Y. pestis strains show reduced virulence during second plague pandemic
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB36413 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR3841650.fastq.gz | Fastqsanger.gz | |||
| ERR3841641.fastq.gz | Fastqsanger.gz | |||
| ERR3841651.fastq.gz | Fastqsanger.gz | |||
| ERR3841642.fastq.gz | Fastqsanger.gz | |||
| ERR3841652.fastq.gz | Fastqsanger.gz |
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Project description:Historical records reveal the temporal patterns of a sequence of plague epidemics in London, United Kingdom, from the 14th to 17th centuries. Analysis of these records shows that later epidemics spread significantly faster ("accelerated"). Between the Black Death of 1348 and the later epidemics that culminated with the Great Plague of 1665, we estimate that the epidemic growth rate increased fourfold. Currently available data do not provide enough information to infer the mode of plague transmission in any given epidemic; nevertheless, order-of-magnitude estimates of epidemic parameters suggest that the observed slow growth rates in the 14th century are inconsistent with direct (pneumonic) transmission. We discuss the potential roles of demographic and ecological factors, such as climate change or human or rat population density, in driving the observed acceleration.
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Project description: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.
| S-EPMC9671091 | biostudies-literature
Project description:Ancient genomic studies have identified Yersinia pestis (Y. pestis) as the causative agent of the second plague pandemic (fourteenth-eighteenth century) that started with the Black Death (1,347-1,353). Most of the Y. pestis strains investigated from this pandemic have been isolated from western Europe, and not much is known about the diversity and microevolution of this bacterium in eastern European countries. In this study, we investigated human remains excavated from two cemeteries in Riga (Latvia). Historical evidence suggests that the burials were a consequence of plague outbreaks during the seventeenth century. DNA was extracted from teeth of 16 individuals and subjected to shotgun sequencing. Analysis of the metagenomic data revealed the presence of Y. pestis sequences in four remains, confirming that the buried individuals were victims of plague. In two samples, Y. pestis DNA coverage was sufficient for genome reconstruction. Subsequent phylogenetic analysis showed that the Riga strains fell within the diversity of the already known post-Black Death genomes. Interestingly, the two Latvian isolates did not cluster together. Moreover, we detected a drop in coverage of the pPCP1 plasmid region containing the pla gene. Further analysis indicated the presence of two pPCP1 plasmids, one with and one without the pla gene region, and only one bacterial chromosome, indicating that the same bacterium carried two distinct pPCP1 plasmids. In addition, we found the same pattern in the majority of previously published post-Black Death strains, but not in the Black Death strains. The pla gene is an important virulence factor for the infection of and transmission in humans. Thus, the spread of pla-depleted strains may, among other causes, have contributed to the disappearance of the second plague pandemic in eighteenth century Europe.
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Project description:Research on the second plague pandemic that swept over Europe from the fourteenth to nineteenth centuries mainly relies on the exegesis of contemporary texts and is prone to interpretive bias. By leveraging certain bioinformatic tools routinely used in biology, we developed a quantitative lexicography of 32 texts describing two major plague outbreaks, using contemporary plague-unrelated texts as negative controls. Nested, network and category analyses of a 207-word pan-lexicome, comprising overrepresented terms in plague-related texts, indicated that 'buboes' and 'carbuncles' are words that were significantly associated with the plague and signalled an ectoparasite-borne plague. Moreover, plague-related words were associated with the terms 'merchandise', 'movable', 'tatters', 'bed' and 'clothes'. Analysing ancient texts using the method reported in this paper can certify plague-related historical records and indicate the particularities of each plague outbreak, which can inform on the potential sources for the causative Yersinia pestis.
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Project description:Bioarchaeological insights into the last plague of Imola (1630-32)
| PRJEB27822 | ENA
Project description:This study used virological, histological, immunological and global gene expression to compare the virlence of two newly emerged 2009 H1N1 isolates (A/Mexico/InDRE4487/2009 and A/Mexico/4108/2009) and current seasonal H1N1 influenza strain (A/Kawasaki/UTK-4/2009) in experimentally infected cynomolgus macaques. We showed that infection of macaques with two genetically similar but clinically distinct SOIV isolates from the early stage of the pandemic (A/Mexico/4108/2009 and A/Mexico/InDRE4487/2009) resulted in upper and lower respiratory tract infections and clinical disease ranging from mild to severe pneumonia. Disease associated with these SOIV isolates was clearly advanced over the mild infection caused by A/Kawasaki/UTK-4/2009, a current seasonal strain.
2011-08-30 | GSE31694 | GEO