Prions
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That one scares me more than current known human prion disease. Mainly because it seems to spread really easily. Other prion diseases seem to practically require cannibalism to spread.
As for why the grazing animals can spread prion, my guess is that the prion protein is highly concentrated in the tongue, and grazing animals are likely to be able to pass the protein down to the ground via the saliva. Scrapie and bse are cross-transmissible
Incidentally, you probably shouldn't eat beef tongue.
According to the CDC, CWD is spread NOT just through saliva, but also feces, blood, urine, etc.
In addition, it CAN spread to Squirrel monkeys. The long-term affects on macaques is still being established (on of the reasons kuru took so long to discover was that it took decades for the monkey to develop symptoms).
If exposure is dangerous to humans, what could we do? In the areas it has been in, it is spread everywhere the deer travel as they shed bodily fluids into the soil.
I thought the theory was that CWD started in a domestic herd that was raised in an area that previously had scrapie infected sheep?
and
"Incidentally, you probably shouldn't eat beef tongue."
Can you clarify?
There is not deer <-> sheep, deer <-> cow, deer <-> humans.
There is cow <-> sheep, maybe cow <-> human. I don't know off the top of my head about sheep <-> human
If there had been, the us food supply would be trashed. Cwd is highly endemic among wild deer and wild deer co-graze with cows all the time.
Also unknown if the relationship can be transitive. There might be a species X where deer <-> X <-> human.
"...in 1996, with the recognition in young people in Britain of a “new variant” of Creutzfeldt-Jakob disease (nvCJD, or the Will-Ironside syndrome) that has since been traced with near certainty to the consumption of tissue from cattle infected with spongiform encephalopathy (BSE), they having in turn consumed meat and bone meal contaminated with rendered sheep carcasses infected with scrapie... There are currently just over 30 verified cases of nvCJD, and four to five new cases a year: whether they represent a small group of susceptible people or are the leading edge of a major epidemic is still moot."
https://www.usatoday.com/story/news/health/2019/02/21/zombie...
Proteins, eventually degrade, even prions. We probably have an enzyme that accelerates degradation of them (my bet is it's insulin-degrading enzyme).
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1114482/
The wiki also indicates that a sheep vaccine distributed in 1935 caused an epidemic, as it contained contaminated neural tissue:
https://en.wikipedia.org/wiki/Scrapie
It also seems to me that the recent mRNA vaccines could be repurposed to target a section of a prion, so the immune system could clean them from the blood. An interesting question would test mRNA vaccine effectiveness in the cerebrospinal fluid, where microglia would be required to perform this function, as macrophages (and friends) are not present there.
You're just as likely to elicit an immune response to the prion plaques, stabilize them, and recruit inflammation to the point of deposit, making matters worse.
Note that "burning to ash" is not that hot.
It seems like prions don't have much chance to evolve/mutate naturally since any change makes them unable to duplicate. However with these simulation systems, are man-made prions a concern?
That's not true.
Don't worry about alphafold. Even if it's a really good extrapolation engine (and not a really good interpolation engine) the amyloid fold is unusual enough that I doubt that alphafold can heuristically solve structures much less assess energetic or kinetic factors (which is not what it was designed to do). Note that I am an alphafold optimist and am on record here saying that I consider alphafold to have solved the basic protein folding problem. More to the point, we don't have many reliable solved structures of amyloid folds, it's clear that they are heterogeneous anyways, and iirc no one has bootstrapped an infectious prion in vitro, which means we don't know exactly what makes something infectious... We can make prion amyloid in vitro but it isn't infectious unless it was seeded by an infectious prion amyloid.
Glad to hear you aren't generally afraid to die though - sounds like a good stance to have.
> imagine if Covid had been even more deadly, for example
It'd have been taken more seriously, and it would have had a higher chance of burning itself out. Covid's such a pain in the ass because it hits such a sweet spot, of spreading fast, being highly infectious, and being benign enough (with many of the infected spreading it asymptomatically). For the hell that it is, the one "saving grace" of Ebola is that it debilitates and kills fast enough it's very hard for it to spread, especially as it doesn't have great transmission vectors.
And to them, prions are just organic matter like any other.
