Evolution of Virulence

Once upon a time, I thought a lot about evolution and pathogens.  I still do, on occasion.

It used to be the case [and still is] that many biologists thought that natural selection would inevitably tend towards a situation in which pathogens did infinitesimal harm to their host.  This despite the epidemics all around them. I remember reading a book on parasitology in which the gormless author mentioned a certain species of parasitic copepod that routinely blinded the fish they attached to.  He said that many a naive grad student would think that that these parasitic copepods were bad for the fish, but sophisticated evolutionists like himself knew (and would explain to the newbies) that of course the fish didn’t suffer any reduction in fitness by going blind – theory said so !  Clearly, that man had a Ph.D.

If a pathogen can gain increased reproduction by tapping host resources, or by doing any damn thing that helps itself and hurts the host,  that tactic may pay, and be selected for. It depends on the balance between the advantages and costs – almost entirely those to the pathogen, since the pathogen evolves much more rapidly than the host.  In some cases, as much as a million times faster – because of  generations that may be 20 minutes long rather than 20 years, because  pathogens often have very large populations, which favors Fisherian acceleration, and in many cases, a relatively high mutation rate.  Pathogen evolution is, at least some cases, so rapid that you see significant evolutionary change within a single host.  Along the same lines, we have seen very significant evolutionary changes in antibiotic resistance among pathogenic bacteria over the past few decades,    but I’m pretty sure that there hasn’t been much evolutionary change in mankind since I was a kid.

So when analyzing  virulence, people mostly consider evolutionary pressures on the pathogens,  rather than the host.  Something like the Born-Oppenheimer approximation.

There are some patterns we have a pretty good understanding of.  Often, a pathogen gains from leaving the host mobile, which generally entails leaving the host alive, except for the well-known zombiefication germ.  Pathogens spread by vectors – mosquito-born diseases such as  malaria and sleeping sickness, or  water-borne diseases such as cholera – tend to do more harm, because host mobility is not so important for them. Thus, a pathogen that is  originally virulent, like myxomatosis,  may evolve towards lower virulence if it’s killing its hosts too rapidly.

Vertical transmission –  usually transmission from a mother to her children –  pushes a pathogen towards being harmless or even beneficial.   If all transmission is vertical, and the organism reduced fitness, it is easy to see that carriers (and pathogen) would go extinct. So pure vertical transmission selects for  beneficial effects – in females.   There are maternally transmitted organisms that cause parthenogenensis and eliminate all males.  Along the same line, there is evidence that male-harming mutations accumulate in mitochondria, an idea called Mother’s Curse. I don’t think this is what is happening with human male homosexuality, but it has been suggested.

Steve Frank ( who is sharp!) suggests another pattern. Consider a parasite cloaking device, something interferes with or avoids host immunity. This reduces the clearance of the parasite.  Second, the cloaking device causes an increase in virulence at later times, by which we mean a greater chance of host death at that later time.  The fitness sensitivity of changes in survival is always weaker at later ages, because the probability of being alive is always smaller at later ages.  So Frank predicts that a parasite always gains by reducing clearance at earlier times even if that causes an equivalent risk to the parasite at a later time by increasing the host death rate.  If the damage to the host appears farther in the future, after the infection is cleared, then of course  such an action is favored by selection.  This seems to often happen in diseases triggered by molecular mimicry (a way of avoiding clearance) , such as  Type-I diabetes or rheumatic fever. With rheumatic fever, the molecular similarity between the strep germs and heart valves causes cross reactions that leave the patient with long-term heart problems.  This also happens with Chagas disease.

If a pathogen action reduced host fitness, but without killing the host or reducing mobility, there would be no cost to the pathogen at all.  Thus you shouldn’t be too surprised to see pathogens cause sterility in their host.  Even the slightest advantage  (such as a slightly increased chance of avoiding early clearance) would be enough to favor this.  For that matter, if happened by accident – if pathogens drifted into a situation did harm to the host but that would not lead to further transmission – it wouldn’t be disfavored by selection.

Most of the infections that cause sterility or reduced fertility are STDs,  and I would guess that those effects happen, to a large extent, because the pathogens are in the right neighborhood. It’s a lot easier to interfere with the reproductive system if you’re already there.  On the other hand, other pathogens also cause sterility:  tuberculosis is one of the most common causes of infertility in backward countries.

