scholarly journals The evolution of cheating in viruses

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Asher Leeks ◽  
Stuart A. West ◽  
Melanie Ghoul

AbstractThe success of many viruses depends upon cooperative interactions between viral genomes. However, whenever cooperation occurs, there is the potential for ‘cheats’ to exploit that cooperation. We suggest that: (1) the biology of viruses makes viral cooperation particularly susceptible to cheating; (2) cheats are common across a wide range of viruses, including viral entities that are already well studied, such as defective interfering genomes, and satellite viruses. Consequently, the evolutionary theory of cheating could help us understand and manipulate viral dynamics, while viruses also offer new opportunities to study the evolution of cheating.

Author(s):  
Asher Leeks ◽  
Stuart A. West ◽  
Melanie Ghoul

The success of many viruses depends upon cooperative interactions between viral genomes. For example, viruses that coinfect the same cell can share essential gene products, such as replicase, the enzyme that replicates the viral genome. However, when cooperation occurs, there is the potential for ‘cheats’ to exploit that cooperation. We suggest that: (1) the biology of viruses makes viral cooperation particularly susceptible to cheating; (2) cheats are common across a wide range of viruses, including viral entities that are already well studied, such as defective interfering genomes, and satellite viruses. Consequently, evolutionary theory developed to explain cheating offers a conceptual framework for understanding and manipulating viral dynamics. At the same time, viruses offer unique opportunities to study how cheats evolve, because cheating is relatively common in viruses, compared with taxa where cooperation is more usually studied, such as animals.


Author(s):  
Lee Cronk ◽  
Beth L. Leech

This book investigates a wide range of ideas, theories, and existing empirical research relevant to the study of the complex and diverse phenomenon of human cooperation. Issues relating to cooperation are examined from the perspective of evolutionary theory, political science, and related social sciences. The book draws upon two bodies of work: Mancur Olson's The Logic of Collective Action (1965) and George C. Williams's Adaptation and Natural Selection (1966). Olson, an economist, and Williams, an evolutionary biologist, both argued that a focus on groups would not provide a complete understanding of collective action and other social behaviors. This introductory chapter discusses some important definitions relating to cooperation, with particular emphasis on collective action and collective action dilemmas, along with coordination and coordination problems. It also provides an overview of the chapters that follow.


Ever since Charles Darwin, scholars have noted that cultural entities such as languages, laws, firms, and theories seem to ‘evolve’ through sequences of variation, selection and replication, in many ways just like living organisms. This book considers whether this comparison is ‘just a metaphor’, or whether modern evolutionary theory can help us to understand the dynamics of different cultural domains. The ‘evolutionary paradigm of rationality’ has a significant role to play throughout the human sciences, but raises complex issues in every cultural context where it is applied. By fostering discussion between scholars from a wide range of research traditions, this book aims to influence the evolution of all of them.


2009 ◽  
Vol 84 (4) ◽  
pp. 1674-1682 ◽  
Author(s):  
Linlin Li ◽  
Amit Kapoor ◽  
Beth Slikas ◽  
Oderinde Soji Bamidele ◽  
Chunlin Wang ◽  
...  

ABSTRACT Circoviruses are known to infect birds and pigs and can cause a wide range of severe symptoms with significant economic impact. Using viral metagenomics, we identified circovirus-like DNA sequences and characterized 15 circular viral DNA genomes in stool samples from humans in Pakistan, Nigeria, Tunisia, and the United States and from wild chimpanzees. Distinct genomic features and phylogenetic analysis indicate that some viral genomes were part of a previously unrecognized genus in the Circoviridae family we tentatively named “Cyclovirus” whose genetic diversity is comparable to that of all the known species in the Circovirus genus. Circoviridae detection in the stools of U.S. adults was limited to porcine circoviruses which were also found in most U.S. pork products. To determine whether the divergent cycloviruses found in non-U.S. human stools were of dietary origin, we genetically compared them to the cycloviruses in muscle tissue samples of commonly eaten farm animals in Pakistan and Nigeria. Limited genetic overlap between cycloviruses in human stool samples and local cow, goat, sheep, camel, and chicken meat samples indicated that the majority of the 25 Cyclovirus species identified might be human viruses. We show that the genetic diversity of small circular DNA viral genomes in various mammals, including humans, is significantly larger than previously recognized, and frequent exposure through meat consumption and contact with animal or human feces provides ample opportunities for cyclovirus transmission. Determining the role of cycloviruses, found in 7 to 17% of non-U.S. human stools and 3 to 55% of non-U.S. meat samples tested, in both human and animal diseases is now facilitated by knowledge of their genomes.


