The population genomic legacy of the second plague pandemic.

Human populations have been shaped by catastrophes that may have left long-lasting signatures in their genomes. One notable example is the second plague pandemic that entered Europe in ca. 1,347 CE and repeatedly returned for over 300 years, with typical village and town mortality estimated at 10%-40%.1 It is assumed that this high mortality affected the gene pools of these populations. First, local population crashes reduced genetic diversity. Second, a change in frequency is expected for sequence variants that may have affected survival or susceptibility to the etiologic agent (Yersinia pestis).2 Third, mass mortality might alter the local gene pools through its impact on subsequent migration patterns. We explored these factors using the Norwegian city of Trondheim as a model, by sequencing 54 genomes spanning three time periods: (1) prior to the plague striking Trondheim in 1,349 CE, (2) the 17th-19th century, and (3) the present. We find that the pandemic period shaped the gene pool by reducing long distance immigration, in particular from the British Isles, and inducing a bottleneck that reduced genetic diversity. Although we also observe an excess of large FST values at multiple loci in the genome, these are shaped by reference biases introduced by mapping our relatively low genome coverage degraded DNA to the reference genome. This implies that attempts to detect selection using ancient DNA (aDNA) datasets that vary by read length and depth of sequencing coverage may be particularly challenging until methods have been developed to account for the impact of differential reference bias on test statistics.

[The complex plague--reconsiderations of an epidemic from the past]. / Den komplekse pesten--revurderinger av en epidemi fra fortiden.

Speculations have arisen about the black plague in recent years - was it a disease caused by YERSINIA PESTIS: or something else? Extensive outbreaks in India in the 1890s have formed the basis for descriptions of the plague, both for those who believe that the medieval plagues and modern plague were different diseases and for those who claim that the plague has been one and the same disease throughout history. The plague was more or less defined as a disease in the 1890s, and the understanding of its clinical course and dissemination at the time has uncritically been understood as the general model for spreading of the plague. But plague is a many-faceted disease. It has spread to five continents in modern times, through an array of ecosystems and under widely different climatic conditions. It can also be passed on to man, and from one individual to another, in different ways. The biological conditions that prevailed in India have not been relevant for medieval Norway. The preconditions for spreading of plague epidemics of the past in a Nordic climate must therefore have been different. It can only be expected that contemporary descriptions of historic epidemics are different from those in modern times.