There is another principle that particularly limits the virulence of pathogens attacking humans.  We know of pathogens that can wipe out species, or come close:  you don’t see many American elms or American chestnuts anymore.  Almost all koalas have a retrovirus that is responsible for > 80% of deaths and threatens to wipe out the species.  Tasmanian Devils are being attacked by an infectious host cell line that threatens to put all of them in the cold, cold ground. The chytrid fungus has wiped out many frog species. What’s our secret?

If we had been hit by something that serious, we probably wouldn’t be here at all, and I wouldn’t be writing this.  The anthropic principle rides again!

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59 Responses to Evolution of Virulence

  1. gwern says:

    > This also happens with Chagas disease,

    Cut off?

  2. The fourth doorman of the apocalypse says:

    I think that is myxomatisis not myxmomatosis.

    Still. Damn good stuff. I wish it was up on Hacker News instead of the other crap.

  3. JH says:

    The anthropic principle works as an account if the rate at which species-destroying plagues arise is low in evolutionary time, as new species can be produced fast enough to replace the lost ones. But if disease evolution is so fast that host evolution mostly can’t keep up, why aren’t all species destroyed by plagues like the frogs or the elms?

    • misreavus says:

      Wouldn’t you think that once the species goes kaput, the pathogen would die along with it?

      But of course, pathogens are unfeeling, insensate sacks of protoplasm that are wholly devoid of rational thought, and thus incapable of projecting short-term trends into the future. (Say, doesn’t that sound familiar?) Genes that surge of the competition are those that win the evolutionary race. If the population momentum is such that the host population has been decimated beyond recovery, and neither host nor pathogen can cope with the loss — well, that’s just the tragedy of the commons.

    • misreavus says:

      *surge AHEAD of the competitoin

      Some plausible scenarios to consider re: pathogen-mediated extinction:

      1) A particularly virulent pathogen spreads itself through host-to-host contact, and the onset of disease is late enough that a critical percentage of the host population has been infiltrated. (See: gay men and HIV, but we have prophylactics and anti-retrovirals. Plus not all gay men are stupid, I hope! — just the vast, vast majority.) Predictably, this causes the host population density to plummet, thereby reducing the likelihood of host-to-host contacts. Uh-oh.

      Unfortunately, this is bad for the host as well, because a low population density makes it harder for certain species to mate and restore their numbers, particularly if they have a narrow habitat range, a low fecundity, a long generation time, or any combination thereof. And this scenario is especially likely to occur if the host population was tiny to begin with. Goodbye host, goodbye pathogen.

      2) The pathogen exploits some kind of defense mechanism that is critical for the host’s own survival, but ultimately results in self-destruction when it is employed against the pathogen. (See: dutch elm disease.)

      This makes it challenging for the host to evolve resistence to the pathogen, because any weakening of the defense mechanism would also induce a critical loss of fitness to the host. If the loss of fitness is even greater than the impact of the pathogen — well, that’s just too bad. Even if the entire gene pool dwindles down to nothing, certain genes will inevitably emit their dying gasp sooner than others.

      3) The host is the last surviving member of an ancient evolutionary clade for which few ecological niches remain today. (See: gingko trees) This not limits species radiation, because there are few environments left for the species to colonize* (or, more likely, other niches *do* exist elsewhere in the world, but the distance is too far to permit species dispersal), but it also limits genetic diversity within the species, because the species is so well-adapted to that unusual environment. For this reason, domesticated plants that are propagated through grafting are especially prone to diseases that threaten to cause host extinction. (See: bananas and grapes)

      (*Moreover, because the species is the sole remaining survivor of an ancient clade, the introgression of resistance-bearing alleles into the host gene pool becomes especially unlikely.)

      4) The bug renders the host unusually popular, charismatic, pleasant in the company of others, or otherwise irresistable to other potential hosts. Unfortunately, it also causes sterility or otherwise impacts fitness in a big way. But that’s ok, because in the very short term, this happens to be the perfect evolutionary strategy for the host. And nothing else matters.

      Eventually, the species plummets to its extinction, with its few surviving members dying in inexorable ecstasy. Perhaps this is the best way for us to depart from this world.

      The most important thing to consider is that no species anywhere, past or present, EVER adopts an evolutionary strategy simply because it benefits the whole species. (Sorry, Wynne-Edwards, but you were dead wrong.)

      If a lucky mutant happens to behave in a way that magnifies its fitness in the short term, but completely destroys its ecosystem in the long term — well, that’s just life. Nobody could foresee it when it was happening, and nobody even wanted to.

