The Red Queen_ Sex and the Evolution of Human Nature - Matt Ridley [38]
Other parasites try to mimic the passwords carried by the host. The selective pressure is on all pathogens to mimic the passwords of their hosts. The selective pressure is on all hosts to keep changing the password. This, according to Bremermann, is where sex comes in.
The histocompatibility genes, which determine more than the passwords, but are themselves responsible for susceptibility to disease, are richly polymorphic. There are over one hundred versions of each histocompatibility gene in the average population of mice, and even more in human beings. Every person carries a unique combination, which is why transplants between people other than identical twins are always rejected, unless special drugs are taken. And without sexual outbreeding, it is impossible to maintain that polymorphism.
Is this conjecture or is there proof? In 1991 Adrian Hill and his colleagues from Oxford University produced the first good evidence that the variability of histocompatibility genes is driven by disease. They found that one kind of histocompatibility gene, HLA-Bw 53, is frequent where malaria is common and very rare elsewhere. Moreover, children ill with malaria generally do not have HLA-Bw53. That may be why they are ill.43 And in an extraordinary discovery made by Wayne Potts at the University of Florida at Gainesville, house mice appear to choose as mates only those house mice that have different histocompatibility genes from their own. They do this by smell. This preference maximizes the variety of genes in mice and makes the young mice more disease-resistant.44
Bill Hamilton and Parasite Power
That sex, polymorphism and parasites have something to do with each other is an idea with many authors. With characteristic prescience, J. B. S. Haldane got most of the way there.
I wish to suggest that [heterozygosity] may play a part in disease resistance, a particular race of bacteria or virus being adapted to individuals of a certain range of biochemical constitutions, while the other constitutions are relatively resistant.
Haldane wrote that in 1949, four years before the structure of DNA was elucidated.45 An Indian colleague of Haldane’s, Suresh Jayakar, got even closer a few years later.46 Then the idea lay dormant for many years until the late 1970s, when five people came up with the same notion independently of each other within the space of a few years: John Jaenike of Rochester, Graham Bell of Montreal, Hans Bremermann of Berkeley, John Tooby of Harvard and Bill Hamilton of Oxford.47
But it is Hamilton who has pursued the connection between sex and disease most doggedly and has become most associated with it. In appearance Hamilton is an almost implausibly perfect example of the absent-minded professor, as he stalks through the streets of Oxford, deep in thought, his spectacles attached umbilically to a string round his neck, his eyes fixed on the ground in front. His unassuming manner and relaxed style of writing and story-telling are deceptive. Hamilton has a habit of being at the right place in biology at the right time. In the 1960s, he moulded the theory of kin selection – the idea that much of animal co-operation and altruism is explained by the success of genes that cause animals to look after close relatives, because close relatives share many of the same genes. Then in 1967 he stumbled on the bizarre internecine warfare of the genes that we shall meet in the next chapter. By the 1980s he was anticipating most of his colleagues in pronouncing reciprocity as the key to human co-operation. Again and again, in this book, we will find we are treading in Hamilton’s footsteps.48
With the help of two colleagues from the University of Michigan, Hamilton built a computer model of sex and disease, a slice of artificial life. It began with an imaginary population of two hundred creatures. They happened to be rather like humans – each began breeding at fourteen,