How deep is that gene pool

In the years that followed, scores of the couple’s friends died of AIDS but he never got ill, despite being as sexually active as them all and not taking any special precautions.

When he realized he was different, he volunteered to work with doctors to find out why.

‘I couldn’t infect the CD4 cells,’ Dr Bill Paxton, who the worked at the Aaron Diamond AIDS Research Center in New York, said. ‘I’d never seen that before.’

Years later, researchers isolated the reason. H.I.V. gets into the white blood cells by fitting into two receptors but Mr Crohn’s second receptor was flawed due to a genetic defect.

The anomaly, found in less that 1 per cent of the population, saved Mr Crohn’s life.

Of course, being childless, this particular instance of this particular set of genes isn’t going to perpetrate down the generations. Bit it’s an interesting example of quite how deep that gene pool is. Quite how difficult it would be for any one disease to kill us all.

The other example I can think of is the way that the Black Death significantly changed the genetic make up of Europe. And of course this is very much Matt Ridley territory, all Red Queen and so on.

And, at the extreme, it explains the existence of sex: which brings us rather full circle giving that we’re talking about HIV.

11 comments on “How deep is that gene pool


    Maybe, maybe not. I suspect it may.

    “In addition to Ms Santagata, Mr Crohn is survived by two other sisters, Carla Crohn Friedman and Judith Bloom, and their children whom he loved.”

    But it all seems a bit pointless. We know how to survive the AIDS epidemic – don’t have anal sex with a lot of other men, don’t shoot up and don’t sleep with Africans. Hardly rocket science.

  2. Random mutations persist and succeed if they are useful. Mr Crohn’s mutation must have arisen to protect against some other virus, since there has been insufficient time since the emergence of HIV. What that virus is or was would be interesting to know.

  3. Or mutation came about as random chance, not targeted against particular problem. Not all mutations will be targeted against something.

    Tim adds: No mutation will be targeted against anything. They’re random, by definition. Although they can turn out to be useful. This is the survival of the fittest part.

  4. This article is a joke, come on! “Dr Bill Paxton”, researching “Mr Crohn’s disease”??

    If I met the Good Doctor, my head would explode.

    “Any questions?”
    “Yeah, how do I get out of this chickenshit outfit?”

  5. Random mutations persist and succeed if they are useful.

    They don’t need to be useful, they just need to be not harmful.

  6. Gildas’s articles are fascinating and well worth a read. One conclusion was that Crohn’s genes had been selected for by the Black Death pandemic.

    I think I commented over at Anna’s- this may be a more general explanation for AIDS distribution worldwide. The civilised world has been suffering epidemics (including STDs such as syphilis) for a long time. This may have led to increased resistance in other ways that Crohn’s immunity, requiring a higher viral load, for instance, for infection.

    Thus, the curious lack of an AIDS epidemic in the West, but not among populations without a long history of urban civilisation, e.g. Africa. Westerners thus are much more likely to require an unusual means of transmission (anal sex, intravenous, etc) than Africans. Otherwise, an STD with such a long incubation before showing symptoms ought to have been epidemic; but it wasn’t.

  7. Thanks SMBL.
    the virus / bacillus controversy has been bubbling away in the groves (or cauldrons?) of academe for quite a while.
    As Henry Kissinger put it: Academic disputes are so virulent because the stakes are so small.
    Hard to get much smaller than a virus.

  8. Gildas’s writings on the Black Death are interesting but mostly wrong. The DNA evidence shows that Black Death was indeed caused by ancestors of modern Y.pestis.

    The patterns of spread he discusses are consistent with pneumonic Y.pestis infection being spread by coughing. And, contrary to what his veterinary advisors seem to have told him, disseminated intravascular coagulation is a known risk of the disease.

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