      Worst of all, in a tragic twist of fate, anybody who COULD foresee it, and acted accordingly, would have been selected out of the gene pool long ago. This has disturbing implications for our species.

      All of us living on earth are assholes, and there is nothing to be done about it.

      • albatross says:

        It seems like the anthropic principle could give you some level of genes that benefit the whole species, at some low or negligible cost to the individual. Species in which such genes arose would tend to be a little less likely to go extinct over time, and so would show up now.

        For pathogens: a pathogen that is successful by quickly killing its host and spreading before the host dies has a relatively good chance of “burning itself out,” by killing all its available hosts and going extinct (along with all its possible hosts in some area). So at any given time, we probably won’t see a lot of those pathogens circulating. (The ones we do see will have some other reservoir they can live in, and they’ll occasionally jump over from bats or monkeys or something.) If that pathogen mutates into a form where it keeps its host alive and infectious for longer, it has a better chance of not going extinct.

        And a pathogen that circulates often enough can do some serious selection on its much-slower-evolving hosts. If the measles go around once every few years, and all the kids in the village catch them, then kids with genes that incline them to survive a childhood measles infection will see a pretty big improvement in their fitness. At the extreme, that can be purifying selection–people without the resistance gene always die in childhood epidemics, so soon everyone in the population has the resistance gene.

      • misdreavus says:

        Unless those genes carried a powerful individual advantage, they would be unlikely to ever reach fixation. I don’t know of very many genes like that where the marginal benefit to the individual is greater than the marginal cost.

        My whole point is that sometimes, a strategy that does wonders for short term fitness might very well cause extinction in the long term. And any mutant that saw this coming, and acted accordingly would therefore be selected out of the gene pool.

        It’s the same story with liberals who voluntarily refuse to have children out of concern for overpopulation. Since political orientation is heritable, you can only guess the consequences in the long term.

      • albatross says:

        I understand the gene-level selection argument you’re making. I’m just saying I think survivorship bias could have some effect on what we see at any given time. Species where some gene arose whose success was disastrous for its species’ long-term survival tend to be extinct species, by the time modern biologists arive on the scene and start thinking about them. I don’t have an intuition for whether that’s especially important, but it seems like an effect that *could* matter. There’s no gene-level selection for behaving in ways beneficial to the species, but there is a survivorship bias that means that, at least, you won’t see a lot of examples of species that have genes that are very good for them and very bad for the species as a whole, just because they won’t be around to be examples.

      • misdreavus says:

        Of course.

  4. The fourth doorman of the apocalypse says:

    I knew about the chlamydia but not the KoRV.

  5. Carl Lumma says:

    Not directly related to this post, but an idea that any lover of controversy might consider, is the possibility that smallpox eradication led to (or accelerated) HIV zoonosis.

    • RS says:

      what, by causing human overpopulation?

      • Carl Lumma says:

        There are a few plausible mechanisms, not mutually exclusive. The viruses are related through their action on the CCR5 receptor and, re. the original post here, may have competed for the same hosts. The use of a related virus (vaccinia) in the vaccine is also potentially a factor. The timing of the zoonosis relative to eradication is also about right. All highly speculative, mind you. But I think it merits investigation.

  6. Jaim Jota says:

    To complicate the equation, parasites are competing with other parasites of the same host, and themselves are targeted by parasites. It’s a hard life!

    • gcochran9 says:

      Yep. And that can influence selection for virulence: a pathogen might, by itself, do better by letting the host live a long time, but if there are competing pathogens, better to have that lunch before someone else does.

      • Lesser Bull says:

        Conversely, a parasite that imposes a cost on the host that by itself doesn’t cripple the host might find itself dead because other parasites are also imposing costs and it exceeded what the host could take. The cost the parasite imposes on the host is going to be a sort of balance between its own benefit, what the host can bear, and the costs other parasites are imposing.

  7. Hideous says:

    Intelligence is an immune mechanism (among other things). It helps humans avoid infections (sometimes by minimizing contact with vectors) and survive illness. Complex social behaviours sometimes have immune benefits; people often recover from illnesses which would be more likely fatal if faced alone because other humans feed and guard them while they are weak. Of course there are tradeoffs since socializing facilitates the transmission of many pathogens.

  8. Matt says:

    Interesting topic, so… if they’re almost totally ineffective (virulence is entirely determined pathogen side by the balance of fitness costs and benefits), immune systems must be fairly simple and cheap? The immune system should be more and more outpaced by pathogens as time goes on, and the faster adaptation rates of pathogens compound.