I think we'd probably handle a more severe disease with much less flippancy than we did COVID and we'd have to treat lockdown and other tools with much more reverence in such a situation.
This does happen with Ebola outbreaks being managed in Africa now so if they can do it there I think we can do it here.
I agree with the first sentence, but not with the second. Yes, governments might eventually put more care onto reducing covid counts. But a) it might be too late. Just check how long it took for travel restrictions to be imposed.
And b) the panic that people will be in will be even bigger, especially those who think that masks and vaccines are a way to spread microchips and 5G. These folks aren't rational.
Last, there is a non zero chance you'll be dying in the next few years. At that point, do you really care about rules? The governments will impose even stricter lockdown measures. But this will cause even more unrest as people are confined to their homes.
Ebola is in the category of "deadly but not easy to spread". Yes, it can be spread but by the time you spread it you physically can't leave your bed. That's a great help in preventing spread. I'm talking about a disease that at the start has few symptoms, allowing for easy spread, then gets severe and deadly further down in disease progression.
It seems to be close to the sweet spot in terms of being able to spread but still occasionally kill.
Surviving airborne before the advent of buildings meant surviving outside in direct sunlight with little in the way of protection from droplets or anything else. Organisms have a limited amount of abstract "evolutionary capital" and the costs, so to speak, of developing adaptations to survive airborne and evade an active immune system are astronomical. It's not impossible, but the two "features" work against each other during the development phase.
My understanding is that the main reason is a biological application of the principle of parsimony: Evolutionarily, organisms don't generally evolve lots of different things all at once. Thus, if you have a novel variant of a virus, it is highly likely to be mostly like existing variants, but with a very small number of changes.
Basically, you can think of it as the virus having to hit a particular threshold of a mutation direction that increases transmissibility to become widely-spread, but also has to hit a particular threshold of a mutation direction that increases lethality in order to become very dangerous.
As soon as it hits that transmissibility threshold, that is the version of the virus that's going to spread, and hitting both those thresholds at the same time is going to be incredibly rare.
What's much more likely (and genuinely concerning) is the possibility that a virus that has already become highly transmissible evolves more in the "lethality" direction and goes from being a widespread nuisance to being a deadly pandemic. The longer we let something like COVID remain widespread, as I understand it, the more likely we are to see a variant emerge that retains its high transmissibility but also gains a higher lethality. However, as we can see from the fact that the bodies are not piling up in the streets, even after nearly a year and a half of a pandemic form of a particular virus, it's by no means guaranteed that something like that will happen, even at a small scale.
We all know the more aggressive a pathogen is, the more it paints itself into a corner because it's burning its bridges. Something like airborne HIV would be really scary.
My guess is that airborne diseases are not weaker, but that evolution has selected for resistance against those because they spread fast among the population.
The more times you roll the dice, the more often you’ll get that magic combo of lethal and highly transmissible. For the most part it doesn’t favor it, but that just makes it an outlier when it does, not impossible.
So yeah, cannibalism and brain spray. Stupid behaviors.
It is basically a juggernaut.
- Prions are resistant to sterilization (since there is nothing to "kill"), but simple soap and water are still highly effective
- Prions don't "last forever". They can live in buried carcasses for a few years, but some studies have shown that even our existing sewage treatment processes already break down a lot of prions.
- While vegans might have some risk, meat multiplies the risk because of how it can concentrate prions. I have to imagine that vegans have an incredibly low risk profile for prions.
- Most importantly, viruses and bacteria innately "want" to spread. Prions do not have any biological mechanism for their own propagation - they are just an unfortunate mistake of nature. And this seems to be key why there has never been a massive prion outbreak.
If you were an anarchist rooting for the collapse of society, as this writer seems to pitching for, sure it seems like it might be a more likely vector than many.
I disagree here, and but it's not fatal to your argument. Anything that reliably reproduces "wants" to. Hell, I bet prions can evolve too on large enough time scales (heterogeneous induced refolding), so we can say they are alive. But sometimes the tortoise is too patient and the race ends before the hare tires.
Virus instead use their own material as the original to make copies, so any new good or bad variation will be copied in the offspring, and they can evolve.
Evolution only requires "descent with modification". DNA is a mechanism for this, but it is not necessarily the only one.
