Marisa Azad "Rational design of antimicrobial peptide-bacteriophage therapy for biofilm-mediated periprosthetic joint infection: an evolution-informed strategy" |
Brendan Bohannan "The social microbiome and public health" |
Trevor Graham |
Johannes Krause |
Lynnette Leidy Sievert "Beyond the end of fertility: evolutionary perspectives on menopause, post-reproductive aging, and women’s health" |
Prize winners
For more information about the prizes, please see this link. |
George C. Williams Prize winner
Daniel Stadtmauer "Proximate and ultimate causes of pregnancy sickness" | Gilbert S. Omenn Prize winners
Johan Nordgren & Richard Ågren "Natural selection of a virus-protective FUT2 variant following the transition to agriculture" |
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Abstract
Periprosthetic joint infection (PJI) is a devastating complication of joint replacement surgery, commonly caused by biofilm-forming multidrug-resistant pathogens that colonize prosthetic surfaces. These complex microbial communities exhibit reduced metabolic activity, phenotypic heterogeneity, and enhanced capacity for persistence, collectively limiting immune clearance and antibiotic efficacy. We developed an evolution-informed combinatorial strategy using rationally designed α-helical antimicrobial peptides (AMPs) with strain-specific lytic bacteriophages to simultaneously disrupt membranes, penetrate biofilms, and constrain antibiotic resistance evolution. Lead AMP M-5W0A demonstrated broad-spectrum activity against clinical PJI isolates, including methicillin-resistant Staphylococcus aureus (MRSA), vancomycin resistant enterococci (VRE), and S. epidermidis, with minimum inhibitory concentration (MIC) ranging from 2–512 µg/mL, including maintained efficacy against highly resistant phenotypes (e.g., Corynebacterium striatum 2 µg/mL; S. epidermidis 8 µg/mL; VRE 32 µg/mL; MRSA 128 µg/mL). In combination therapy, we observed synergistic killing, accelerating clearance of both planktonic and biofilm-associated populations at reduced effective doses. On implant-relevant stainless-steel surfaces, this approach achieved up to 85% reduction in biofilm metabolic activity and multi-log reductions in viable bacterial burden. Hemocompatibility assays confirmed minimal erythrocyte toxicity at bactericidal concentrations, supporting translational feasibility. These results establish a scalable, evolution-informed framework for treating hardware-associated infections. More broadly, they demonstrate how combining antimicrobials with distinct mechanisms of action can impose ecological and evolutionary constraints on pathogenic populations, offering an effective strategy for addressing biofilm-associated antimicrobial resistance in healthcare.
About the speaker
Marisa completed a combined MD/PhD in Biochemistry and a residency in Internal Medicine at McMaster University in 2019. She completed a fellowship in Infectious Diseases at the University of Ottawa and followed up with an advanced fellowship in Orthopedic Infectious Diseases at the Mayo Clinic in 2022. She is currently an Assistant Professor of Medicine in the Division of Infectious Diseases at The Ottawa Hospital, an Associate Clinical Scientist and a Mayo Clinic Research Collaborator at the Ottawa Hospital Research Institute. Her research focuses on exploiting the molecular and microbial mechanisms of periprosthetic joint infections to develop novel rapid diagnostics and therapeutics.
