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Abstract COVID‐19 has highlighted a brutal reality known for decades, that Black, Indigenous, and People of Color bear a disproportionate burden of US annual sepsis cases. While plentiful research funds have been spent investigating genetic reasons for racial disparities in sepsis, an abundance of research shows that sepsis incidence and mortality maps to indicators of colonial practices including residential segregation, economic and marginalization sepsis, and denial of care. Here we argue that sepsis risk is an immunological embodiment of racism in colonial states, that the factors contributing to sepsis disparities are insidious and systemic. We show that regardless of causative pathogen, or host ancestry, racialized people get and die of sepsis most frequently in a pattern repeatedly reiterated worldwide. Lastly, we argue that while alleviation of sepsis disparities requires radical, multiscale intervention, biological anthropologists have a responsibility in this crisis. While some of us can harness our expertise to take on the ground action in sepsis prevention, all of us can leverage our positions as the first point of contact for in depth human biology instruction on most college campuses. As a leading cause of death worldwide, and a syndrome that exhibits the interplay between human physiology, race and environment, sepsis is at the nexus of major themes in biological anthropology and is a natural fit for the field's curriculum. In adopting a discussion of race and sepsis in our courses, we not only develop new research areas but increase public awareness of both sepsis and the factors contributing to uneven sepsis burden. 

Abstract Among mammals, humans are exquisitely sensitive to lipopolysaccharide (LPS), an environmentally pervasive bacterial cell membrane component. Very small doses of LPS trigger powerful immune responses in humans and can even initiate symptoms of sepsis. Close evolutionary relatives such as African and Asian monkeys require doses that are an order of magnitude higher to do the same. Why humans have evolved such an energetically expensive antimicrobial strategy is a question that biological anthropologists are positioned to help address. Here we compare LPS sensitivity in primate/mammalian models and propose that human high sensitivity to LPS is adaptive, linked to multiple immune tactics against pathogens, and part of multi‐faceted anti‐microbial strategy that strongly overlaps with that of other mammals. We support a notion that LPS sensitivity in humans has been driven by microorganisms that constitutively live on us, and has been informed by human behavioral changes over our species' evolution (e.g., meat eating, agricultural practices, and smoking). 

The COVID-19 pandemic is extraordinary, but many ordinary events have contributed to its becoming and persistence. Here, we argue that the emergence of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus, which has radically altered day-to-day life for people across the globe, was an inevitability of contemporary human ecology, presaged by spillovers past. We show the ways in which the emergence of this virus reiterates other infectious disease crises, from its origin via habitat encroachment and animal use by humans to its evolution of troublesome features, and we spotlight a long-running crisis of inequitable infectious disease incidence and death. We conclude by describing aspects of SARS-CoV-2 and the COVID-19 pandemic that present opportunities for disease control: spaces for intervention in infection and recovery that reduce transmission and impact. There are no more “before times”; therefore, we encourage embracing a future using old mitigation tactics and government support for ongoing disease control. 

Many genes that respond to infection have functions outside of immunity and have been found to be under natural selection. Pathogens may therefore incidentally alter nonimmune physiology through engagement with immune system genes. This raises a logical question of how genetically promiscuous the immune system is, here defined as how heavily cross-referenced the immune system is into other physiological systems. This work examined immune gene promiscuity across physiological systems in primates by assessing the baseline (unperturbed) expression of key tissue and cell types for differences, and primate genomes for signatures of selection. These efforts revealed “immune” gene expression to be cross-referenced extensively in other physiological systems in primates. When immune and nonimmune tissues diverge in expression, the differentially expressed genes at baseline are enriched for cell biological activities not immediately identifiable as immune function based. Individual comparisons of immune and nonimmune tissues in primates revealed low divergence in gene expression between tissues, with the exception of whole blood. Immune gene promiscuity increases over evolutionary time, with hominoids exhibiting the most cross-referencing of such genes among primates. An assessment of genetic sequences also found positive selection in the coding regions of differentially expressed genes between tissues functionally associated with immunity. This suggests that, with increasing promiscuity, divergent gene expression between the immune system and other physiological systems tends to be adaptive and enriched for immune functions in hominoids.