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The Evolutionary Significance of Drug Toxicity Over Reward
Published in Hanna Pickard, Serge H. Ahmed, The Routledge Handbook of Philosophy and Science of Addiction, 2019
Edward H. Hagen, Roger J. Sullivan
Unfortunately for these autotrophs, heterotrophs evolved that feed on them, sparking an evolutionary arms race (Dawkins and Krebs 1979) that continues to this day: heterotrophs evolved to exploit autotroph tissues and energy stores; autotrophs, in turn, evolved numerous defenses; heterotrophs then co-evolved countermeasures, and so forth.1 Key events in this arms race include the evolution of marine animals more than 600 million years ago (Knoll and Carroll 1999), and the evolution of terrestrial plants ~400 million years ago, along with the terrestrial bacterial, fungal, nematode, invertebrate and vertebrate herbivores that feed on them (Herrera and Pellmyr 2009).
Industrial Agricultural Environments
Published in Kezia Barker, Robert A. Francis, Routledge Handbook of Biosecurity and Invasive Species, 2021
Robert G. Wallace, Alex Liebman, David Weisberger, Tammi Jonas, Luke Bergmann, Richard Kock, Rodrick Wallace
Considerable effort has been spent describing Palmer amaranth’s development, growth habits and impact upon cropping systems (see reviews Ward et al., 2013; Chahal et al., 2015), as well as in introducing chemical and non-chemical forms of management (e.g. Culpepper et al., 2010; Culpepper et al., 2011; Price et al., 2011; Gaines et al., 2012). Such efforts presently dominate weed management science, extension literature and popular farm press, the latter two representing major arbiters of information reaching farmers. Current status quo recommendations for the management of Palmer amaranth involve the continued use of herbicides, with increasingly expensive products and mixtures. While such programmes may provide temporary respite to farmers, this management paradigm continues to fuel what has become an evolutionary arms race, leading to more herbicide-resistant Palmer amaranth. Those that stand to gain the most in the long-term from this trajectory are the agribusiness giants involved in chemical and bio-technology development and sales. As popular herbicides such as glyphosate have become less efficacious in controlling Palmer amaranth over the past ten-plus years, companies have returned to the promotion and sale of older, more volatile herbicide chemistries (group 4 herbicides, specifically 2,4-D and dicamba), concomitantly breeding transgenic crops with tolerance to these chemistries in addition to glyphosate. Unsurprisingly, farmer adoption has quickly followed in the Cotton Belt. This ‘solution’ merely reproduces the same logic that facilitated Palmer amaranth’s exceptional adaptation in the first place. Palmer amaranth plants with resistance to these new mixtures of glyphosate, 2,4-D and dicamba have already been discovered in Kansas, suggesting a limited timeline for this technology at the very outset of its implementation (Kumar et al., 2019).
