The Th1 cell regulatory circuitry is largely conserved between human and mouse

Gene expression programs controlled by lineage-determining transcription factors are often conserved between species. However, infectious diseases have exerted profound evolutionary pressure, and therefore the genes regulated by immune-specific transcription factors might be expected to exhibit greater divergence. T-bet (Tbx21) is the immune-specific, lineage-specifying transcription factor for T helper type I (Th1) immunity, which is fundamental for the immune response to intracellular pathogens but also underlies inflammatory diseases. We compared T-bet genomic targets between mouse and human CD4+ T cells and correlated T-bet binding patterns with species-specific gene expression. Remarkably, we found that the majority of T-bet target genes are conserved between mouse and human, either via preservation of binding sites or via alternative binding sites associated with transposon-linked insertion. Species-specific T-bet binding was associated with differences in transcription factor–binding motifs and species-specific expression of associated genes. These results provide a genome-wide cross-species comparison of Th1 gene regulation that will enable more accurate translation of genetic targets and therapeutics from pre-clinical models of inflammatory and infectious diseases and cancer into human clinical trials

Parasite-stress promotes in-group assortative sociality: the cases of strong family ties and heightened religiosity

Throughout the world people differ in the magnitude with which they value strong family ties or heightened religiosity. We propose that this cross-cultural variation is a result of a contingent psychological adaptation that facilitates in-group assortative sociality in the face of high levels of parasite-stress while devaluing in-group assortative sociality in areas with low levels of parasite-stress. This is because in-group assortative sociality is more important for the avoidance of infection from novel parasites and for the management of infection in regions with high levels of parasite-stress compared with regions of low infectious disease stress. We examined this hypothesis by testing the predictions that there would be a positive association between parasite-stress and strength of family ties or religiosity. We conducted this study by comparing among nations and among states in the United States of America. We found for both the international and the interstate analyses that in-group assortative sociality was positively associated with parasite-stress. This was true when controlling for potentially confounding factors such as human freedom and economic development. The findings support the parasite-stress theory of sociality, that is, the proposal that parasite-stress is central to the evolution of social life in humans and other animals

Prediction and prevention of the next pandemic zoonosis.

Most pandemics--eg, HIV/AIDS, severe acute respiratory syndrome, pandemic influenza--originate in animals, are caused by viruses, and are driven to emerge by ecological, behavioural, or socioeconomic changes. Despite their substantial effects on global public health and growing understanding of the process by which they emerge, no pandemic has been predicted before infecting human beings. We review what is known about the pathogens that emerge, the hosts that they originate in, and the factors that drive their emergence. We discuss challenges to their control and new efforts to predict pandemics, target surveillance to the most crucial interfaces, and identify prevention strategies. New mathematical modelling, diagnostic, communications, and informatics technologies can identify and report hitherto unknown microbes in other species, and thus new risk assessment approaches are needed to identify microbes most likely to cause human disease. We lay out a series of research and surveillance opportunities and goals that could help to overcome these challenges and move the global pandemic strategy from response to pre-emption

One Health – an Ecological and Evolutionary Framework for tackling Neglected Zoonotic Diseases

Understanding the complex population biology and transmission ecology of multihost parasites has been declared as one of the major challenges of biomedical sciences for the 21st century and the Neglected Zoonotic Diseases (NZDs) are perhaps the most neglected of all the Neglected Tropical Diseases (NTDs). Here we consider how multihost parasite transmission and evolutionary dynamics may affect the success of human and animal disease control programmes, particularly neglected diseases of the developing world. We review the different types of zoonotic interactions that occur, both ecological and evolutionary, their potential relevance for current human control activities, and make suggestions for the development of an empirical evidence base and theoretical framework to better understand and predict the outcome of such interactions. In particular, we consider whether preventive chemotherapy, the current mainstay of NTD control, can be successful without a One Health approach. Transmission within and between animal reservoirs and humans can have important ecological and evolutionary consequences, driving the evolution and establishment of drug resistance, as well as providing selective pressures for spill‐over, host switching, hybridizations and introgressions between animal and human parasites. Our aim here is to highlight the importance of both elucidating disease ecology, including identifying key hosts and tailoring control effort accordingly, and understanding parasite evolution, such as precisely how infectious agents may respond and adapt to anthropogenic change. Both elements are essential if we are to alleviate disease risks from NZDs in humans, domestic animals and wildlife

Guns, germs, and stealing: exploring the link between infectious disease and crime.

