The population genomic legacy of the second plague pandemic in Trondheim, Norway

SHYAM GOPALAKRISHNAN; INGE LUNDSTRØM; SIGRIDUR S. EBENESERSDOTTIR; LUCY VAN DORP; PIERRE LUISI; 40 AUTORES; THOMAS GILBERT

Manchester

Encuentro; SMBE2019; 2019

Society for Molecular Biology and Evolution

Human populations have been shaped by past catastrophes, some of which may have leftlong-lasting signatures in our genomes. The second plague pandemic represented the most importantdemographic collapse in historical Europe, with mortality rates estimated to possibly >50% of the population. Itis widely assumed this must have significantly affected the genetic makeup of the populations. We explored itsconsequences on the Norwegian city of Trondheim, which like most European cities suffered a pandemicinduced bottleneck, with estimates ranging from 50-70% reduction in census population size attributable to thesecond plague pandemic.To explore the genomic effects of the second plague pandemic in Trondheim, we collected 54 genomesspanning 3 time periods, specifically 11 samples from before 1349 AD, 13 samples from the 16-18thcenturies, and 30 samples from modern Trondheim. Using whole genome sequencing on these samples, weexamined the global genome-wide changes in the ancestry composition of the population, and identifiedregions of the genome which showed radical changes in allele freuquencies through the period of the secondplague pandemic.Despite the relatively small sample sizes of our dataset, our results validate with the hypothesis that thesecond plague pandemic played a significant role in shaping the genomic diversity of Trondheim - somethingexpected given the large estimated change in population size that occurred during this period. In particular,our data is compatible with a major decrease in migration from previous population sources (e.g. the BritishIsles) during this time, consistent with the decrease in Trondheim?s political and economic importance. Theaverage proportion of ancestry derived from British Isles decreases from ~30-40% in the pre-1349 samples, tounder 5% in the post-1349 samples.Additionally, we find allele frequency changes in genes that can be plausibly linked to resistance againstbacterial infections. We note that it is impossible to pinpoint the pathogen Yersinia pestis as the driver of thesechanges - in theory other pathogens or even non pathogenic factors may have lead to the observeddecreases in population diversity and shifts in allele frequencies at key genomic loci. Ultimately this leads usto propose that genetically encoded immune defense and ability to deal with septicemic states may have beena relevant factor for surviving bubonic plague.