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Abstract It has long been known that pathogenic microbes can be transmitted through social interactions among host individuals. Recent studies of insects, mammals, birds, non-human primates, and humans have revealed that non-pathogenic (i.e. beneficial or commensal) microbes can also be socially transmitted, and that socially interacting hosts have more similar microbiomes. These observations have led to the concept of the social microbiome—the community of microbes exchanged among host individuals that share a social network. Social transmission has important consequences for evolution, providing for example a mechanism for microbiome heritability across host generations. The social transmission of non-pathogenic microbes also has important implications for medicine and public health. Recent studies suggest that socially transmitted non-pathogenic microbes share unique traits, and that socially assembled microbiomes can make unique, positive contributions to host health, implying that health may be transmissible in ways analogous to the transmission of disease. Given this possibility, strategies for reducing the spread of infectious disease (such as social distancing and quarantine) may have unintended negative impacts on the transmission of beneficial microbes, which could lead to negative consequences for health. Public health strategies that reduce the spread of disease while minimally impacting the transmission of health are thus needed. Designing such strategies will require a much deeper understanding of the social microbiome, especially the dispersal biology of pathogenic vs non-pathogenic microbes. |
About the speaker Brendan is the Alec and Kay Keith Professor at the University of Oregon and the director of the university’s Institute of Ecology and Evolution. He is a contributor to the Proceedings of the National Academy of Sciences. In 2019, he was awarded a $7.6 million grant from the U.S. National Institutes of Health to investigate the potential health benefits of bacteria. His research focuses on understanding the causes and consequences of microbial biodiversity. With his research group, he examines the fundamental drivers of biodiversity, the effects of environmental change on microbial communities, and how microbial diversity changes in human-dominated environments—including those within the human body and other host organisms. |
About the speaker Trevor joined the Institute of Cancer Research as Director of the Centre
for Evolution and Cancer in 2022 and is a group leader of the Genomics
and Evolutionary Dynamics laboratory. For the previous 8.5 years Trevor
led the Evolution and Cancer laboratory at the Cancer Research UK Barts
Cancer Institute within Queen Mary University of London. Trevor’s
laboratory was the first mathematical theory-led laboratory in the
Institute. He co-led the development of computational biology as core
research theme at Barts, culminating in the establishment of the Centre
for Genomics and Computational Biology in 2019, where Trevor was deputy
lead. Trevor’s research is focused on understanding the evolutionary
dynamics of cancer development and translating this knowledge to improve
clinical management of disease. His laboratory combines expertise in
evolutionary theory, mathematical modelling and bioinformatics, together
with cutting-edge wet-lab analyses foremost in genomics, single cell
sequencing and molecular pathology. |
About the speaker Johannes is the Managing Director of the Max Planck Institute for
Evolutionary Anthropology and a leading expert in ancient DNA research.
He focuses on the analysis of ancient DNA to investigate such topics as
pathogens from historic and prehistoric epidemics, human genetic
history, and human evolution. He has contributed to deciphering
Neanderthal genetics and the shared genetic heritage of Neanderthals and
modern humans. In 2010, he discovered the first genetic evidence of the
Denisovans, an extinct hominin found in the Altai Mountains in Siberia.
His recent work includes revealing the genetic heritage of ancient
Egyptians, reconstructing the oldest modern human genome, studying late
Pleistocene genomes from Africa, Central Asia and Europe, uncovering the
source of the epidemic plague bacteria that periodically caused
historic and prehistoric epidemics in Eurasia, studying the evolution
and genetic history of pathogens such as Mycobacterium leprae, M. tuberculosis, Treponema pallidum, Hepatitis B virus, Salmonella enterica, Helicobacter pylori
and the Herpes virus, as well as clarifying the complex history of
Western Eurasia’s prehistoric mass migrations. He has authored more than 250 publications, mainly in peer-reviewed journals, including Nature, Science, Cell, Nature Reviews Genetics, etc. He has given more than 400 invited presentations and his research has been featured in numerous television, radio, print and online media sources, including The New York Times, Washington Post, BBC, NPR, Discovery Channel, National Geographic, Zweites Deutsches Fernsehen, 3Sat, ARTE, Der Spiegel, FAS, FAZ, Die Zeit, Die Welt, Süddeutsche Zeitung, Science, Nature, and considerably more. He has also authored two international bestsellers focusing on human history: A Short History of Humanity: How Migration Made Us Who We Are and Hubris: The Journey of Humankind. |