2008 ◽  
Vol 7 (2) ◽  
pp. 193-201 ◽  
Author(s):  
Judy Perry ◽  
Eli Meir ◽  
Jon C. Herron ◽  
Susan Maruca ◽  
Derek Stal

To understand evolutionary theory, students must be able to understand and use evolutionary trees and their underlying concepts. Active, hands-on curricula relevant to macroevolution can be challenging to implement across large college-level classes where textbook learning is the norm. We evaluated two approaches to helping students learn macroevolutionary topics. Treatment 1 is a laboratory for the software program EvoBeaker designed to teach students about evolutionary trees. We tested Treatment 1 among nine college-level biology classes and administered pre/posttests to assess learning gains. We then sought to determine whether the learning gains from Treatment 1 were comparable to those derived from an alternate hands-on treatment, specifically the combination of a prerecorded lecture on DVD and paper-based activity based on Goldsmith's Great Clade Race (Treatment 2). Comparisons of pre- and posttests among participants using either Treatment 1 or 2 show large learning gains on some misconceptions and skills beyond knowledge gained from reading standard textbook entries. Both treatments performed equivalently in overall learning gains, though both had areas where they performed better or worse. Furthermore, gains among students who used Treatment 1 representing a wide range of universities suggest that outcomes are potentially applicable to a variety of “real-world” biology classes.


Author(s):  
Jack Zipes

If there is one genre that has captured the imagination of people in all walks of life throughout the world, it is the fairy tale. Yet we still have great difficulty understanding how it originated, evolved, and spread—or why so many people cannot resist its appeal, no matter how it changes or what form it takes. This book presents a provocative new theory about why fairy tales were created and retold—and why they became such an indelible and infinitely adaptable part of cultures around the world. Drawing on cognitive science, evolutionary theory, anthropology, psychology, literary theory, and other fields, the book presents a nuanced argument about how fairy tales originated in ancient oral cultures, how they evolved through the rise of literary culture and print, and how, in our own time, they continue to change through their adaptation in an ever-growing variety of media. In making its case, the book considers a wide range of fascinating examples, including fairy tales told, collected, and written by women in the nineteenth century; Catherine Breillat's film adaptation of Perrault's “Bluebeard”; and contemporary fairy-tale drawings, paintings, sculptures, and photographs that critique canonical print versions. While we may never be able to fully explain fairy tales, this book provides a powerful theory of how and why they evolved—and why we still use them to make meaning of our lives.


The concept of epistasis was introduced into evolutionary theory more than a hundred years ago. Its history is marked by controversies regarding its importance for the evolutionary process, as exemplified by the debate between Ronald Fisher and Sewall Wright in the wake of the modern synthesis. In this case the disagreement was about the shape of the adaptive landscape, which is determined by epistasis. Wright believed that epistasis causes the adaptive landscape to be rugged with many local peaks, whereas Fisher viewed evolution as a smooth, steady progression toward a unique optimum. Even today, the different meanings attributed to epistasis continue to spawn confusion. Nevertheless, a consensus is emerging, according to which the term should be used to designate interactions between genetic effects on phenotypes in the broadest sense. Stated differently, in the presence of epistasis the phenotypic effects of a gene depend on its genetic context. In evolutionary theory the phenotype of primary interest is organismal fitness, but principally the concept applies to any genotype-phenotype map. Reflecting the Fisherian view, throughout the 20th century epistasis was often considered to be a residual perturbation on the main effects of individual genes. Following the advent of sequencing techniques providing insights into the molecular basis of genotype-phenotype maps, over the past two decades it has become clear, however, that epistasis is the rule rather than an exception. This has motivated a large number of empirical studies exploring the patterns and evolutionary consequences of epistasis across a wide range of scales of organismal and genomic complexity. Correspondingly, mathematical and computational tools have been developed for the analysis of experimental data, and models have been constructed to elucidate the mechanistic and statistical origins of genetic interactions. Despite a certain inherent vagueness, the concept takes center stage in modern evolutionary thought as a framework for organizing the accumulating understanding of the relationship among genotype, phenotype, and organism.


Author(s):  
R. S. Thorpe

SynopsisThe racial affinities of the widely distributed (palearctic) ringed snake, Natrix natrix were assessed using a large number of phenotypic characters from a wide range of features. These characters show a considerable amount of complex geographic variation which is further complicated by geographic variation in the extent of their sexual, ontogenetic and local variation. Nevertheless, extensive analysis of the data using univariate statistics, numerical taxonomy and a wide range of multivariate statistics allowed the primary patterns of ‘racial’ differentiation to be elucidated.The dominant feature of the racial affinities is the division of the majority of the complex into distinct eastern and western forms which meet along a ‘hybrid zone’. The nature of this zone is analysed in detail and discussed in relation to aspects of evolutionary theory such as gene flow. The island populations of Corsica and Sardinia are also extremely divergent. The evolution and taxonomy of the four primary subdivisions of the complex (east, west, Corsica, Sardinia) are discussed in relation to Pleistocene history, evolutionary theory, species concepts (phenetic and biological) and subspecies concepts, etc. These four subdivisions border on the species rank and may be regarded by some as semispecies. They are formally recognised as subspecies. Attention is drawn to the difficulties of intraspecific taxonomy and the arbitrary nature of the four taxa given formal recognition.


