Zoonoses Adaptations

The resurgence of Ebola in Congo (with a new strain), news about the Andean hantavirus that can transmit among humans, and the evolving history of Covid all bring to mind the necessary steps for animal bugs to a) transmit to humans and b) adapt to interhuman transmission. I’d like to learn more of the necessary setting and adaptations for such bugs to become problems–from rodent poop (Hanta and Lassa), bats (Ebola), monkeys (SIV/HIV), sheep and cattle (mad cow disease/prions) if any of you have good resources, maybe here would be fun to discuss. Thank you.

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I am not an expert but some basic points:

  • many viruses in animals can transmit to humans but the consequences vary from symptomless to deadly. For example, there are Hantaviruses that do not cause notable symptoms in humans while some cause a relatively high mortality rate (like Sin Nombre and Andes).
  • many dangerous viruses require a close contact with the virus - blood or excreta - to cause a disease. Some viruses like Hantavirus can ride on specks of dust and be inhaled with dust but some need a more direct contact between the sick and the potential new host.
  • for many zoonoses, humans are not the primary target and what happens to the humans does not matter much for the evolution of the virus. An exception may be if the virus manages to adapt to interhuman transmission. In such a case, that starts a separate virus-human evolutionary path.
  • with interhuman transmissions, the virus-human evolution is likely to lead to virus strains that do not kill the host rapidly. A dead host may be a dead end for the virus if the host dies before the virus had spread to some other hosts. I assume that that has already happened in the case of Covid as the strains that seldom kill the host have swamped the more deadly ones.
  • In many cases, the seriousness of an infection depends on the genes of the host. For example, the Hantavirus Puumala seldom kills humans but those who die seem to have an identical gene sequence that makes them vulnerable to a deadly infection. That may act as a factor in natural selection, acting against such gene sequences that are likely to increase the mortality rate where the virus is in contact with humans.
  • airborne interhuman transmission may be the worst case for humans but luckily, many deadly viruses cannot spread in such a way unless there happens multiple critical mutations in the viruses that have ended in humans or some similar kind of host (mostly pigs or apes).
  • there are animal viruses that are potential zoonoses but have not caused known infections in humans because humans have not had much contact with the wild hosts. As humans destroy habitats and spread to the remaining spots where the wild hosts live, the increased contacts are likely to start novel epidemics at some point. We just do not know where and when. Small mammals, including bats, are among the likely sources for novel epidemics.
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A friend of mine just got back from Africa. He is somewhat of a germaphobe, but was relating how the local fauna follow the jeep trails through the landscape as it makes for easy passage, pooping along the way, and the dust raised by the lead Jeep is primarily animal poop, making it worrisome for disease vectors being spread.
We often see just the tip of the iceberg in these cases, and I wonder if there is a lot more cases of zoonotic illness we do not see. With Covid, there was evidence that many mutations were created in immunodepressed individuals who did not clear the infection, but carried the virus long term, and I wonder if that happened in the wild there from initial sporadic but unrecognized infections until it mutated in an immunodepressed person to a form that was able to be passed person to person. There might be a similar process happening with other zoonotic illnesses, and with the USA withdrawal of AIDS treatment and prevention, we may well be contributing to it. That is all conjecture, as I have no training in virology, but would be a good conspiracy theory :wink:

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I don’t have a particular book or website off the top of my head anymore but to me it always seems to come down to mostly the same few things.

  1. Wilderness fragmentation leading to more wildlife bottlenecking causing sick animals to overlap with other animals including humans .

  2. The wildest parts seem to be more remote and farms seem to be pushed up against it. Ranchers won’t to drive off Buffalo because they are worried of diseases jumping to cows. Predators are pushed out more to protect livestock meaning more sick animals able to carry on.

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While that’s a reasonable scenario in general, I think it’s unlikely in the case of SARS-CoV-2. The clustering of early cases around a market selling live wild animals suggests that the initial vector was one of the animals. Not definitive, of course, but pretty solid.

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Just going by these sort of studies:

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Thanks. That is a mechanism I’d never heard of

Oh, there’s no question that the virus can accumulate a bunch of mutations in immune-compromised humans, and that was very likely the origin of several of the major variants (including the Omicron variant, whose descendants we still live with today). There was even a case I heard about where researchers were tracking a highly divergent strain of SARS-CoV-2 in wastewater that they were monitoring. They were able to trace the signal to wastewater coming from (IIRC) a single apartment block, where there must have been a single long-term infected individual.

All I was saying was that I don’t think that phenomenon led to the original spread of the virus.

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