Can variation in crime rates be traced to the threat of infectious disease? Pathogens pose an ongoing challenge to survival, leading humans to adapt defenses to manage this threat. In addition to the biological immune system, humans have psychological and behavioral responses designed to protect against disease. Under persistent disease threat, xenophobia increases and people constrict social interactions to known in-group members. Though these responses reduce disease transmission, they can generate favorable crime conditions in two ways. First, xenophobia reduces inhibitions against harming and exploiting out-group members. Second, segregation into in-group factions erodes people's concern for the welfare of their community and weakens the collective ability to prevent crime. The present study examined the effects of infection incidence on crime rates across the United States. Infection rates predicted violent and property crime more strongly than other crime covariates. Infections also predicted homicides against strangers but not family or acquaintances, supporting the hypothesis that in-group-out-group discrimination was responsible for the infections-crime link. Overall, the results add to evidence that disease threat shapes interpersonal behavior and structural characteristics of groups

Before the Pandemic Ends: Making Sure This Never Happens Again

Introduction On 30 January 2020, the World Health Organization (WHO) declared a Global Health Emergency of international concern attendant to the emergence and spread of SARS-CoV-2, nearly two months after the first reported emergence of human cases in Wuhan, China. In the subsequent two months, global, national and local health personnel and infrastructures have been overwhelmed, leading to suffering and death for infected people, and the threat of socio-economic instability and potential collapse for humanity as a whole. This shows that our current and traditional mode of coping, anchored in responses after the fact, is not capable of dealing with the crisis of emerging infectious disease. Given all of our technological expertise, why is there an emerging disease crisis, and why are we losing the battle to contain and diminish emerging diseases? Part of the reason is that the prevailing paradigm explaining the biology of pathogen-host associations (coevolution, evolutionary arms races) has assumed that pathogens must evolve new capacities - special mutations – in order to colonize new hosts and produce emergent disease (e.g. Parrish and Kawaoka, 2005). In this erroneous but broadly prevalent view, the evolution of new capacities creates new opportunities for pathogens. Further, given that mutations are both rare and undirected, the highly specialized nature of pathogen-host relationships should produce an evolutionary firewall limiting dissemination; by those definitions, emergences should be rare (for a historical review see Brooks et al., 2019). Pathogens, however, have become far better at finding us than our traditional understanding predicts. We face considerable risk space for pathogens and disease that directly threaten us, our crops and livestock – through expanding interfaces bringing pathogens and hosts into increasing proximity, exacerbated by environmental disruption and urban density, fueled by globalized trade and travel. We need a new paradigm that explains what we are seeing. Additional section headers: The Stockholm Paradigm The DAMA Protocol A Sense of Urgency and Long-Term Commitment Reference

Hybridization in parasites: consequences for adaptive evolution, pathogenesis and public health in a changing world

[No abstract available

The influence of biological rhythms on host–parasite interactions

Biological rhythms, from circadian control of cellular processes to annual cycles in life history, are a main structural element of biology. Biological rhythms are considered adaptive because they enable organisms to partition activities to cope with, and take advantage of, predictable fluctuations in environmental conditions. A flourishing area of immunology is uncovering rhythms in the immune system of animals, including humans. Given the temporal structure of immunity, and rhythms in parasite activity and disease incidence, we propose that the intersection of chronobiology, disease ecology, and evolutionary biology holds the key to understanding host–parasite interactions. Here, we review host–parasite interactions while explicitly considering biological rhythms, and propose that rhythms: influence within-host infection dynamics and transmission between hosts, might account for diel and annual periodicity in host–parasite systems, and can lead to a host–parasite arms race in the temporal domain

Representations of swine flu: Perspectives from a Malaysian pig farm

© The Author(s), 2010. This is the author's accepted manuscript. The final published article is available from the link below.Novel influenza viruses are seen, internationally, as posing considerable health challenges, but public responses to such viruses are often rooted in cultural representations of disease and risk. However, little research has been conducted in locations associated with the origin of a pandemic. We examined representations and risk perceptions associated with swine flu amongst 120 Malaysian pig farmers. Thirty-seven per cent of respondents felt at particular risk of infection, two-thirds were somewhat or very concerned about being infected. Those respondents who were the most anxious believed particular societal “out-groups” (homosexuals, the homeless and prostitutes) to be at higher infection risk. Although few (4%) reported direct discrimination, 46% claimed friends had avoided them since the swine flu outbreak. Findings are discussed in the context of evolutionary, social representations and terror management theories of response to pandemic threat

Decisions and disease: a mechanism for the evolution of cooperation

In numerous contexts, individuals may decide whether they take actions to mitigate the spread of disease, or not. Mitigating the spread of disease requires an individual to change their routine behaviours to benefit others, resulting in a 'disease dilemma' similar to the seminal prisoner's dilemma. In the classical prisoner's dilemma, evolutionary game dynamics predict that all individuals evolve to 'defect.' We have discovered that when the rate of cooperation within a population is directly linked to the rate of spread of the disease, cooperation evolves under certain conditions. For diseases which do not confer immunity to recovered individuals, if the time scale at which individuals receive information is sufficiently rapid compared to the time scale at which the disease spreads, then cooperation emerges. Moreover, in the limit as mitigation measures become increasingly effective, the disease can be controlled, and the rate of infections tends to zero. Our model is based on theoretical mathematics and therefore unconstrained to any single context. For example, the disease spreading model considered here could also be used to describe social and group dynamics. In this sense, we may have discovered a fundamental and novel mechanism for the evolution of cooperation in a broad sense