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The medieval Black Death (c. 1347-1351) was one of the most devastating epidemics in human history. It killed tens of millions of Europeans, and recent analyses have shown that the disease targeted elderly adults and individuals who had been previously exposed to physiological stressors. Following the epidemic, there were improvements in standards of living, particularly in dietary quality for all socioeconomic strata. This study investigates whether the combination of the selective mortality of the Black Death and post-epidemic improvements in standards of living had detectable effects on survival and mortality in London. Samples are drawn from several pre- and post-Black Death London cemeteries. The pre-Black Death sample comes from the Guildhall Yard (n = 75) and St. Nicholas Shambles (n = 246) cemeteries, which date to the 11th-12th centuries, and from two phases within the St. Mary Spital cemetery, which date to between 1120-1300 (n = 143). The St. Mary Graces cemetery (n = 133) was in use from 1350-1538 and thus represents post-epidemic demographic conditions. By applying Kaplan-Meier analysis and the Gompertz hazard model to transition analysis age estimates, and controlling for changes in birth rates, this study examines differences in survivorship and mortality risk between the pre- and post-Black Death populations of London. The results indicate that there are significant differences in survival and mortality risk, but not birth rates, between the two time periods, which suggest improvements in health following the Black Death, despite repeated outbreaks of plague in the centuries after the Black Death.

Was the mortality associated with the deadliest known epidemic in human history, the Black Death of 1347-1351, selective with respect to preexisting health conditions (\"frailty\")? Many researchers have assumed that the Black Death was so virulent, and the European population so immunologically naïve, that the epidemic killed indiscriminately, irrespective of age, sex, or frailty. If this were true, Black Death cemeteries would provide unbiased cross-sections of demographic and epidemiological conditions in 14th-century Europe. Using skeletal remains from medieval England and Denmark, new methods of paleodemographic age estimation, and a recent multistate model of selective mortality, we test the assumption that the mid-14th-century Black Death killed indiscriminately. Skeletons from the East Smithfield Black Death cemetery in London are compared with normal, nonepidemic cemetery samples from two medieval Danish towns (Viborg and Odense). The results suggest that the Black Death did not kill indiscriminately--that it was, in fact, selective with respect to frailty, although probably not as strongly selective as normal mortality.

Crisis mortality events such as disease epidemics and famines have long had major impacts on human health and demography, and clarifying variation in susceptibility to crisis mortality is crucial for enhancing our understanding of the larger-scale phenomena of human adaptation and biological variation. Previous bioarchaeological research using data from human skeletal remains has revealed variable patterns of biological, and by inference, social determinants of vulnerability to medieval famine and plague mortality. However, such previous work did not account for missing data and the potential associated biases. For this study, we apply a novel approach integrating dietary isotope, pathological, and demographic data into multinomial logistic regression analyses of mortality differentials during famine and plague events in medieval London, while controlling for missing data. The results suggest higher risks of famine and plague mortality for males and for individuals previously exposed to stressors, and higher risks of plague (but not famine) mortality for older adults. Further, we find evidence that protein-rich diets were protective against famine and plague mortality. Our findings highlight how various biological and social factors shaped risks of mortality in medieval London, even in the context of major mortality crises, which are often assumed to be indiscriminate in nature.

