak up the virus (with antibodies) fast enough, your lung function deteriorated until you basically drown.
Thank you for clearing up the reason for ventilators.
Yes, but there are also factors that tend towards higher virulence
I’m way out of my depth here but I wonder if high blood pressure isn’t one such factor. Or ppl w/high BP are just… weaker.
“higher virulence” means that the nature of the virus is different, so that, ceteris paribus, it is more likely to make you very sick or kill you.
Copy number must count.
Now that the extint American chestnut (RIP) was mentioned, consider the thriving Chinese chestnut. Diversity is strength!
It’s not extinct, but barely hanging on. Scientists were trying to get approval to begin planning genetically-modified American Chestnuts that had resistance to the blight, but a bunch of hippies is trying to thwart their effort.
https://psmag.com/ideas/most-controversial-tree-in-the-world-gmo-genetic-engineering
Interesting that the blight originated from SE Asia.
I’ve seen many American Chestnut saplings and once even a few nuts on the ground in Tennessee. I doubt they’re actually propagating enough to avoid eventual extinction though. I hope the GM method works and they can apply to a large number of lines from different areas to maintain diversity. The backcrossing effort is impressive but too slow and expensive to do that.
A well written article. The total number of chestnut trees in eastern North America was estimated at over three billion… The number of surviving trees … is
fewer than 100. (from wiki). In these days of pandemic, let’s drop the subject of the American chestnut. My parents were so supersticious that when I fell ill, they changed my name to confound the Angel of Death. (It worked).
originated from SE Asia
But brought to the US by a person. That’s the way it always happens. Jackrabbits and cane toads, something in Hawaii (I forget – mongoose?), starlings by some Shakespeare-addled dope…
OTOH, this is the most useful article I’ve read about the disease:
https://www.cbsnews.com/news/coronavirus-digestive-symptoms-diarrhea-almost-half-of-patients
Reblogged this on Nicht-Linke Blogs.
Trees cannot reproduce fast enough to evolve against a virus. They have co -evolved over millennia. Hence introducing, authoritarian, morally ambiguous, face saving, ego centric culture to the “western”economic system was not a strength. And leaves the ecosystem weaker just like in North Eastern Forests. Read Rackham on that.
Read Rackham on anything to do with landscape history or woodlands. Top man.
“Eat Bambi” was his cry.
A little off topic, but it occurs to me that there’s a lot of flight attendants sitting about without pay. Simultaneously countries are going to need a hell of a lot of triage nurses. They should be trained in how to deal with covid-19 cases.
“Originally, it kill < 99% of infected rabbits.”
When tired… Fixed.
“ Myomatosis”?
There is such a thing:
https://medical-dictionary.thefreedictionary.com/myomatosis
But probably not what you meant.
Reblogged this on The zombie apocalypse survival homestead.
Myxomatosos was “accidentslly” released. They say.
It destroyed the market in Australia for rabbit meat, and thus the availability of domestic rabbit pelts for use by the iconic Australian felt hat company Akubra. They import from Belgium or somewhere now.
“American chestnut. How are they doing nowadays?”
Hanging in there, with a little help from its friends.
https://kwoa.net/2019/05/13/update-on-the-status-of-the-american-chestnut/
I thought it likely that early on Covid-19 would evolve to be less virulent because asymptomatic carriers would be the spreaders rather than the very sick. But now we know the young are very commonly the asymptomatic spreaders and therefore it wasn’t pushed in that direction.
Evolution depends on the details. Even with the greatest incentive to do so, mosquitos haven’t evolved wire cutters to get through window screens. They just can’t, and that’s a matter of the mechanical details of how mosquitos work. Likewise, there may simply be no evolutionary path for a virus to become milder and yet remain transmissible, purely because of mechanical details of how it works.
Continuing with your mosquito getting through the screen analogy I will jump to this. https://www.youtube.com/watch?v=1vZDVbqRhyM . The mosquito being the virus and the screen being the wall of a cell it is trying to penetrate. Scientists around the world are studying this means of access the virus has to the inside of the cell. If Covid-19 mutations make access to the cell easier, then the mortality rate can go up. On the other hand if scientists can find a way to block access to the cell, then the mortality rate can be manipulated to go down.
If the window screens are effective to prevent mosquitoes, they cannot develop wire cutters. Evolution works step by step. Should be a small hole that allows the entrance of a few mosquitoes, the next generations may develop ways to improve the access to blood. For example, enlarging existing holes. Coming generations may improve to the point of creating holes.
That’s exactly the kind of reasoning that results from ignoring the details, in particular the details that (1) window screens are made of tough stuff (usually fiberglass or aluminum), and (2) mosquitoes aren’t (as anyone knows who’s ever squashed one). Even slightly enlarging an existing opening in a window screen is far beyond what mosquitoes can do.
The power of evolution may surprise you. Look up hercules beetle at https://eol.org/pages/1026724
The best way to deal with mosquitoes is a fan.
Since I no longer employ punkah wallahs due to straightened circumstances, I use the electric type.
I’ve seen that ACE receptor blockers can help reduce cytokine storm … that’s why high blood pressure is the higher % killer for most who get this coronavirus, it attaches to the receptors to cause a greater chemo/endotaxis
I asked Greg on the other thread where is the sweetspot for calling off the economic collapse dogs. More than a month still ok with the economic damage even if it collapses the system? Rioting or violence might just be a worse way to go in our big blue cities … than from a virus that won’t barely even cause much of a cough for 80% of people.
During World War II we devoted about 40% of the economy to the war effort. We did this for almost 4 years. Did that “collapse the system”? In the event of serious unrest, we have the National Guard (and the draft). The potential American fatalities from coronavirus are much higher than those we sustained in the War. Also, there is a reasonable chance that medical treatments will permit a loosening of the suppression efforts within a few months. If not, we should have a vaccine within 18 months.
Why are we so confident we will have a vaccine within 18 months? I’ve read that we’ve never had a vaccine for a coronavirus before. Is that true?
If true, is it relevant?
If true and relevant, is it for lack of trying?
We started to try with SARS, but quit after it got suppressed and went away. There are vaccines against several coronaviruses that infect animals.
Thanks! Did we try with MERS? If not, was it for the same reason?
Logically you want to weigh up the trade-off of death by the Contagion from Cathay versus death by impoverishment. I’ve no idea whether an economist exists who could give you a useful estimate of the second.
Nor am I entirely confident in any estimate of the first that an epidemiologist might give you. First you must bear his incentive structure in mind: we live in an age of dishonest scientists.
Secondly, the disease is new and so there’s great doubt (it seems to me) about many of its characteristics. Maybe the fact that it discriminates against ill codgers is the thing we know that’s most soundly based? On the Diamond Princess seven passengers died of whom none were under seventy. The average age of the passengers was 58.
Riots are easy to put down, if you’re in the right mood.
Individual rabbits didn’t “evolve” resistance, the rabbit population evolved resistance. Each successive generation of rabbits were descended from survivors of the virus, who had an inherent, and hereditary, resistance.