Some heterozygote advantages in humans are:

  1. People with sickle-cell trait are resistant to malaria, but people with sickle-cell disease tend to die young.
  2. Depending of the source we believe, people with one copy of a cystic fibrosis allele are immune to tuberculosis, or cholera, or typhoid fever (or two of them or all the three!) (it has been debunked).
  3. People with one copy the CCR5-delta 32 allele are resistant to AIDS, when they have two copies, they are immune to AIDS, but they are at higher risk for West Nile virus disease complications.
  4. People with Niemann-Pick disease type C are completely immune to ebolavirus-related hemorrhagic fever, and their heterozygous parents seem to be resistant against this disease caused by a filovirus.

So, I wonder what would a heterozygote advantage against pork tapeworm (Taenia solium) look like. I ask because my story is set in a future where tapeworms have evolved to be able to survive MUCH higher temperatures, and therefore, it has become more difficult to cook mammalian meats without burning them. Therefore, many humans died from neurocysticercosis.

The molecular mechanism behind this is three genes linked to Hirschsprung's disease (RET, EDNRB, and GDNF, respectively on chromosome 10, on chromosome 13, and on chromosome 5).

  • $\begingroup$ Heterozygot: an individual having two different alleles of a particular gene or genes, and so giving rise to varying offspring. Alleles: one of two or more alternative forms of a gene that arise by mutation and are found at the same place on a chromosome. Question: Can you explain why I shouldn't VTC as too story-based? Because those definitions imply that you can randomly choose what it "looks like" to suit your story needs. (Note that all your examples are bacteria/virus sized critters and a tape worm... isn't...). $\endgroup$
    – JBH
    Jul 19, 2022 at 23:57
  • $\begingroup$ This seems like a brainstorming question where you're asking us to generate ideas for you. Such questions are not permitted on this site. $\endgroup$
    – sphennings
    Jul 20, 2022 at 0:13
  • 2
    $\begingroup$ @sphennings - it actually seems to me the opposite. The idea is pretty much had. Are answers constrained to those 3 genes? If you are positing that heterozygosity of one of those genes confers protections vs the tapeworm are you looking for mechanism? I suspect you know mechanism since you specified the genes! If you want to know how the homozygotes would be sick you can just look up the phenotypes of the mouse knockouts of those genes. $\endgroup$
    – Willk
    Jul 20, 2022 at 0:20
  • $\begingroup$ All your examples are small things like virus and plasmodiums. Are there any real examples of a heterozygote protecting you from big things like tapeworm? $\endgroup$
    – Daron
    Jul 20, 2022 at 12:27
  • $\begingroup$ I am also unsure what an example would look like. Please give the answer in the desired level of depth for one of your four real examples. Then we will know what an answer for your invented example would look like. $\endgroup$
    – Daron
    Jul 20, 2022 at 12:32

1 Answer 1


Different Conditions

From Wikipedia:

Each [tape worm larva] is oval in shape, containing an inverted scolex (specifically "protoscolex"), which everts once the organism is inside the small intestine. This process of evagination is stimulated by bile juice and digestive enzymes (of the host). Then, the protoscolex lodges in the host's upper intestine by using its crowned hooks and 4 suckers to enter the intestinal mucosa. Then, the scolex is fixed into the intestine by having the suckers attached to the villi and hooks extended.

This suggests three good modifications for tapeworm immunity:

  1. Different stomach enzymes that do not wake up the larva.

  2. Different mucosal layer that makes it hard for the larva to attach due to tooth shape.

  3. Different or absent villi that makes it hard for the larva to attach due to tooth shape. These are villi by the way:

enter image description here

Tiny tentacles on the skin of the intestine.

These three changes occur in people with a single copy of a bad gene.


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