Tasmanian devils 'adapting to coexist with cancer'
bbc.com
bbc.com
https://www.nytimes.com/2017/10/04/science/ancient-viruses-d...
Theoretically it /is/ possible for the right sequence of say radiation damage and auto-repair to give rise to segments of a virus in DNA but the odds are stupidly lower. To use an example technically you could scatter scrabble tiles randomly to get quotes from Shakespeare if you do it enough but you are far more likely to occasionally get gibberish than "WHAT LIGHT THROUGH YONDER WINDOW BREAKS" - let alone in the right order.
Nobody claimed sickle cell had anything to do with viruses; I claimed that sickle cell is a mutation which provides a protection to malaria — which it does.
From the person I was replying to:
> We might find that every N years a new disease emerges, spreads, and then is adapted to - and we're just lucky enough to be around to observe this current wave
Sickle cell seems like precisely that in response to malaria, in human history.
In addition to sickle cell as a trait which shows that adaptation, our DNA is full of evidence of wide spread viruses, eg wide spread infection, because of the patterns in junk DNA. It’s not just mutation — it’s also a chemical signature of the rate of retrovirus epidemics.
Your post seems not to have understood mine, talking about nonsense with radiation — which is nonsense because I never mentioned a means of adaptation, but merely signatures of historic disease spread (and a case of adaptation).
Some selective pressure emerges that didn't previously exist, whether that be a predator; change in nutrient availability; disease; climate; etc.
It's possible the loss of habitat in Tasmania has either slowed spread of the DFTD, because the Devils are more widely dispersed, or hastened the spread because there are fewer Devils reproducing to potentially adapt to it.
I find it interesting to ponder how it has come about that the Earth isn't just covered in, say, that pathogenic fungus¹ reported on recently, but rather something like 8.7 million species².
1. https://news.ycombinator.com/item?id=19515362
2. https://www.nature.com/news/2011/110823/full/news.2011.498.h...
Existing inside an organism with a functioning immune system long enough to cause death requires completely different adaptations than existing outside of one. By their very nature, most pathogens spend too much energy on biochemistry that does diddly squat (without an immune system to fight) to help them compete against the innumerable species of garden variety bacteria floating around.
The reason they didn't have problems before was that the parasite didn't exist before.
If I remember correctly it was only recently they were reintoduced into the wild en-masse.
This article is kind of celebrating the birth of a new genetic disorder as a form of survival.
I actually find that aspect of it moderately disturbing.
Presumably, both disorders developed for the same reason: One copy of the gene is protective, but not crippling. Two copies are crippling.
So those with one copy had higher survival rates when epidemics of certain diseases hit. This meant that more of their children survived, even though some of their children were born with terrible impairment and worse survival rates.
People with CF tend to not reproduce. In fact, 97 percent of males with CF lack a vas deferens, making them effectively sterile. It's mostly the carriers who create new people with CF. Some of them had no idea they were carriers until they had a child with CF.
> In 2007, it was predicted that populations could become locally extinct within 10–15 years of DFTD occurring, and predicted that the disease would spread across the entire range of the Tasmanian devils causing the devils to become extinct within 25–35 years.
Oh man :(
Is this kind of stuff "normal" (historically), or is it likely to be another result of our general poisoning of everything? There is this,
> In 2004, Kathryn Medlock found three oddly shaped devil skulls in European museums and found a description of a devil in London Zoo dying, which showed a similarity to DFTD
but that's a.) not much and b.) the source for that is dead or had the URL changed, and I can't find it: https://www.google.com/search?q=abc+%22Devil+Disease%22+medl...
Fortunately, Tasmanian Devils are very easy to breed in captivity, and there’s at least a handful of sanctuaries open to the public that have breeding programs, and rehabilitation services that cater to for injured Devils.
So it looks like the Tasmanian Devil will continue on.
[0] https://en.wikipedia.org/wiki/Devil_facial_tumour_disease#Hi...
> Calicivirus, 1080 poison, agricultural chemicals, and habitat fragmentation combined with a retrovirus were other proposed causes. Environmental toxins had also been suspected.
