A common explanation for the massive population decreases of isolated societies upon contact with Europeans during the Age of Discovery is that the natives lacked immunity to newly introduced diseases.

What does this actually mean?

Is it just a shorthand for "the adult population was not subjected to these pathogenes during childhood and is therefore more susceptible to them" or is there maybe a certain genetic component to it?

  • $\begingroup$ This is a very interesting question. 1) You might want to narrow your question down to a single disease (such as smallpox for example) because otherwise the question might be too broad. 2) You might also want to consider the possibility of a cultural difference in response to specific diseases. Maybe in Europe, the people knew how to deal with a specific disease they were used to encounter (quarantine, specific treatments, ...) but the native, having never encountered this specific disease, did not know how to deal with it. $\endgroup$ – Remi.b Jul 24 '18 at 19:55
  • $\begingroup$ Related posts: Why was disease transfer to the Americas one-way? and Why Can't The Immune Systems of Uncontacted Tribes Handle Our Common Colds?. This second post might actually be a duplicate. You might want to address this other post in your question. $\endgroup$ – Remi.b Jul 24 '18 at 19:57
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    $\begingroup$ @Remi.b I'm a complete layman and really wouldn't know which disease would be suitable for narrowing down the scope though. $\endgroup$ – T Nierath Jul 24 '18 at 19:59
  • $\begingroup$ @Remi.b I don't think this is a duplicate. This question, to me, focuses on the heritable vs. non-heritable factors in susceptibility in general. The proposed duplicate, to me, reads as a question about how the common cold can be relatively innocuous in one population but fatal in another. That's a different question entirely (and is poorly answered right now). Both are questions about host-pathogen interactions on a population level, but I read them as very different. $\endgroup$ – De Novo Jul 25 '18 at 18:06
  • $\begingroup$ It would also help to consider the response of European populations to newly-introduced diseases. For instance, bubonic plague killed tens of millions of Europeans in several episodes. Yet now it's endemic amoung rodents in the western US, yet only about 10 human cases per year are reported: livescience.com/51792-plague-united-states.html Similarly the Antonine Plague (either smallpox or measles). $\endgroup$ – jamesqf Jul 26 '18 at 16:39

Is it just a shorthand for "the adult population was not subjected to these patogenes during childhood and is therefore more susceptible to them" or is there maybe a certain genetic component to it?

It's a little of both. You can read some of the math behind this in Infectious Diseases of Humans: Dynamics and Control, by Anderson and May. Chapter 2 gives an overview. The behavior of an epidemic depends a great deal on the specifics of the host-pathogen interaction, but generally you can say that the epidemic curve in a a naive population will have a larger and sharper upswing than in a previously exposed population. You can attribute some of this different behavior to lack of adaptive immunity in the adult population. Again, depending on the pathogen, you can also attribute some of this different behavior to lack of selective pressure in the naive population on highly variable loci involved in the immune response.

To address more directly what seems to be your primary question: yes, there is a genetic component to the susceptibility of a host (e.g., a human) to a pathogen (e.g., a microbe that can cause disease).

Non-heritable aspects:

There are certain aspects of what we call the adaptive immune system in jawed vertebrates that are not directly heritable. You are a jawed vertebrate, and the DNA in each of your B-cells and T-cells that produces B-cell receptors (BCR) and T-cell receptors (TCR) goes through a number of changes outside of the germ line. You can read about these changes in, for example, How the Immune System Works, Chapter 3, by Lauren Sompayrac. It's an excellent introduction if this is new to you.

In addition to the exact set of BCRs and TCRs in the pre-immune state, your current repertoire of cells and molecules is determined by your history of exposure. While some of this can be vertically transmitted, the majority of it is not. This is one of the reasons why, when you look at this repertoire, much of the variability is attributable to non-heritable factors. A not insignificant proportion is attributable to heritable factors, though. So if TCRs and BCRs are not encoded in your germ-line, and your environment obviously has a strong influence on your current immune state, where does the heritable component come from?