Reconstruction of Black Death genome The latest DNA recovery and sequencing technologies have been used to reconstruct the genome of the Yersinia pestis bacterium responsible for the Black Death pandemic of bubonic plague that spread across Europe in the fourteenth century. The genome was pieced together from total DNA extracted from the skeletal remains of four individuals excavated from a large cemetery on the site of the Royal Mint in East Smithfield in London, where more than 2,000 plague victims were buried in 1348 and 1349. The draft genome sequence does not differ substantially from modern Y. pestis strains, providing no answer to the question of why the Black Death was more deadly than modern bubonic plague outbreaks. Technological advances in DNA recovery and sequencing have drastically expanded the scope of genetic analyses of ancient specimens to the extent that full genomic investigations are now feasible and are quickly becoming standard 1 . This trend has important implications for infectious disease research because genomic data from ancient microbes may help to elucidate mechanisms of pathogen evolution and adaptation for emerging and re-emerging infections. Here we report a reconstructed ancient genome of Yersinia pestis at 30-fold average coverage from Black Death victims securely dated to episodes of pestilence-associated mortality in London, England, 1348–1350. Genetic architecture and phylogenetic analysis indicate that the ancient organism is ancestral to most extant strains and sits very close to the ancestral node of all Y. pestis commonly associated with human infection. Temporal estimates suggest that the Black Death of 1347–1351 was the main historical event responsible for the introduction and widespread dissemination of the ancestor to all currently circulating Y. pestis strains pathogenic to humans, and further indicates that contemporary Y. pestis epidemics have their origins in the medieval era. Comparisons against modern genomes reveal no unique derived positions in the medieval organism, indicating that the perceived increased virulence of the disease during the Black Death may not have been due to bacterial phenotype. These findings support the notion that factors other than microbial genetics, such as environment, vector dynamics and host susceptibility, should be at the forefront of epidemiological discussions regarding emerging Y. pestis infections.

More than 20 years ago, Wood et al. (Curr Anthropol 33:343-370, 1992) published \"The Osteological Paradox: Problems of Inferring Prehistoric Health from Skeletal Samples,\" in which they challenged bioarchaeologists to consider the effects of heterogeneous frailty and selective mortality on health inferences in past populations. Here, we review the paper's impact on bioarchaeology and paleopathology, focusing on recent advancements in studies of ancient health. We find the paper is often cited but infrequently engaged in a meaningful way. Despite an initial decade of limited progress, numerous researchers are now addressing components of the Paradox in more informed ways. We identify four areas of fruitful research: (1) intrasite, contextual perspectives, (2) subadults, (3) associating stress markers with demographic phenomena, and (4) skeletal lesion-formation processes. Although often seen as a problematic assumption, understanding the sources of heterogeneous frailty within human populations is a worthy research question in and of itself, and one that clearly links past and present health research within a global framework.

The successful reconstruction of an ancient bacterial genome from archaeological material presents an important methodological advancement for infectious disease research. The reliability of evolutionary histories inferred by the incorporation of ancient data, however, are highly contingent upon the level of genetic diversity represented in modern genomic sequences that are publicly accessible, and the paucity of available complete genomes restricts the level of phylogenetic resolution that can be obtained. Here we add to our original analysis of the Yersinia pestis strain implicated in the Black Death by consolidating our dataset for 18 modern genomes with single nucleotide polymorphism (SNP) data for an additional 289 strains at over 600 positions. The inclusion of this additional data reveals a cluster of Y. pestis strains that diverge at a time significantly in advance of the Black Death, with divergence dates roughly coincident with the Plague of Justinian (6(th) to 8(th) century AD). In addition, the analysis reveals further clues regarding potential radiation events that occurred immediately preceding the Black Death, and the legacy it may have left in modern Y. pestis populations. This work reiterates the need for more publicly available complete genomes, both modern and ancient, to achieve an accurate understanding of the history of this bacterium.

The recent Ebola epidemic provides a dramatic example of the devastation and fear generated by epidemics, particularly those caused by new emerging or reemerging diseases. A focus on the control and prevention of diseases in living populations dominates most epidemic disease research. However, research on epidemics in the past provides a temporal depth to our understanding of the context and consequences of diseases and is crucial for predicting how diseases might shape human biology and demography in the future. This article reviews recent research on historic epidemics of plague and tuberculosis, both of which have affected human populations for millennia. Research on these diseases demonstrates the range (and differential availability) of various lines of evidence (e.g., burial context, diagnostic skeletal lesions, molecular data) that inform about past disease in general. I highlight how research on past epidemics may be informative in ways that benefit living populations.