    I would have intuitively thought that pathogens may have a faster rate of adaptation, but their low complexity tends to limit the amount that they can *do* with this faster rate (there aren’t many places they can go which are effective) and the more complex host systems can often deal with them? But this is probably a wealthy world, high medicine availability, good public health control delusion.

    • greg kai says:

      Not sure that their low complexity is a limit, but there sure are a lot of limit o what biological entities can do: even with unlimited time for evolution, one can not bend the law of physics. And a pathogen is in a very hostile milieu, even if very rich in nutrient and very stable conditions. It will be surrounded be a huge amount of hostile non-reproducing clones which thus cooperate much more strongly than the pathogen, and can specialise much more. So the host also have inherent advantages, to counterbalance the evolution rate.

    • gcochran9 says:

      It’s not so much that immune systems are ineffective, more that they don’t change very rapidly. It has been argued that sex pays for itself (probably in part) by speeding up host evolution, primarily in a race against pathogens.

      You are probably right about the lower complexity.

      One other point: vertebrates have more complex immune systems, with adaptive immunity. But it’s not clear that they get sick any less than plants and invertebrates that don’t have the adaptive component. Perhaps pathogens have risen to the occasion. In the same way, zebras may run faster than their distant ancestors, but lions do too, so they may be in about the same place.

      • albatross says:

        I think you have to think of an immune system as both evolving in competition with pathogens, and also evolving in competiton with other members of your species. If I’m better at fighing off infections than my neighbors, that pays off in fitness terms. And you can see that, because we’ve got immune systems tuned far enough in the paranoid direction that they sometimes kill their owners through overzealous responses (anaphalaxis) or mistargeting (autoimmune diseases).

        How much is known about plant and insect immune systems? ISTR there are some kinda-sorta adaptive mechanisms (siRNAs made in response to some previously-seen viruses), but nothing like what you see in jawed-fish-and-higher vertebrates.

  9. Greying Wanderer says:

    “It used to be the case [and still is] that many biologists thought that natural selection would inevitably tend towards a situation in which pathogens did infinitesimal harm to their host. This despite the epidemics all around them.”

    Didn’t many/most of the worst ones come from somewhere else though? So the source population had developed some immunity but the target population hadn’t e.g. American Indians, lots of the big European plagues etc.

    The assumption that homosexuality has always been c. 3% leads down one set of paths but what if it wasn’t. What if it’s been < 1% for most of history and only started to increase relatively recently i.e. homosexuality ~ globalization.

  10. Intelligence is an immune system against most threats to life. If one accepts that wealthy people in the US are more likely to be intelligent, then they avoid all causes of deaths more effectively than poorer and putatively less bright Americans, save one: deaths in private planes.

  11. J. Cotton says:

    A layman here…
    I find this topic very fascinating. I have a question though. If the homosexuality germ theory holds, to my uninformed view, this would mean someone can be “infected” late in life (e.g. adulthood), right? If no, why not?
    Also, any suggestions for a book on evolutionary theory, accessible to a layman?

    • RS says:

      Dawkins’ Selfish Gene is not all that different from an undergrad textbook which you can find on the syllabus of some good uni. The textbook has useful diagrams and is probably more essential if you have to pick one. The Dawkins is better-written and can be profitably added.

      Unless you have some special disinterest in humans I would also read 10k Year Explosion ; given that it’s about people, which tends to drive high interest in the brain, you can pretty much read it in two or three sittings. Wade’s Before the dawn is similarly engrossing and covers the pre-agri period.

      • albatross says:

        A hypothetical gay germ could affect development, and so only have an effect within some window of time. And it could easily be some otherwise harmless childhood germ that, like polio, occasionally gets into the brain and messes something up.

        One thing I think we should see if the gay germ idea is true: we should see examples where there is a sudden change in the level of homosexuality of a culture, as the germ shows up and affects them. For example, was there a big change in the rate of homosexuality among American Indians after European contact? Or pacific islanders? Even if the germ had been with us forever, small isolated populations could lose it over time, and then have it re-introduced. And people with long contact with the germ would be expected to have more immunity to it, since the germ has a noticable fitness cost. (That could be partly cultural–say, a universal idea that a man has a duty to leave an heir or two even if he prefers boys, which would decrease the fitness cost of being gay.)