2021 ◽  
Author(s):  
Natalia Rego ◽  
Tamara Fernandez-Calero ◽  
Ighor Arantes ◽  
Veronica Noya ◽  
daiana mir ◽  
...  

During the first nine months of the SARS-CoV-2 pandemic, Uruguay successfully kept it under control, even when our previous studies support a recurrent viral flux across the Uruguayan-Brazilian border that sourced several local outbreaks in Uruguay. However, towards the end of 2020, a remarkable exponential growth was observed and the TETRIS strategy was lost. Here, we aimed to understand the factors that fueled SARS-CoV-2 viral dynamics during the first epidemic wave in the country. We recovered 84 whole viral genomes from patients diagnosed between November, 2020 and February, 2021 in Rocha, a sentinel eastern Uruguayan department bordering Brazil. The lineage B.1.1.28 was the most prevalent in Rocha during November-December 2020, P.2 became the dominant one during January-February 2021, while the first P.1 sequences corresponds to February, 2021. The lineage replacement process agrees with that observed in several Brazilian states, including Rio Grande do Sul (RS). We observed a one to three month delay between the appearance of P.2 and P.1 in RS and their subsequent detection in Rocha. The phylogenetic analysis detected two B.1.1.28 and one P.2 main Uruguayan SARS-CoV-2 clades, introduced from the southern and southeastern Brazilian regions into Rocha between early November and mid December, 2020. One synonymous mutation distinguishes the sequences of the main B.1.1.28 clade in Rocha from those widely distributed in RS. The minor B.1.1.28 cluster, distinguished by several mutations, harbours non-synonymous changes in the Spike protein: Q675H and Q677H, so far not concurrently reported. The convergent appearance of S:Q677H in different viral lineages and its proximity to the S1/S2 cleavage site raise concerns about its functional relevance. The observed S:E484K-VOI P.2 partial replacement of previously circulating lineages in Rocha might have increased transmissibility as suggested by the significant decrease in Ct values. Our study emphasizes the impact of Brazilian SARS-CoV-2 epidemics in Uruguay and the need of reinforcing real-time genomic surveillance on specific Uruguayan border locations, as one of the key elements for achieving long-term COVID-19 epidemic control.


2018 ◽  
Author(s):  
Katia Koelle ◽  
Alex Farrell ◽  
Christopher Brooke ◽  
Ruian Ke

AbstractWithin-host models are useful tools for understanding the processes regulating viral load dynamics. While existing models have considered a wide range of within-host processes, at their core these models have shown remarkable structural similarity. Specifically, the structure of these models generally consider target cells to be either uninfected or infected, with the possibility of accommodating further resolution (for example, cells that are refractory to infection and cells that are in an eclipse phase). Recent findings, however, indicate that cellular coinfection is the norm rather than the exception for many viral infectious diseases, and that cells with high multiplicity of infection are present over at least some duration of an infection. The reality of these cellular coinfection dynamics is not accommodated in current within-host models although it may be critical for understanding within-host dynamics. This is particularly the case if multiplicity of infection impacts infected cell phenotypes such as their death rate and their viral production rates. Here, we present a new class of within-host disease models that allow for cellular coinfection in a scalable manner by retaining the low-dimensionality that is a desirable feature of many current within-host models. The models we propose adopt the general structure of epidemiological ‘macroparasite’ models that allow hosts to be variably infected by parasites such as nematodes and host phenotypes to flexibly depend on parasite burden. Specifically, our within-host models consider target cells as ‘hosts’ and viral particles as ‘macroparasites’, and allow viral output and infected cell lifespans, among other phenotypes, to depend on a cell’s multiplicity of infection. We show with an application to influenza that these models can be statistically fit to viral load and other within-host data, that they can reproduce notable features of within-host viral dynamics, and that important in vivo quantities such as the mean multiplicity of cellular infection can be easily quantified with these models once parameterized. The within-host model structure we develop here provides an alternative approach for modeling within-host viral load dynamics and allows for a new class of questions to be addressed that consider the effects of cellular coinfection, collective viral interactions, and viral complementation in within-host viral dynamics and evolution.


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