Heritable aspects:

All of the other proteins involved in the immune system response are encoded in the germ line, and are thus heritable. Some of them are highly variable, and since they are very important they are under strong selective pressure. You can see important changes in the population distribution of these loci over a relatively small number of generations. There are many other heritable components of an individual or population's susceptibility to infectious disease. There is a great deal of work on this. Casanova has a great article about this in PNAS, which I've linked to in another answer to a related question. A more traditional review of his is here. Of course, he's not the only one working on this. I just like the way he writes. Here's a good one by Baker and Antonovics.

A simplified and speculative example

Re: your comment about measles in the Polynesian islands, we don't have scientific consensus about the relative importance of non-heritable and heritable factors for this particular case. Instead of getting into the nitty gritty details, I'll walk you through a hypothetical:

Imagine an isolated population with a lot of variability in germline genes that code for a special protein that helps their immune system mount a full response to viruses.

A very nasty, very contagious virus is introduced to this previously isolated population. The characteristics of the population help determine the outcome of their interaction with this new virus. Here are 3 important characteristics:

  1. Because nobody has ever been exposed to this virus, nobody has neutralizing antibodies or the rapid immune response that happens the second time you're exposed to a pathogen.

  2. Some versions of that special protein with all that variability don't do a good job of helping the immune system mount a response to this new virus.

  3. Luckily though, some other versions of that special protein with all that variability do an especially good job of helping the immune system mount a response to this new virus.

Because of (1) the disease spreads broadly throughout the population. Because of (2), a specific group of people get especially sick, die, and (because they are dead) don't reproduce, and don't pass on their version of the gene that codes for special protein. Because of (3) a specific group of people do very well, are only sick for a little while, and do an especially good job at generating long lived immunity, and (because they are alive and well) reproduce a lot, and pass on their version of the gene that codes for that special protein.

The epidemic is eventually controlled. Years go by, and the virus starts circulating again.

Now the characteristics of the population are quite different, so the dynamics of the host-pathogen interaction will be different.

Many of the people that were alive during the first epidemic now have neutralizing antibodies and a memory response, so this second epidemic will not spread as quickly or as broadly. This is a non-heritable factor. Previous exposure to the virus has changed the repertoire of cells and molecules in people's blood.

Among the younger generation, more of them have the helpful version of the special protein that helps the immune system generate a response, so not as many of them will die. This is a heritable factor. Previous exposure of the population to the virus has exerted selective pressure, changing the frequency of the helpful and unhelpful alleles in the population.

  • $\begingroup$ Thank you. I'm still having trouble reconciling my (naive!) ideas of how evolution works with the phenomenon at hand. Say, after 40% of Polynesians were wiped out after the first wave of (e.g.) measles, were the surviors genetically "hardier" to the germ? I understand that most likely the best answer is "go read a textbook" (thank you for the references), but maybe you could address this point (more). $\endgroup$ – T Nierath Jul 25 '18 at 9:40
  • $\begingroup$ @TNierath It's very plausible that those who survived were genetically more resistant to measles (on average). Don't think of this as an on/off switch, more on a gradient. People can be more likely to survive for many reasons. Perhaps some people had stronger lungs (partially for genetic reasons, but also partially due to non-genetic reasons). Perhaps some people had a stronger immunity system. All kinds of factors can be involved, and all these factors may influence how much at risk any individual is. $\endgroup$ – Eff Jul 25 '18 at 10:19
  • $\begingroup$ @TNierath I've added a hypothetical example that may help you understand. $\endgroup$ – De Novo Jul 25 '18 at 17:39
  • $\begingroup$ Thank you again for taking the time. I understand the evolutionary logic (I think), but have trouble with some of the terminology and concepts: What are germline genes and how are they different from other genes? The "same" protein can have varieties? Are proteins themselves uniform across human populations and only differ in their varieties coded by genes? What is a "memory response"? $\endgroup$ – T Nierath Jul 25 '18 at 18:49
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    $\begingroup$ @TNierath Germline genes are passed on to your children. My first paragraph on non-heritable factors talks about how some genes involved in the immune response are changed outside the germline, so can't be passed on to your children. Variability is what makes evolution work. Genes are not uniform across human populations, they are variable. The proteins they code for are not uniform either. Different versions of a gene (and the protein it codes for) are called alleles. Small differences in a protein may not have an impact in certain conditions, but will in other conditions. This is an example $\endgroup$ – De Novo Jul 25 '18 at 19:00

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