    • Carl Lumma says:

      “If the homosexuality germ theory holds, to my uninformed view, this would mean someone can be “infected” late in life (e.g. adulthood), right? If no, why not?”

      Shhh. Don’t disturb the natives’ delicate thinking patterns.

      What does your uninformed view tell you about the germ that causes heterosexual couples in cities all over the world to have 1 or 0 children? That one’s spreading like wildfire.

  12. The fourth doorman of the apocalypse says:

    Can I assume you are taking a jab at the anthropic principle?

  13. dave chamberlin says:

    Your blog had got me thinking alot about pathogens, evolution, and human history. I’ve read a fair amount of history and damned if the rise and fall of empires isn’t always attributed to the competence or incompetence of Big Al the Great or Little Fred the Wimpy. Funny how those barbarian hordes always come sweeping down from the north (colder climate=less diseases that can survive=lower infant mortality rates=population expantion). Seems like the history books don’t like to give germs much credit for shaping human history. You can read five books on the decline of the Roman Empire and not find one single reference to the influence of disease even though the same climate differences made a huge impact on the size of surviving families in the United states in the 18th century. Just about as shunned an idea as your gay germ theory is any mention that maybe, just maybe, that human evolution could give a bit more push to higher intelligence in colder regions because the battle against pathogens wasn’t quite so intense.

    • a very knowing American says:

      “Plagues and Peoples” by William H. McNeill makes the argument at length that new diseases spread by the opening of trade routes across Eurasia brought down the Roman Empire and, around the same time, the Han dynasty in China. Later, bubonic plague spread though Eurasia along trade routes opened by the Mongol empire. Lots of good stuff there, although he repeats the conventional wisdom about germs evolving to be less harmful over time.

  14. For whatever it’s worth I tweeted: pathogen evolution (put into context of selfish-genetic-elements and aging/entropy), (snipped out the URL to this blog here) — Richard Harper ‏@harpersnotes

  15. Dahlia says:

    “Vertical transmission – usually transmission from a mother to her children – pushes a pathogen towards being harmless or even beneficial. If all transmission is vertical, and the organism reduced fitness, it is easy to see that carriers (and pathogen) would go extinct.”

    HIV’s primary mode of transmission is not vertical, which explains it’s virulence and in the absence of treatment, the risk of vertical transmission (mother-to-baby) of HIV is as high as 25-30%. What is it for the other known stds? And the unknown stds?

    At Unz’s thread of his latest post, in the context of saying we should not take STDs off the table as an explanation for homosexuality, I neglected to point out that we’re too used to thinking of STDs as something caused mainly by individual behavior.

    • albatross says:

      HIV would benefit from longer coexistence with its hosts–a longer healthy period for the host = more time to spread to the host’s gay bathhouse buddies or prostitutes or plasma recipients or whatever. The problem is that HIV mutates very quickly, so at any time, a patient has a really astonishing number of viral variants in him–even if some of those variants would help the host survive longer (say, not trashing the lymphatic system, not infecting the brain, etc.) they have a gazillion destructive roommates who will still trash the place.

      On the other hand, there are people who get HIV and live a long time with it, even without treatment–called long-term non-progressors. If I understand correctly, the mechanism involves their adaptive immune system being able to present a somewhat wider-than-usual set of antigens on the surface of B cells and macrophages and T cells, so that the virus takes a very long time (perhaps a natural lifetime) to evolve entirely around the immune response. (There are also people who are almost immune to infection, because they have a mutant coreceptor for the virus.)

      Imagine a world where there’s no modern medicine when HIV shows up. It spreads through the population, kills a hell of a lot of people. At the end of that, centuries later, almost the only people left are people with MHC genes that allow a wide enough range of antigens to be presented that they can keep AIDS at bay for a long lifetime, or with the variant coreceptor that prevents infection. Imagine that modern medicine arises several centuries later. Wouldn’t those hypothetical doctors see HIV (which at that point, occasionally makes someone really sick, but usually seems pretty harmless until you get very sick or old) as an example of pathogen/host evolution toward less virulence?

  16. Andrew Ryan says:

    Our secret is genetic diversity. I imagine Greg knows this and is being a bit coy.

    In the case of American elms they are all descended from a single clone which left them vulnerable to infection. I’m not sure what the deal is with the frogs or koalas, but I’m betting a similar bottleneck reduced diversity as well.

    Host selection for resistance (or at least tolerance) underscores why epidemics and high mortality are often seen when a pathogen is introduced into a new, previously unexposed population–think smallpox with Native Americans, respiratory diseases in slaves in New England, malaria in Europeans traveling in Africa, etc.