> Prion replication is subject to epimutation and natural selection just as for other forms of replication, and their structure varies slightly between species.[19]
[19] is https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2848070
My impression is that DNA / RNA-based organisms have a high tolerance for changes to their DNA / RNA, such that many genetic changes won't cause them to lose their self-replicating ability. This is great for evolution.
Prions, on the other hand, seem like they would have a low reproductive tolerance for changes to their structure.
What do you reckon the risk profile of vegetarians would be? Are prions likely to end up in eggs and milk?
Remember that all risks are relative. Just like radiation, there's likely to be a background level of prions in the soil that you can't avoid even if you only eat vegetables. The question is how much prion exposure you can tolerate without having noticeable symptoms within your lifetime.
I eat meat occasionally as well. I tried going vegetarian for a six months, but I lost an unhealthy amount of weight (my BMI dropped from 19.2 to 17.8) and I think the health risk from malnutrition, as you also mention having struggled with, is much more severe than that of prion disease
It turns out that there is genetic resistance to it. There's a specific gene, of which there are two forms, called Q and R. If a sheep is Q-Q, it has no resistance. If it is Q-R is has some resistance. If it is R-R it is completely immune.
All of which is to say: we should not just assume that exposure to prions results in a 100% disease rate, nor should we assume that prion disease itself has a 100% mortality rate. Because the diagnosis for prion disease is clinical. In other words, we only know someone has the prion if they show signs of the disease. And we only look for the disease once someone starts showing significant signs of disease. But there is no test that shows that you ave been exposed, nor is there a test that shows you have been infected but that your infection is spreading so slowly that (say) prostate cancer or heart disease will kill you long before the prion does.
The majority of research into prions happens post mortem, and is usually trying to pin down the cause of death. Statistically, there must be prions that are not lethal.
I'm reminded of the issues with people that work at pig processing plants, who had the job of blowing the brains out of the skull cavity with compressed air. Many were not issued proper PPE and ended up with a wide variety of symptoms.
https://www.twincities.com/2008/02/06/minn-to-question-25-mo...
It makes sense to me that non-lethal cases wouldn't be discovered, as it's probably prohibitively expensive to screen for non-lethal/dormant infections. It could also be that the progression is so slow for most people, that they die from unrelated causes before the disease becomes a problem (this is pure conjecture on my part)
https://www.nih.gov/news-events/nih-research-matters/new-met...
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5538786/
Scientists have since developed a promising method that relies on analyzing the retina.
https://www.nih.gov/news-events/news-releases/scientists-ide...
Suffice it to say, the prion disaster did not materialize, so I'm skeptical about the same story being repeated almost verbatim today. My guess is that prions aren't all that contagious after all, especially after basic food preparation measures.
It is a bit unnerving to know you may or may not have a disease that there is no test for, and symptoms may not appear until decades later.
> It is a bit unnerving to know you may or may not have a disease that there is no test for, and symptoms may not appear until decades later.
That's true for many neurodegenerative diseases. If that's unnerving to you, better stay away from WebMD...
There is NO single, conclusive test for Alzheimer's disease. The symptoms are almost identical to CJD (human mad cow) with the biggest differentiator being time from diagnosis to death. Even Amyloid-beta plaque buildup is often (though not always) noted in CJD patients [0][2]. Likewise the other Alzheimer's marker tau protein is also elevated in CJD patients [3]. I'd note that we don't actually know that CJD must progress over 1-2 years rather than a decade -- it is an observational assumption.
Between 15-30% of Alzheimer's diagnosed patients also don't have the normal Alzheimer's brain symptom (presumably amyloid buildup) either. Alzheimer's as cause of death was 17.6% in 2000, but is now 37.3% in 2020.[1] Because CJD is defined as killing quickly, it isn't even checked for in such cases (a kind of self-fulfilling prophecy if the diagnosis criteria aren't actually accurate). It doesn't help that cleanup of a contaminated area is time consuming and costly (not to mention potential negative press and panic).
This isn't a new idea, but perhaps those fears were somewhat true, but have been buried under our lack of knowledge of protein diseases.
