Jessica Brinkworth. Ekaterina Pechenkina. Primates, Pathogens and Evolution: An Introduction. Brinkworth and Kate Pechenkina Introduction Primate immune systems have evolved to interact with pathogens in different ways Mandl et al. Human and nonhuman primate immune systems have diverged with some species exhibiting strong differences in immune response to certain pathogens including immunodeficiency viruses [reviewed by Pandrea and Apetrei , Toxoplasma gondii Epiphanio et al.
Why closely related primates have evolved such divergent pathogen interaction strategies is not well understood. Our understanding of how primate immunity evolved is hindered by disconnected research on primate—pathogen molecular interaction, an uneven focus on primate coevolution with a limited number of pathogens, and the discon- nect between research on primate molecular phylogeny and primate physiology.
The objective of the present collection of papers is to integrate research on the evolution of primate genomes, primate immune function, primate—pathogen biochemical interaction, and infectious disease emergence to provide a knowledge base for future research on human and nonhuman primate speciation, immunity, and disease. Pechenkina The Role of Long-Term Evolutionary Processes in Shaping the Primate Immune System Evolution of the immune system is tied to the evolutionary history of a species and intertwined with the evolution of physiological functions and developmental stages of an organism.
The majority of cold-blooded vertebrates appear to experience functional shifts in their immune response depending on external temperatures, resulting, in some cases, in impaired immune responses such as the inhibition of immunoglobulin class switching Jackson and Tinsley To interpret variation in primate immune response within and between species, the evolutionary forces that shaped the underlying molecular differences need to be examined. Of these forces, pathogen-mediated natural selection has likely been the leading factor in increasing the frequency of pathogen resistance in host popula- tions.
Complete or partial resis- tance of specific human genotypes to certain pathogenic strains and the patterned distribution of these genotypes among indigenous populations around the globe is fairly well documented Hamblin and Di Rienzo ; Hraber et al. While the genetic variability of nonhuman primate immune factors is comparatively less well studied, specific disease resistance genotypes in some of these species have been identified.
Ecological differences between savanna dwelling Guinea baboons Papio papio and chimpan- zees Pan troglodytes are likely responsible for resistance on the part of the former species to the savannah-based pathogen Trypanosoma brucei gambiensis, and high susceptibility to fatal T.
Baboons are more involved in grassland ground foraging than chimpanzees, which also exploit savannah resources but are tied to forested regions and tend to retreat to the forest for sleep Kageruka et al. In the course of their evolution in open habitats, baboons have likely been continuously exposed to the low flying tsetse fly—the vector for T. The selective pressure generated by T. In humans, two unrelated mutations in ApoLI that increase sleeping sickness resistance are geographically restricted to Africa and absent in European populations.
The pathogen-directed evolutionary mechanisms that contribute to the divergence of immune systems remain hypothetical. In the simplest case, an epidemic of a highly virulent infectious disease eliminates a large number of susceptible organisms very quickly, thereby favoring the disproportional reproductive success of resistant indi- viduals. In such a scenario pathogen-mediated selection is assumed to be strong.
However, such a model of host—pathogen coevolution is pertinent in extreme cases only. Pathogens of moderate-to-low virulence can also affect host immune allele frequencies by, for example, contributing to lowered fertility in the form of physical inability to produce offspring after being infected or causing a lesser ability to acquire mates as a result of decreased mobility Cheney et al. Pathogens that do not kill a host, therefore, can affect sexual selection and gene flow. Of course, the consequences of a deadly epidemic may not be limited to removal of the alleles that contribute to disease susceptibility, such as those of surface antigens recruited by a pathogen to penetrate the host.
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Such strong selective pressure may also affect alleles that contribute to increased susceptibility to coinfections or to overt immune activity that leads to the development of secondary conditions e. Pathogen pressure may also select for resistance traits and in doing so affect the frequency of linked alleles in a population through selective sweeps.
