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Evolutionary Biology of Parasitism
Published in Eric S. Loker, Bruce V. Hofkin, Parasitology, 2023
Eric S. Loker, Bruce V. Hofkin
What is coevolution, and what are some of its outcomes? How does coevolution differ from “evolution”? Hint: don’t confuse this term with cospeciation. How is our view of the commonness and importance of coevolution changing?
Role of Engineered Proteins as Therapeutic Formulations
Published in Peter Grunwald, Pharmaceutical Biocatalysis, 2019
Khushboo Gulati, Krishna Mohan Poluri
The word “Coevolution” itself indicates the simultaneous evolution. This coevolution implies that there are several residues in the protein which are quiet far away from each other in the sequence; however, they come closer during the structure formation (Lovell and Robertson, 2010). Such residues are involved in making essential interactions to hold the structural fold of the protein. Decoding coevolving residues in the protein aids in figuring out the ingrained elements in the protein that exert huge influence on the structural and functional aspects of the protein (Horner et al., 2008). Several research groups are focusing on identification of coevolving residues and targeting them for mutations to inculcate novelties in the existing protein (Socolich et al., 2005; Yip et al., 2008; Chen et al., 2011).
Complexity, guidelines and ethics
Published in Deborah Bowman, John Spicer, Roger Higgs, Primary Care Ethics, 2018
In biological terms, coevolution means that adaptation by one organism alters the fitness and the fitness landscapes of other organisms. In human systems, coevolution emphasises the relationships between the coevolving entities. Through a complexity lens, it makes no sense to examine the evolution or performance of one individual in isolation – the GPR and patient coevolve.
Bacterial infection during wars, conflicts and post-natural disasters in Asia and the Middle East: a narrative review
Published in Expert Review of Anti-infective Therapy, 2020
Tania Nawfal Dagher, Charbel Al-Bayssari, Seydina M. Diene, Eid Azar, Jean-Marc Rolain
Dissemination of bacterial infections was and will always be a major worldwide problem. Wars and natural disasters have worsened this situation. Historically, the Asian continent is well known as one of the major continents in which natural disasters occur especially earthquakes and tsunamis. In addition, the Middle East region and Afghanistan are considered as the worldwide war regions. This review provides an overview of bacterial infections resulting from these two phenomena in Asia and the Middle East. Countries of this region of the world are afflicted with repeated arm conflicts affecting both civilians and soldiers. In addition, countries of East Asia are considered as the most natural disasters prone countries in the world. The coevolution of Human beings with the microorganisms that infect them often develops faster than does the understanding of the resulting infectious diseases, mainly during wars and natural disasters. Historically, during wars, diseases, such as plague, typhoid, cholera, smallpox, have been responsible for enormous deaths. Bacterial infections have been shown to spread during wars in either refugees or soldiers. In military settings, infections are linked to wounded soldiers through environmental contaminations or during their transit from one setting to another. However, refugees can spread the dissemination of these infections while leaving in inadequate and crowded shelters suffering from poor hygiene conditions.
Human antimicrobial peptides in autoimmunity
Published in Autoimmunity, 2020
Ekaterina S. Umnyakova, Maria S. Zharkova, Mikhail N. Berlov, Olga V. Shamova, Vladimir N. Kokryakov
The complement system and AMPs are known to be vital humoral factors of innate immunity [136,137]. Their coevolution and colocalization give the opportunity to assume the existence of close interactions between different components of these systems. However, nowadays there are a lot of blank spots and gaps in this field. The data about interactions between the complement system and AMPs and consequences of such interplay are not so numerous and some of them are rather contradictory, that might be because of using fundamentally different approaches and models. The majority of literature data [55–57,138,139] devoted to this question is about the interaction of human defensins with the receptor molecules of classical and lectin complement activation pathways: C1q protein and mannose-binding lectin (MBL), respectively. These two molecules can be also called “scaffold molecules” of initiation complexes that switch on complement in two different ways but they lead to the same result: C3-convertase formation. The initiation complex of classical pathway consists of С1q molecule and tetramer of serine proteinases C1r and C1s (C1r2C1s2) that is located in the collagen-like domain of receptor molecule [140,141]. The dysregulation of the classical pathway is a most common feature for the autoimmune diseases [142], that is why it is more beneficial to find the modulator for this pathway of activation, to keep it in balance, and not to bother other pathways.
The molecular immunology of human susceptibility to fungal diseases: lessons from single gene defects of immunity
Published in Expert Review of Clinical Immunology, 2019
The fungal kingdom is estimated to contain 1.5- to 5 million species [1] and is estimated to have split from animals and plants approximately 1.5 billion years ago [2]. Thus, there has been an abundance of time for competition, capitulation, coevolution, and coadaptation that has allowed for indifferent, symbiotic and predatory relations to develop. Although fungi are major pathogens of plants, insects, amphibians, and certain mammals, only a discrete number (perhaps a few hundred species) are pathogenic to humans. Chief among the successful human defense factors are body temperature and immunity [3]. Indeed, it is dogma that fungal diseases affect humans with compromised immune systems. Yet, despite its clear importance, our understanding of human immunity to fungi is nascent. In this review, we first revisit the fascinating concept of natural variability to mycoses. Then, using human monogenic immunodeficiencies in which fungal diseases naturally develop, we map out critical processes by which the human immune system mitigates distinct fungal pathogens.