What do you mean by this? Like COVID is the result of an evolutionary process that selected a disease that kept humans away?
That doesn’t make sense, in fact, it’s way more likely for diseases to become less deadly over time. Killing humans or making them very weak is bad for its survival.
I'm making a few assumptions in order to lump COVID in here, I'm just not familiar enough with it's dynamics in bats to argue about it specifically. I do think the principle is the same though. 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. If a tick bites an infected mouse and later bites you, you are likely to become infected.
Neither ticks nor mice experience significant negative affects from being infected (I'm told that bats are this way with COVID). Although it must at least be an energy drain on the mouse (or the bat), whose metabolism supports the manufacture of high concentrations of the pathogen.
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.) You're going to take the path of least resistance, and that path is determined not by your eventual target, but by all of the paths not taken--by the degree to which the other hosts put up a fight.
Then look at it from the perspective of all of the potential host immune systems. There's an incentive to not being in last place--then you'll be chosen for specialization against--but there's also no need to overallocate resources to this fight. It's like a multiparty prisoner's dilemma except the optimal solution is that we all defect against one of us.
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. (of course it's not a decision, it's evolution, but it's convoluted to talk about collaboration in terms of deleterious coincidences and selective pressures).
For reasons unknown, B. Bergdorferi's ancestor's 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. The impact of human settlement is uneven: It bothers the raptors more than it bothers the mice. So we have this situation where Lyme-disease-causing bacteria is concentrating in tick guts specifically where humans 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.
> Killing humans or making them very weak is bad for its survival.
That B. Bergdorferi harms humans is good for the survival of the deer and the owls and the snakes and the bears which share a habitat with ticks. It is the collective adaptations in their immune systems which determine that mice are competent hosts, which is what causes B. Bergdorferi to come in contact with humans at an increased frequency. So no, killing humans is not bad for the organisms that matter in this case. I'm sure they would be quite happy to be rid of us.
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.
I was perhaps too zoomed in on the details of how interspecies evolutionary pressure would work. Sorry for the wall of text.
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.
That doesn’t make sense, in fact, it’s way more likely for diseases to become less deadly over time. Killing humans or making them very weak is bad for its survival.