[0] https://pubmed.ncbi.nlm.nih.gov/3092727/
[1] https://alz-journals.onlinelibrary.wiley.com/doi/full/10.100...
Ordinary CJD has a much lower median age of death (68 years) than Alzheimer's (88 years), but vCJD (the form that is believed to be caused by contaminated food) has a median age of death of only 28 years.
https://en.wikipedia.org/wiki/Creutzfeldt%E2%80%93Jakob_dise...
A surge in young or middle-aged dementia cases would likely not have fallen under the radar.
> Between 15-30% of Alzheimer's diagnosed patients also don't have the normal Alzheimer's brain symptom (presumably amyloid buildup) either. Alzheimer's as cause of death was 17.6% in 2000, but is now 37.3% in 2020.[1]
You have mistaken the rate of deaths (per 100,000) for the percentage. When judging this increase, one must consider that in the same timeframe, the mean age of the population has risen by 10% and life expectancy increased by more than two years.
Sorry, knew what I meant, but messed up what I typed. In any case, doubling the death rate per 100k is still much greater than the 10% age and 2-3% lifespan increase would indicate. Alzheimer's mortality had increased 16x between 79 and 91 (from a mere 857 to 13,768 in 1991[0]. The previous study I quoted above put the 2018 mortality at 122,019. Alzheimer's is now the 6th leading cause of death and continues to rise at a rapid rate.
> Ordinary CJD has a much lower median age of death (68 years) than Alzheimer's (88 years), but vCJD (the form that is believed to be caused by contaminated food) has a median age of death of only 28 years.
This is the crux of the problem.
We have experimental knowledge about this from kuru. The last patient displayed symptomatic kuru some 5 decades after the cannibalistic practices had stopped.
Do only young people eat meat? If all age groups eat meat at equivalent rates and infection rates in cattle are constant (believed to be around 1 in a million IIRC), then the median age should be the population median age PLUS a shift for however long it takes to become symptomatic.
Linkage is also important. How do we know that CJD and vCJD are different? We made that distinction arbitrarily and don't have evidence that "normal" CJD is not caused by external sources. Official vCJD cases are around 200 over the past 30 years, so there isn't exactly huge amounts of data to pull from either.
If CJD really did explode in the 80s-90s, then you would expect the older generation to become symptomatic at an older age than would be typical if the disease were common in the decades before.
There seems to be a connection with being vegetarian/vegan and alzheimer's but how much is due to not eating meat and how much is due to overall healthy lifestyle is hard to determine.
Something weird is going on with Alzheimer's disease and the legit explosion in cases over the last 30 years (both per capita and as cause of death in the elderly) give reason to wonder what weirdness is going on.
"We know that the β-A4 amyloid of Alzheimer’s disease also derives from a normal host protein that in diseased people accumulates in the brain, but it does not have the ability to transmit disease to a healthy person. Why this difference?"
So unlike Europe we never reckoned with the problem and don't know if it is currently spreading. For human exposure we would not yet be far enough along to know if the US Beef supply either is or was contaminated.
Personally I have basically stopped eating beef for this reason.
Feeding practices that led to BSE have changed, the USDA is still testing for BSE, and if the disease was spreading, we'd probably notice it at some point.
Personally, I'd be far more worried about cattle farming practices spawning some sort of super-resistant flesh-eating bacteria than anything related to BSE.
Huh? Why would they prohibit testing?
> NOT A FOOD SAFETY TEST
> BSE tests are not conducted on cuts of meat, but involve taking samples from the brain of a dead animal to see if the infectious agent is present. We know that the earliest point at which current tests can accurately detect BSE is 2-to-3 months before the animal begins to show symptoms. The time between initial infection and the appearance of symptoms is about 5 years. Since most cattle that go to slaughter in the United States are both young and clinically normal, testing all slaughter cattle for BSE might offer misleading assurances of safety to the public.
> ...
> Why doesn't USDA test every animal at slaughter?
> There is currently no test to detect the disease in a live animal. BSE is confirmed by taking samples from the brain of an animal and testing to see if the infectious agent - the abnormal form of the prion protein - is present. The earliest point at which current tests can accurately detect BSE is 2 to 3 months before the animal begins to show symptoms, and the time between initial infection and the appearance of symptoms is about 5 years. Therefore, there is a long period of time during which current tests would not be able to detect the disease in an infected animal.