Infectious diseases are among the strongest selective pressures driving human evolution 1 , 2 . This includes the single greatest mortality event in recorded history, the first outbreak of the second pandemic of plague, commonly called the Black Death, which was caused by the bacterium Yersinia pestis 3 . This pandemic devastated Afro-Eurasia, killing up to 30–50% of the population 4 . To identify loci that may have been under selection during the Black Death, we characterized genetic variation around immune-related genes from 206 ancient DNA extracts, stemming from two different European populations before, during and after the Black Death. Immune loci are strongly enriched for highly differentiated sites relative to a set of non-immune loci, suggesting positive selection. We identify 201 variants that are highly differentiated within the London dataset. Combining evidence from during the Black Death, our replicate population in Denmark, and function evidence, rs2549794 near ERAP2 emerges as the strongest candidate for positive selection. The selected allele at rs2549794 is associated with the production of a full-length (versus truncated) ERAP2 transcript, variation in cytokine response to Y. pestis and increased ability to control intracellular Y. pestis in macrophages. Finally, we show that protective variants overlap with alleles that are today associated with increased susceptibility to autoimmune diseases, providing empirical evidence for the role played by past pandemics in shaping present-day susceptibility to disease. Klunk and colleagues identify signatures of natural selection imposed by Yersinia pestis and demonstrate their effect on genetic diversity and susceptibility to certain diseases in the present day.

The ongoing COVID-19 pandemic has justifiably captured the attention of people around the world since late 2019. It has produced in many people a new perspective on or, indeed, a new realization about our potential vulnerability to emerging infectious diseases. However, our species has experienced numerous catastrophic disease pandemics in the past, and in addition to concerns about the harm being produced during the pandemic and the potential long-term sequelae of the disease, what has been frustrating for many public health experts, anthropologists, and historians is awareness that many of the outcomes of COVID-19 are not inevitable and might have been preventable had we actually heeded lessons from the past. We are currently witnessing variation in exposure risk, symptoms, and mortality from COVID-19, but these patterns are not surprising given what we know about past pandemics. We review here the literature on the demographic and evolutionary consequences of the Second Pandemic of Plague (ca. fourteenth–nineteenth centuries C.E.) and the 1918 influenza pandemic, two of the most devastating pandemics in recorded human history. These both provide case studies of the ways in which sociocultural and environmental contexts shape the experiences and outcomes of pandemic disease. Many of the factors at work during these past pandemics continue to be reproduced in modern contexts, and ultimately our hope is that by highlighting the outcomes that are at least theoretically preventable, we can leverage our knowledge about past experiences to prepare for and respond to disease today.

Climate change is an indisputable threat to human health, especially for societies already confronted with rising social inequality, political and economic uncertainty, and a cascade of concurrent environmental challenges. Archaeological data about past climate and environment provide an important source of evidence about the potential challenges humans face and the long-term outcomes of alternative short-term adaptive strategies. Evidence from well-dated archaeological human skeletons and mummified remains speaks directly to patterns of human health over time through changing circumstances. Here, we describe variation in human epidemiological patterns in the context of past rapid climate change (RCC) events and other periods of past environmental change. Case studies confirm that human communities responded to environmental changes in diverse ways depending on historical, sociocultural, and biological contingencies. Certain factors, such as social inequality and disproportionate access to resources in large, complex societies may influence the probability of major sociopolitical disruptions and reorganizations—commonly known as “collapse.” This survey of Holocene human–environmental relations demonstrates how flexibility, variation, and maintenance of Indigenous knowledge can be mitigating factors in the face of environmental challenges. Although contemporary climate change is more rapid and of greater magnitude than the RCC events and other environmental changes we discuss here, these lessons from the past provide clarity about potential priorities for equitable, sustainable development and the constraints of modernity we must address.