Today’s title refers to the perhaps unexpected origins of the recent swine ’flu outbreak, that apparently  comes not from the widespread intermingling of wildfowl and table ducks in Asia but via as yet uncertain processes in the western hemisphere. In the previous blog, I summarised some of the issues of swine flu as I saw them. Meanwhile, the e-print scientific literature is starting to become populated with some epidemiological and related analyses (I thank Fiona Tomley of our Institute for Animal Health for drawing my attention to some of them). The general consensus remains that the present outbreak is of a strain that is not excessively virulent, but that during the northern summer (southern winter) a reservoir of infection (in pigs, birds and humans) will build up and the likelihood of mutations or reassortment events producing something considerably nastier will increase significantly. [...]

That genetic differences account for a substantial part of biological variability is hardly in dispute, and the inclusion of genetics (and increasingly molecular genetics) was arguably the key contribution that created neo-Darwinism and led to the ‘modern synthesis’ of evolutionary theory.

Selective breeding programmes amply illustrate the contribution to the phenotype that can be effected by genetic variation. Thus in a very nice summary, Hill (2005) describes an experiment at the University of Illinois (Laurie et al. 2004) that has been running since 1896. In this experiment, scientists have selected (and bred) strains of maize (corn) that are either high or low in the content of oil in their kernels (a trait of considerable agronomic importance). Over the years, the initial 5% oil has changed to 20% in the high-oil lines, and has decreased almost to zero in the low-oil strains. (A similar experiment using protein as the trait of interest gave a similar result, save that the ‘low-protein’ lines retain about 5% of protein.) Genetic analysis (of the quantitative trait loci) showed that a great many parts of the genome contributed this variation in oil content, that the largest could account for a difference of only 0.3% in oil content, and most accounted for just 0.1 – 0.2%. Given this, it is possibly unsurprising that these (small) effects were seen as additive (i.e. independent); put another way, there was negligible epistasis observed in these populations in which all other genes were also segregating. [...]