> Since most cattle are slaughtered in the United States at a young age, they are in that period where tests would not be able to detect the disease if present. Testing all slaughter cattle for BSE could produce an exceedingly high rate of false negative test results and offer misleading assurances of the presence or absence of disease.
> Simply put, the most effective way to detect BSE is not to test all animals, which could lead to false security, but to test those animals most likely to have the disease, which is the basis of USDA's current program.
The ban might not be warranted (I don't believe it is myself), but it is important to be aware that testing for BSE may not be accurate at the time most cows are slaughtered.
https://www.usda.gov/topics/animals/bse-surveillance-informa...
1. https://en.wikipedia.org/wiki/Variant_Creutzfeldt–Jakob_dise...
1. https://www.cdc.gov/prions/vcjd/vcjd-reported.html
2. See table 3 in the PDF on this page: https://www.termedia.pl/Review-article-r-n-r-nVariant-Creutz...
Proceeds to peddle the "horrors" of prions.
I don't entirely dismiss this article since I have a friend who worked with prions in a bio lab at the Univ. of Chicago and I remember he was absolutely terrified of them. (And IIRC he reported having some doubts about laboratory safety protocols...) But I don't think he was afraid of this kind of apocalyptic endgame either; he just thought they were horrendously nasty stuff.
No citations
Lots of fear
Thinly veiled far right rhetoric
But perhaps horseshoe theory strikes again.
Even if 1 prion can kill you, even if prions will survive in the soil indefinitely, I think we are going to erode all the topsoil faster than the prions can accumulate in concentrations sufficient to cause issues.
Get in line.
/* reads TFA about prions binding in soil */
Please move to the front of the line.
Prions don't live forever, they are susceptible to soap and water. Prions are proteins, anything that can break down a protein will work to break down a prion. They are not some form of mystical protein. They will break down naturally over time. This is why regions that have had Kuru outbreaks have been able to stop those outbreaks.
Since prions are literally just a chemical (albeit a complex one), they are not trying to propagate themselves. There have been outbreaks, but no massive ones with prions because that's simply not how they work. As well, since they are proteins and proteins eventually break down when they are removed from a living being, they will also eventually break down.
This article is a whole lotta fear with not a whole lotta valid info.
>The prion’s structure is corruptive because it is not a copy but a mirror image of the protein, flipped in the opposite direction. In technical terms, some groups of prions have the opposite chirality—Greek for “handedness”—of their normal cousin proteins. The prion is doubly corruptive because it does not keep its inversion to itself: when it encounters its mirror image—a normal protein—it convinces that image to flip, to change chiralities and join the prion group.
The amino acids don't change their chirality, only the protein's secondary structure.
You could just as well ask, "in a world with solar UV rays, wouldn't we evolve cancer resistance?"
Cancer mainly takes the old, and is certainly no threat to the survival of mankind.
I couldn't find the exact one that I read a year ago... the one I read talked about a test where the vaccinated mice survived while the unvaccinated mice died quickly.
Prion diseases are scary psychologically because the early stages are almost the same as any other neurodegenerative disease. For those who are suffering from one, who would likely develop some sort of depression early on, really gives them doubts about their lifespan. This is from personal experience.
Here's a bunch of articles about it:
https://pubmed.ncbi.nlm.nih.gov/18215090/
https://pubmed.ncbi.nlm.nih.gov/17234125/
https://www.eurekalert.org/pub_releases/2014-12/nlmc-fsv1217...
This site hosts white-supremacist aligned articles (like this one supporting the dehumanizing NPC meme: https://www.countere.com/home/how-to-spot-an-npc) so I wouldn't be too worried about an article here about the "end of the world"
Wouldn't this be more for the lunatic who either hopes to take humanity down in the long run, or just does not give an f?
More of a 12 Monkeys scenario?
Regardless, happy Monday, indeed...
Terrorism is first and foremost a propaganda strategy to destabilise the political system in the target country and recruit new members to the organisations cause
Since prions take decades to progress, a terrorist attack using such a weapon, would probably not create the shock and outrage, that makes headlines