Highlights in PNAS

New for October 21, 2020

Ecology

Ancient DNA and range of bovids and rhinoceroses

Prehistoric bovid remains are common in the northeastern Tibetan Plateau (NETP). However, the lineage and range of NETP bovid species are unknown. Ningbo Chen, Lele Ren, Linyao Du, Jiawen Hou, et al. analyzed DNA of approximately 5,200-years-old bovid and rhinoceros specimens from the Neolithic NETP site of Shannashuzha (SNSZ). Comparisons of ancient bovid DNA with the DNA of modern Bovini species found that SNSZ bovid were genetically similar to modern Asian wild gaur and diverged from extant gaur and gayal lineages approximately 18,000 years ago. Comparisons of ancient and extant rhinoceroses revealed that SNSZ rhinoceroses were a sister clade of Sumatran rhinoceroses. The range of extant tropical gaurs and Sumatran-like rhinoceroses extended up to 34.06°N approximately 5,200 years ago. Population reconstructions revealed declining SNSZ gaur populations approximately 5,000 years ago, consistent with paleoclimatic records of the NETP transitioning to a cold climate around that time. However, rhinoceroses roamed throughout the NETP between 8,000 to 6,000 years ago, revealing a warm and moist environment at the time. Radiocarbon dating of NETP archaeological sites found an increase in human settlements with domestic animal pastures between 6,000 and 3,000 years ago. The findings suggest that climatic change and human activities contributed to the disappearance of gaur and Sumatran-like rhinoceroses from middle and high latitudes, leading to the animals’ distribution in tropical regions, according to the authors. — M.S.

"Ancient genomes reveal tropical bovid species in the Tibetan Plateau contributed to the prevalence of hunting game until the late Neolithic," by Ningbo Chen, Lele Ren, Linyao Du, Jiawen Hou, et al.
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Immunology and Inflammation

Probiotic bacteria and multiple sclerosis severity

Multiple sclerosis is an autoimmune disease and a leading cause of nontraumatic neurological disability in young adults. Recent evidence suggests that the gut microbiome modulates disease risk, but the specific bacterial species and the role of host genetics have not been clear. Theresa Montgomery, Axel Ku?nstner, et al. modulated the gut microbiome of genetically diverse mice with experimental autoimmune encephalomyelitis (EAE), an animal model for multiple sclerosis. Wild-derived PWD strain of mice and conventional laboratory B6 mice had different levels of susceptibility to EAE and different gut microbiome profiles. Transplantation of gut microbes from PWD mice to B6 mice resulted in more severe EAE compared with transplantation between B6 mice. Additional analysis revealed that Lactobacillus reuteri, a commensal species commonly found in the gut and often used in probiotics, was almost completely absent in B6 mice but highly abundant in PWD mice. Moreover, B6 mice that were colonized with L. reuteri isolated from PWD mice developed more severe EAE, compared with control B6 mice lacking this bacterial species. According to the authors, antibiotic or probiotic strategies to prevent or treat multiple sclerosis should take into account host genetics and the preexisting gut microbiome. — J.W.

"Interactions between host genetics and gut microbiota determine susceptibility to CNS autoimmunity," by Theresa L. Montgomery, Axel Ku?nstner, et al.
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Medical Sciences; Environmental Sciences

Great Chinese Famine and tuberculosis risk

The Great Chinese Famine, which spanned 1958 to 1962, was among the deadliest famines in human history. Yet the famine’s long-term impact on infectious diseases remains uncertain. To assess the impact of the famine on pulmonary tuberculosis (PTB) over subsequent decades, Qu Cheng et al. analyzed data from more than one million PTB cases reported between 2005 and 2018 in Sichuan Province, which experienced high mortality rates during the famine. The authors also used a model that accounted for risks associated with aging as well as trends in tuberculosis incidence over time. When compared with neighboring cohorts, people born during the famine and their putative children exhibited significantly higher rates of tuberculosis, suggesting an intergenerational effect of prenatal and early life exposure to famine. A comparison of cohorts that were and were not affected by the famine found that more than 12,000 active PTB cases reported between 2005 and 2018 in Sichuan province were attributable to the famine. The findings suggest that individuals who experience severe malnourishment early in life, as well as their children, are at a heightened risk of contracting PTB in adulthood, according to the authors. — M.S.

"Prenatal and early-life exposure to the Great Chinese Famine increased the risk of tuberculosis in adulthood across two generations," by Qu Cheng, et al.
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Population Biology

Plague outbreaks during the second pandemic

Plague outbreaks during the second pandemic spanning the 14th to 17th centuries decimated human populations in Europe and Asia. Although genetic studies of the causative pathogen, Yersinia pestis, have yielded important insights, several aspects of the disease transmission mode and dynamics remain unclear. David Earn et al. analyzed historical, demographic, and epidemiological data from London, England, and estimated mortality using three datasets assembled between 1348 and 1666. The archival records included the London Bills of Mortality, parish registers, and wills and testaments. The data revealed that the epidemic growth rate increased by a factor of four from the Black Death of 1348 to later epidemics, ending with the Great Plague of 1665. Additional analyses of mortality rates suggest that the 14th-century epidemics, and possibly later epidemics, likely did not spread primarily through direct, or pneumonic, human-to-human transmission. Instead, the growth rates for both the early and late epidemics are consistent with bubonic, or indirect, flea-driven, transmission. In addition, climatic changes such as cooling temperatures and the substantial increase in human population density during the 300-year period may have contributed to the increase in the plague epidemic growth rate, according to the authors. — J.W.

"Acceleration of plague outbreaks in the second pandemic," by David J.D. Earn, Junling Ma, Hendrik Poinar, Jonathan Dushoff, and Benjamin M. Bolker
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Some of the highlights have previously appeared on the PNAS media tipsheet. The articles in PNAS report original research by independent authors and do not necessarily represent the view of the National Academy of Sciences.

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