The most popularized perception of host—pathogen evolutionary interaction is the concept of a host—pathogen evolutionary arms race. The Red Queen hypothesis proposes that closely associated organ- isms may coevolve so tightly that the likelihood of extinction for one or the other is constant over geological time. Changes in one species affect the tightly coevolved interface with another species, threatening either species with extinction. However, some pathogens actually co-opt normal mechanisms of primate immune recognition and the subsequent responses, such as cytokine release, cell trafficking, and tissue destruction, using them to their advantage.
Mycobacterium tuberculosis tuberculosis infection is enhanced by the release of host anti- inflammatory cytokine IL Redford et al. Pechenkina macrophage, Yersinia pestis plague migrates to its main point of dissemination, the lymph nodes, while acquiring phagocytosis resistance Oyston et al. Similarly, HIV can disseminate to the lymph nodes and other regions through antigen-presenting cells Koppensteiner et al. Moreover, exaggerated and uncontrolled immune cell responses may result in host death—such is the case of severe sepsis and septic shock triggered by strong innate immune cell recognition of immune system insult e.
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In viruses lacking E3L, K3L rapidly becomes amplified 10—fold via serial dupli- cation, which increases viral fitness. However, the tradeoff for increased genome size is less efficient replication. Remarkably, an expanded genomic array of identi- cal resistance genes in a pathogen increases the probability of emergence, fixation, and spreading of additional K3L mutants with improved host avoidance; these viruses subsequently lose the K3L duplicated array but retain the novel resistance mutation Elde et al. Two limiting factors for pathogen-driven evolution of the immune system are disadvantages rendered to the host by hyper-responsiveness, leading to autoimmune disorders, and inadvertent pressure on symbiotic and commensal organisms.
An overactive immune system is responsible for the development of chronic conditions mediated by the immune system itself, such as systemic lupus erythematosus, antiphospholipid syndrome, polycystic ovary syndrome, and diabetes, among oth- ers, that negatively affect reproductive fitness and may therefore contribute to immune system evolution Carp et al. Consequently, immune system divergence between species is not driven by host— pathogen interaction alone but is profoundly affected by the living environment, which includes a complex network of interspecies interactions between hosts, sym- bionts, commensals, and pathogens Klimovich ; Lee and Mazmanian Changes in the fitness of any holobiont-involved species affect the system as a whole, rather than just the fitness of the host species.
Indeed, changes in the compo- sition of intestinal microbiota may promote outgrowth or invasion by pathogenic microorganisms or induce an exaggerated host response that results in the onset of various autoimmune disorders such as inflammatory bowel disease Maynard et al. Establishing whether new species-specific pathogens are effectors or consequences of speciation is a daunting task.
The Role of Pathogens in Primate Speciation Interaction with pathogens likely played an important role in primate speciation in several ways. Pathogens have contributed to primate genome divergence through direct integration of microorganismal genomes into the genomes of primate germ- line cells. Over millions of years, viral integration into host genomes has changed genome sequences and affected multiple biological functions Arnaud et al.
For instance, Dunlap et al. Once incorporated, viral genomes were inherited by offspring. Due to different histories of pathogen exposure, primate genomes differ from one another in terms of the types and numbers of integrated viral sequences Horie et al. As such, viral pathogens have contributed to the divergence of primate genomes and the divergent functions of primate genes Gogvadze et al. While portions of primate genomes have diverged because of species-specific viral integration, some loci appear to have evolved under pathogen-driven selection.
Multiple pathogens have been identified as having exerted selective pressure on pri- mate immune factors for millions of years [i. Primate immune genes, proteins, and cells have structurally and functionally diverged. Primate immune factors show evidence of selection [CC-motif receptor 5 Wooding et al. Reconstructions of primate evolutionary relationships based on the regulatory and coding sections of immune system genes deviate significantly from generally accepted primate phylogenies [Toll-like receptor 2 Yim et al.
Pechenkina of immune function.
