A new kind of evidence for a known conclusion
Variola virus DNA has been extracted from the remains of two individuals at the Camarones 9 site in northern Chile, both dated to between 1492 and 1631. The genomes belong to a now-extinct branch that split off after medieval European strains, and they are near-identical to one another, a resemblance pointing to two people falling ill in the same outbreak.[1]
The novelty here lies elsewhere than in the conclusion itself. That colonisation carried the disease has been inferred for centuries from chronicles, baptismal registers and population estimates; the team presents its findings as the first molecular confirmation of that transfer. When a claim moves from testimony to material evidence, what changes is less its degree of truth than the ground of the argument: objections built on the reliability of a written source no longer land in the same place.[1]
Two centuries slow, then fast
The team's second finding is more interesting and more fragile. The virus shows slow genome evolution across roughly two centuries coinciding with colonial expansion, after which the mutation rate accelerates around the period of widespread vaccination. One reading is that the virus reached a form good enough to spread and needed no further adaptation.[1]
The researchers stop here and draw the line themselves: no proper causation can be claimed for the overlap, though the correlation is at least notable. That caution is well placed, because something more prosaic can produce the same pattern: the number of genomes recovered from different periods is not equal, and a change in sampling density can create an apparent shift in rate without any real change in rate. The molecule is no less talkative than testimony; it simply errs in a different language.[1]
Where two kinds of evidence check each other
In this column's 25 July piece I argued that plague genomes had made the unwritten Eurasia of about 5,300 years ago legible. The two graves in Chile put the same instrument into a period rich in written sources, and that is what matters: in prehistory the genome was the only witness, here it is the second. Two kinds of evidence look at the same event from different places and can check one another. The first test of that checking is already clear: once more genomes from the same period are recovered, we will see whether the reported change in rate survives. That a five-century argument about who passed an epidemic to whom can now be continued by asking both who told the story and what remains in whose bone quietly changes the question of on whose behalf we speak for the past.[1], [2]