    • gcochran9 says:

      I believe you’re mistaken about the American elm.

      • Andrew Ryan says:

        You’re right, I was thinking of Dutch Elm Disease in England, which was even worse:

        Nature. 2004 Oct 28;431(7012):1053.
        Phylogeography: English elm is a 2,000-year-old Roman clone.

        “Its highly efficient vegetative reproduction and its inability to set seeds have preserved this clone unaltered for 2,000 years as the core of the English elm population — and the preponderance of this susceptible variety may have favoured a rapid spread of the disease.”

    • Richard Sharpe says:

      Our secret is genetic diversity.

      I recall reading somewhere that we have less diversity than chimps. Is that wrong?

  17. Greying Wanderer says:

    “One thing I think we should see if the gay germ idea is true: we should see examples where there is a sudden change in the level of homosexuality of a culture, as the germ shows up and affects them.”

    If just for the sake of argument it was West African in origin and immunity only develops over time with long exposure then it will be proved quite soon with a tsunami of sexual dysfunction in China due to China’s relatively sudden and massive exposure over the last 20 years.

    • misdreavus says:

      Well, it’s not true, so stop making the argument.

      • Greying Wanderer says:

        There’s two possibilities
        1) The rate of homosexuality among European populations has always been the same.
        2) It increased at some point in the past.

        Taking 2) as the premise for the purpose of process of elimination then if it increased at some point then one possibility – if it’s some kind of bug – is that the bug came from somewhere else.

        There are a number of possibilities for that “somewhere else” e.g. Asia, America, Africa etc and if you take each of them one by one that creates a grid of possibilities.

        One of the options on that grid is source Africa – which is being put to the test right now because of China’s relatively sudden and massive exposure.

        It’s a testable proposition. I thought that’s what you science types were all about?

      • misdreavus says:

        Logic is not your forte. #2 is the *only* plausible scenario, because if lifelong homosexuality exists in few species of mammal other than our own, and if our ancestors did not have it, by definition, it had to have started from a frequency of zero! What you say is trivial information. Nothing more.

        None of your other goofy speculations even follow logically from this premise.

  18. anonymous says:

    if the gay germ idea is true: we should see examples where there is a sudden change in the level of homosexuality of a culture, as the germ shows up and affects them.”

    American Indians exhibited a considerable level of homosexulity in many tribes. Gotta wonder — was it there pre-Columbus? OR was it new?

    We know that Old World livestock-origin diseases — smallpox, measles,flu, TB — which were brought by the Spaniards inthe early 1500s, swept the New World natives with terrible cruelty. In particular, they nearly emptied out North America, clearing way for the AngloAmericans to move in rather easily 2 centuries later.

    Perhaps an Old World homosexuality-inducing microbe also swept the New World at that time?

  19. nameless37 says:

    It’s funny that one of the first examples cited by the post – myxomatosis – is actually a counterexample to the given thesis.

    Myxomatosis is a vector borne disease. As such it does not care much whether it kills its victims or not. On the other hand, rabbits are among the likeliest mammal species to demonstrate evolution within a single human lifespan (only smaller rodents – mice and rats – evolve even faster.) In 1950 there were more rabbits in the UK than humans, and rabbits reach sexual maturity at the age of 3 months. When myxomatosis was introduced in the UK, it killed 99% of all infected rabbits. Within 25 years, the disease indeed mutated towards longer survival of its victims (killing them in weeks instead of days), but rabbits themselves mutated too, to the point where they exhibited mortality rates of only ~50% even when exposed to fully virulent strains of the disease.

  20. The fourth doorman of the apocalypse says:

    Let’s talk about where size matters? Is phallus size a reproductive barrier among some waterfowl?

  21. Greying Wanderer says:

    Might this tie in to the idea that bugs affecting sexual attraction may not be restricted to homosexuality and that rather homosexuality is possibly merely the canary in the coalmine of a wider phenomenon?


    “Antibiotic Protects Men from Being Too Trusting of Attractive Women”

  22. JayMan says:

    On the topic of homosexuality, here is an example of what discordant (possibly) MZ twins look like (via Steve Sailer’s).

  23. Pingback: Dark Enlightenment News from Around the Web | Occam's Razor

  24. Pingback: Greg Cochran’s “Gay Germ” Hypothesis – An Exercise in the Power of Germs | JayMan's Blog

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