We find patterns consistent with this possibility in mice infected with flu, a pathogen that doesn't naturally infect them and could not nave selected for germline-encoded specificities: some genes consistently dominate early on but individual responses diverge over time. 12/n

Weaker initial advantages lead to similar responses early on but are later overcome by B cell evolution playing out differently in each individual due to chance events (historical contingencies, as Stephen J. Gould put it), leading to decreasing similarity 10/n

When the initial advantage is large relative to the effects of mutation, B cells using those high-affinity germline genes consistently dominate the response across individuals, leading to similar gene frequencies between them. 9/n

But if fitness depends more strongly on subsequent evolution than on the initial germline genes, chance events will likely cause lineages using different genes to win out in different individuals, leading to genetically different B cell responses between them. 7/n

This question informs the predictability of the antibody response: If B cells with specific germline genes consistently outcompete the others, we expect similar gene frequencies in the response of different individuals. 6/n