Multivalent IgM scaffold enhances the therapeutic potential of variant-agnostic ACE2 decoys against SARS-CoV-2
Published in mAbs, 2023
Meghan M. Verstraete, Florian Heinkel, Janessa Li, Siran Cao, Anh Tran, Elizabeth C. Halverson, Robert Gene, Elizabeth Stangle, Begonia Silva-Moreno, Sifa Arrafi, Jegarubee Bavananthasivam, Madeline Fung, Mariam Eji-Lasisi, Stephanie Masterman, Steve Xanthoudakis, Surjit Dixit, John Babcook, Brandon Clavette, Mark Fogg, Eric Escobar-Cabrera
In response to the changing immune profile of the human population, a real-time evolutionary arms race has transpired between SARS-CoV-2 and host. The recent rise of the SARS-CoV-2 Omicron (B.1.1.529) strain and its subvariants (BA.1, BA.2, BA.3, BA.2.12.1, BA.2.13, BA.4, and BA.5) has underscored how mutations affecting the antigenic phenotype have led to failure of all mAbs granted an emergency use authorization (EUA) in the United States and evasion of humoral immunity from natural infection or vaccination.5,6,21–24 Development of new therapeutic mAbs and updated vaccine sequences, however, is inherently “reactive”, typically shows diminished neutralization capacity against emerging variants,22,25 and relies on continued surveillance of genetic and antigenic changes in the global virus population. Although modeling approaches to predict emerging phenotypic trajectories may be developed, as is the case for influenza virus,26 prediction of the mutational pathways by which a virus such as SARS-CoV-2 will evolve is extremely challenging and limits the ability to proactively approach the pandemic, as the Omicron variant showed.27
“I will survive”: A tale of bacteriophage-bacteria coevolution in the gut
Published in Gut Microbes, 2019
Luisa De Sordi, Marta Lourenço, Laurent Debarbieux
It could, therefore, be argued that bacteriophage adaptation in the gut led to a two-step coevolution pathway, in which the evolutionary arms race was initially characterised by the rapid development of bacterial resistance followed by a refining of bacteriophage adaptation. The two populations subsequently continued to coexist, with no evidence of renewed bacterial resistance, suggesting that transient resistance occurred in situ, protecting the bacteria against bacteriophage predation, as discussed below.
The barrier and beyond: Roles of intestinal mucus and mucin-type O-glycosylation in resistance and tolerance defense strategies guiding host-microbe symbiosis
Published in Gut Microbes, 2022
Host defense is an integral part of living with our gut microbiota. Whether the symbiotic microbiota represent resident commensals, mutualists, or overt parasites (pathogens), host innate defense strategies are in place to defend against – or regulate interactions with – all classes of symbionts with the same end goal: to prevent disease, and, ideally, promote a mutualism to enhance fitness of host and symbiont. Two fundamental ways exist in which to achieve this goal: First, we can “resist” the pathogen by regulating numbers via preventing colonization or through direct killing mechanisms.1,2 Resistance strategies are well characterized, i.e., colonization resistance, production of antimicrobials that lyse target cells, opsonization with complement and antibodies, and phagocytosis. By reducing pathogen burdens, we reduce the stimulus and number of virulence factors and toxins that cause damage and disease and thereby enhance host fitness. However, resistance comes at a cost – an ongoing evolutionary arms race and selection pressures as both host and microbe fight for survival over generations.2,3 Further, tissues such as the lung, skin, and reproductive and digestive tracts are constantly exposed to the environment: The digestive tract is an extreme example where >10 trillion bacteria alone exist, making resistance effectively futile. This necessitates the second strategy: promoting “tolerance” to the microbe (or microbially-derived toxin) so as to prevent its ability to cause tissue damage and reduced host fitness.1,4 Indeed, tolerance strategies are required and employed that not only preserve the gut microbiota, but can ultimately enhance their fitness in ways that enhance our own.1 Such strategies include dampening host inflammatory potential, for example, through IL-101 or other negative regulators of inflammation, which maintains a stable microbiota rich in alpha diversity5 that promotes colonization resistance against pathogens,6 and increases our energy extraction from the diet.7 Importantly, these strategies are not always clear-cut: Situations arise where a defense strategy is an asset in one context (promoting resistance or tolerance), but a liability in another, by promoting infection and disease. One major feature of host innate defenses that has emerged to promote resistance and tolerance to the microbes – and sometimes disease susceptibility – is the heavily O-glycosylated mucus system. A number of recent reviews have highlighted the importance of how mucin-type O-glycans contribute to homeostasis.8–10 However, the broader significance of the relationship between host glycans, host–microbe interactions, and host defense is still poorly defined, especially at the interface where host and microbe interact, which largely dictates the physiologic outcome – and evolutionary trajectories – of both host and microbe. This review focuses on how intestinal secretory mucins, by virtue of their O-glycone, specifically contribute to host defense strategies, with an emphasis on emerging tolerance defense mechanisms against the bacterial symbiotic microbiota.