Primates, Pathogens, and Evolution
Until the functional effects of these changes are considered, it is impossible to appreciate how they contributed to speciation or disease suscepti- bility and progression. A goal of this volume is to integrate available information on structural and functional differences in primate immunity with data on the evolu- tionary analysis of gene sequences, pathogen life cycles, and evolutionary history. Clinical Implications of Primate—Pathogen Coevolution As a consequence of primate—pathogen evolutionary interactions, primates exhibit strong interspecies and interpopulation differences in immune response to a broad range of pathogens, some of which are major agents of human disease.
Many lin- eages of African nonhuman primates have hosted immunodeficiency viruses IV over millions of years and their extant descendents do not develop the overt immune activation and white blood cell loss that typifies late stage IV infection AIDS in comparatively new hosts such as humans or Asian monkeys [reviewed in Pandrea and Apetrei ; see also Greenwood et al.
Infectious Diseases in Primates: Behavior, Ecology and Evolution
Nonhuman primate Herpes simian B virus infections in their natural hosts are fairly asymptomatic or manifest mildly, in a manner similar to human herpes simplex mucosal blisters. Unless severely immunocompromised, humans infected with the brain and muscle parasite Toxoplasma gondii are asymptomatic or develop a self-limited disease characterized by fever and enlarged lymph nodes Jones et al. By contrast, T.
Research on the molecular mechanisms responsible for such variation in disease manifestation among different primate species involves multiple, often disparate areas of study, which contributes to gulfs between research on immune function, research on primate—pathogen evolution, and the clinical application of the resultant findings. Arguably, the molecular mechanisms of immunodeficiency virus infection in primates are the best understood primate—pathogen interactions.
The severity of the HIV pandemic and a strong interest in developing viable therapies have encouraged the examination of disease susceptibility and progression in primates, but mainly in a limited selection of catarrhine species.
Primate-IV studies often use a comparative evolutionary approach as a starting point for the analysis of primate immunity and disease progression. An important advance in HIV therapy research has been the finding that IVs have emerged multiple times in the course of primate evolution and have closely coevolved with their hosts over millions of years Pandrea and Apetrei ; Santiago et al.
A limited number of broader interspecies differences in the proportion of immune cell types, activation of immune cells, expression of immune genes, and stimulation of cell death that may affect disease progression have also been noted Kim et al. While primates serve as models for the study of other diseases and have been examined as xenotransplantation subjects, what we currently know about interspecies differences in primate immune function is largely derived from comparative IV-primate research.
Although the genetic and functional differences identified through IV research may also contribute to a clearer picture of general immune responses to pathogens, we do not know how many of these immune factors are activated across primate species or whether this activation is stimulated in a similar way by other pathogens. Ihr Warenkorb 0. Der neue Herold ist da! Modelle Anatomische Modelle Somso-Modelle.
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Lehmanns Verlag. Primates, Pathogens, and Evolution. This book details how pathogens affect the evolution of primate genome diversity, cell and immune function, and health-integrating research from fields on primate-pathogen molecular interactions, primate immune function and primate-pathogen co-evolution. The immune systems of human and non-human primates have diverged over time, such that some species differ considerably in their susceptibility, symptoms, and survival of particular infectious diseases.
Variation in primate immunity is such that major human pathogens - such as immunodeficiency viruses, herpesviruses and malaria-inducing species of Plasmodium - elicit striking differences in immune response between closely related species and within primate populations. The success of some pathogens in establishing persistent infections in humans and other primates has been determined not just by the molecular evolution of the pathogen and its interactions with the host, but also by the evolution of primate behavior and ecology, microflora, immune factors and the evolution of other biological systems.
To explore how interactions between primates and their pathogens have shaped their mutual molecular evolution, Primates, Pathogens and Evolution brings together research that explores comparative primate immune function, the emergence of major and neglected primate diseases, primate-microorganism molecular interactions, and related topics.