But the source for that is also kinda useless... someone with the last name Owen wrote a book in 2005, great. I'm used to footnotes containing quotes from the material they reference, and even when it links to a source, since link rot is out of their scope, that doesn't really help.
> suggests that the cancer is spreads though allograft (i.e. a form of direct transfer of the cancer from one individual to another)
Yes, but why is that a recent disease? 1996 is super recent.
> It also reports that "The devils have, in a way, fought back the extinction by developing the gene that is immune to face tumors" - a positive development in the long run.
The long run is the last 100k years, IMO. When I think about cancer historically, I am interested in that timeframe, not starting with 1996.
I wrote this reply 21 minutes after your comment, but apparently I was throttled so I had to keep the tab open to post it much later. I'm done here, good luck and bye everybody.
In humans, each cancer is unique and the cancerous cells are just mutated versions of the cells of the person, so they are very related. A difficult task of the inmune system is to distinguish the normal cells, from the cancerous cells. Another problem is that the mutations in each person are different, son what is useful to cure one person may not work to cure another person.
In the Tasmanian devil case, all of them have exact same cancer. [Actually, there are two transmisible types. Most of them have one transmissible type, a few have the other transmissible type, and I guess that a small minority has it's own non transmissible variant, like in humans. To simplify the discussion, let's ignore all but the first type, and assume that all of them have the exact same cancer.] This cancer is transmissible, the cell are mutated versions of the cells of a Tasmanian devil that died many years ago. A bunch of cells go from the cancer in one devil to another devil, and start to grow. This is very difficult because the cells of the cancer are very different from the cell of the new devil, so they should be an easy identificable target for the inmune system. For this reason, transmisible cancer are very rare in mammals, there are only 3 or 4 known cases.
I'm not sure what is happening here, but a usual trick to distinguish the cells is that each cell produce some molecules that are a mix of some kind of sugar and some king of protein. There are many sugars to select and many protein parts to select, so there is a lot of possible variation. Each person produces only some of them, not every variant, so the inmune system can learn which of this are the normal one, and if it finds a cell with another combination will attract it.
This is one of the reason why organ transplant is so hard. The inmune system of the host detect that the cells in the new organ have a different variants, and start to attack the organ. This is also the reason why transmisible cancer are so rare. Even if a part of the cancer goes to another person, the inmune system of the new host will detect the unknown molecules and attack them.
Somehow, in the Tasmanian devil case the transmissible cancer can avoid this check and continue growing in the new host.
My guess of the "cure" is that some of the offspring of the Tasmanian devil mutated and get a new molecule that is not in the cells of the cancer that are like the cells of the very ancient Tasmanian devil. Or perhaps the mutation was to not build one of the molecules, or build a different variant. So the inmune system of the new mutated Tasmanian devil can learn that the old protein is not normal, and attack the cells without/with it. I'm not sure what happened here.
Once the mutant Tasmanian devil with the weird molecule survives, it increase the probability of having offspring, that may inherid the mutation, and increase the probability or survival, that increase the number of offspring, ... And sooner or later you get a world full of Teenage Mutant Tasmanian Devils :).
And, as this cancer is transmissible and all have the same kind of cells, the mutation will make the mutated offspring inmune too. [There are actually two transmissible cancers in the Tasmanian devil, so to survive they probably will have to be double mutated, perhaps they can inherit one mutation from the father and other from the mother, or a mutated one can get a new mutation.]
The cancer may also mutate to be more difficult to be detected producing the new version of the molecules, and then the devils will have to wait until one of them get a lucky mutation, and so on ...
The problem to copy this to humans is that each humans gets it own version of cancer, with cells that have the same molecules than the person. So you must:
a) Modify the cancer cells (and not the normal ones) to make them produce a weird molecule so the inmune system identify and attack them. But this is very difficult.
b) Modify the normal cells (and not the cancer ones) to make them produce a weird molecule, and retrain the inmune system to make it attack the cells with the old version of the molecule. I think this is even more difficult, or to be more precise totally impossible.