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Abstract For comparative biologists, menopause is the end of female fertility observed across mammalian taxa. For human biologists, female menopause is a universal life history event within the genus Homo. For perimenopausal women, evolution may seem to be irrelevant as complaints at midlife range from hot flashes to itchy ears. Why does menopause occur, and why is it accompanied by hot flashes, vaginal dryness, risk of osteoporosis, and other complaints and concerns? Post-reproductive life occurs when female longevity extends beyond the supply of gametes. Our own longevity lengthened more than one million years ago, alongside an increase in cranial capacity, tool use, the benefits of fire, and protection from predators. Among all female mammals, the depletion of gametes across the lifespan is a highly conserved trait. The gradual loss of ovarian follicles and concomitant decline in levels of estradiol contribute to symptoms attributed to menopause, although naturally occurring hot flashes appear limited to humans. From an evolutionary perspective, the lengthened somatic lifespan is a mismatch. Alternatively, we can identify the importance of estrogen early in life for thermoregulation, vaginal health, and bone strength to explain the deleterious effects of estrogen withdrawal at menopause and beyond. About the speaker Lynnette has studied variation in age at menopause and symptoms at midlife for more than 30 years. In collaboration with local researchers, she carried out studies of menopause in western Massachusetts; Hilo, Hawaii; the Selška Valley, Slovenia; Asunción and Mbaracayu, Paraguay; Puebla and Campeche, Mexico; Sylhet, Bangladesh; and London, UK, as well as pilot studies in Odisha, India, and Ulaanbaatar, Mongolia. Lynnette also studies and writes about the evolution of menopause and post-reproductive life. Of late, she has been disentangling the experience of hot flashes from the heat and humidity of Campeche, Mexico, and planning to study hot flashes in the winter cold of Mongolia. Her current study is on hot flashes in relation to estimates of brown adipose tissue. Lynnette is an elected Fellow of the AAAS, served on the Board of Trustees of the North American Menopause Society, and was the Editor-in-Chief of the American Journal of Human Biology, the journal of the Human Biology Association. |
George C. Williams Prize winner |
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Abstract Evolutionary biologists have long been fascinated by pregnancy sickness, the heritable, stereotyped syndrome in early pregnancy that usually consists of benign nausea and vomiting and in around 1% of cases progresses to the pathological extreme hyperemesis gravidarum. Identification of the placental hormone GDF15 as a principal causal factor justifies reassessment of its proximate and ultimate causes. This Review synthesizes knowledge of pregnancy sickness at the four levels of analysis of classical ethology-mechanism, development, phylogeny, and adaptive function. Emerging insight into GDF15's role in innate sickness behaviors suggests pregnancy sickness is a heightened state of pre-existing behavioral defenses triggered by placental production of an emetogenic hormone which may hold a different primary function. Comparison of transcriptomes reveals that placental GDF15 production rose 100- to 1000-fold to human-like levels in catarrhine primates, and is low or absent in New World monkeys, rodents, and other mammals, with the possible exception of elephants. This suggests that pregnancy sickness is phylogenetically restricted yet not human-specific, and associates with innovations in syncytiotrophoblast biology rather than diet. I re-evaluate leading adaptive hypotheses (prophylactic, metabolic rewiring, placental growth, and anti-rejection) and argue that the key to adjudicating among them hinges on whether GDF15 acts locally through non-canonical receptors and whether additional factors distinguish pregnancy sickness from sickness behavior. Finally, I evaluate explanations for the persistent risk of hyperemesis gravidarum in modern humans, including trade-offs, mismatch, and conflict. With recent advances, pregnancy sickness is not just a curiosity of human evolution, but a compelling opportunity to investigate the mechanistic bases of complex adaptive behaviors. |
Gilbert S. Omenn Prize winners |
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Abstract Common enteric viruses rely on sugars mediated by the galactoside 2-alpha-L-fucosyltransferase 2 (FUT2) enzyme to infect host cells. Analyzing 4,343 ancient genomes, we map a premature stop codon in FUT2, which was introduced into Europe by migrating Anatolian farmers ∼6000 BC and provide evidence for positive selection. Using data from ∼700,000 present-day individuals, we confirm its protective effect against viral gastroenteritis. Experiments with intestinal organoids reveal that only homozygous carriers are protected against noroviruses and rotaviruses but not sapovirus. Our rotavirus findings resolve a long-standing contradiction between epidemiological data and experiments. Contrary to previous reports, we find no association between FUT2 loss of function and Helicobacter pylori infection. However, carriers exhibit an increased risk of gastric ulcers and gallbladder disease, associations replicated with an independent loss-of-function variant in East Asia. These findings suggest that the transition to agriculture and increased pathogen exposure drove positive selection of this allele. |