“Diseases from animals have evolutionary pressure to hurt humans because hurting humans is better for the survival of its preferred host.”
That does make sense to me, but I think it doesn’t track with how slow evolution works.
According to Yale, Lyme disease has likely been around in North America since 60,000 years ago: https://medicine.yale.edu/news-article/ancient-history-of-ly...
Natives were not very destructive to forests and I don’t think very destructive to mice.
Mass deforestation to the level of evolutionary pressure would have come when Europeans first settled. Meaning Lyme disease would have had to specialize after that, which I would assume is unlikely.
Maybe the diseases do specialize to harm humans, but it feels like the period where diseases can effectively stop humans and humans were doing mass deforestation is too short. Lyme disease is problematic, but it hasn’t stopped anyone from chopping down trees.
You could argue it has the opposite effect. We drain swamps because of malaria, destroying its habitat.
My theory is that some ecosystems have a niche for pathogens that remain at low concentrations in healthy circumstances, but that become amplified in cases where the ecosystem is taking damage.
The article you linked describes such an amplification:
> “The Lyme disease bacterium has long been endemic,” she said. “But the deforestation and subsequent suburbanization of much of New England and the Midwest created conditions for deer ticks—and the Lyme disease bacterium—to thrive.”...
> Ticks expanded into suburbanized landscapes—full of animals like white-footed mice and robins, excellent hosts for B. burgdorferi
It may not have been humans that posed the initial differential threat to everything-but-the-mice-and-robins. But something did, and that created the pressure to arm mice and robins with invader-discouraging pathogens, and that pressure made B Burgdorferi what it is today.
The increased pathogen concentration is an immune response. The stimulus is a reduction of predators (which are known to be more sensitive to habitat disruption) and the response is that the prey, left unchecked, amplify the pathogen and infect the invaders.
In a recent biology class we spent a few lectures talking about Lyme disease, so I am familiar with that one. Here's the idea:
Ticks aren't born with Lyme disease, they get it from an animal and then transfer it to another animal. Not all animals are competent hosts for Borrelia Burgdorferi (the bacteria that causes Lyme disease). If a tick bites an infected deer and then bites you, you're unlikely to be infected (although if you do, then both you and the deer will suffer for it).
Mice however, are competent hosts for B. Bergdorferi. Also, neither ticks nor mice experience any negative affects from being infected (I'm told that bats are this way with COVID).
So look at it from the perspective of the pathogen. You have a limited complexity budget. You can't hack every single immune system, you have to be choosy. (Bacteria get their diversity from horizonal gene transfer, so data about which adaptations are effective in the current environment is sort of gossiped around.)
Meanwhile, look at it from the perspective of all of the potential host immune systems. Nobody wants to be infected, but certain organisms may be able tolerate infection better then others.
So there's this tension where B. Bergdorferi is looking to specialize re: hosts and each host genome has to "decide" how to handle it.
For reasons unknown, the B. Bergdorferi genome chose to specialize with the mouse. The effect of this "choice" is that it is more concentrated in areas where mice don't have many predators, and less common in places where they are well-hunted.
It's known that the impact of human settlement is uneven: It bothers the raptors more than it bothers the mice. So coincidentally, we have this situation where Lyme disease causing bacteria is concentrating in tick guts specifically where humans settle and upset the preditor/prey balances around the mouse.
And recall that this outcome, where it's the mouse and not some other tick-victim that ends up being the competent host, it's the result of tension between the genomes of all the things that ticks bite.
So I ask: is it mere coincidence that it ended up being the mouse that B. Bergdorferi specialized against? Or have the forest dweller genomes "collaborated" to achieve this outcome.
I don't think it's that wild to assume collaboration. Sure, they didn't sit down and discuss it, but given that human-driven habitat loss is a significant driver of extinction, I think there would be a selective pressure towards collaborative outcomes that keep humans out of the forest and away from ones that make the forest more inviting to humans. Perhaps there were cases where the B. Bergdorferi ancestor specialized in other ways, but we don't know about them because instead of forests there are parking lots in those places.
In this way, I expect that zoonotic diseases are a sort of immune system against habitat loss
Hypotheses are no good if not falsifiable, so here's the prediction: novel zoonotic diseases will spring up in places where human-caused habitat loss proceeds in novel ways. If we change how we live such that we don't create a safe haven for mice but do create one for some other creature, then the ecosystems that we're destroying will collaborate in new ways to cause that creature to be a threat to us.
I'm not sure where to look in history for examples of this, otherwise I'd be writing a paper about it, but I hope you can see how it would plausibly be applied to COVID as well.