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PubMed2006

Minority memory genomes can influence the evolution of HIV-1 quasispecies in vivo.

One of the consequences of viral quasispecies dynamics is the presence, in the mutant spectrum, of minority memory genomes that reflect those variants that were dominant at an earlier phase of the same evolutionary lineage. Replicative and cellular (or anatomical) contributions to quasispecies memory were previously defined during intrahost evolution of human immunodeficiency virus type 1 (HIV-1) [Briones, C., Domingo, E., Molina-París, C., 2003. Memory in retroviral quasispecies: experimental evidence and theoretical model for human immunodeficiency virus. J. Mol. Biol. 331, 213-229.]. However, the effects of replicative memory regarding virus evolution in vivo have not been investigated. Here we document that a multidrug-resistant (MDR) HIV-1, present at memory level, determined the ensuing evolution of the virus in an infected patient. Nucleotide sequencing and detailed phylogenetic analyses of sequential viral populations and individual molecular clones evidenced that the progeny of a minority MDR genome during a treatment interruption contributed the dominant genomes when an antiretroviral treatment was restored. An extension of a mathematical model of establishment and maintenance of memory, based on quasispecies theory, supports the experimental data. Therefore a replicative memory subpopulation, not detectable in a consensus nucleotide sequence, affected decisively subsequent states of viral evolution in vivo.

Anti-HIV Agents↗

PubMed2005

Evolution of host specificity in fleas: is it directional and irreversible?

Evolutionary trends in the evolution of host specificity have been the focus of much discussion but little rigorous empirical testing. On the one hand, specialization is often presumed to lead irreversibly into evolutionary dead ends and little diversification; this would mean that generalists might evolve into specialists, but not vice versa. On the other hand, low host specificity may limit the risk of extinction and provide more immediate fitness benefits to parasites, such that selection may favour evolution toward a generalist strategy. Here, we test for directionality in the evolution of host specificity using a large data set and phylogenetic information on 297 species of fleas parasitic on small mammals. The analyses determined whether host specificity, measured both as the number of host species exploited and their taxonomic diversity, was related to clade rank of the flea species, or the number of branching events between an extant species and the root of the phylogenetic tree (i.e., the total path length from the root of the tree to the species). Based on regression analyses, we found positive relationships between the number of host species used and clade rank across all 297 species, as well as within one (Hystrichopsyllidae) of four large families and one of seven large genera investigated separately; in addition, we found a positive relationship between the taxonomic diversity of host species used and clade rank in another of the seven genera. These results suggest a slight evolutionary trend of decreasing host specificity. Using a much more conservative likelihood ratio test, however, a random walk, or null model, of evolution could not be discarded in favour of the directional trends in all cases mentioned above. Still, these results suggest that host specificity may have tended to decrease in many flea lineages, a process that could have been driven by the benefits of exploiting a wide range of host species.

Adaptation, Biological↗

PubMed2005

Evolution of mechanoregulation of bone growth will lead to non-optimal bone phenotypes.

Mechanical forces acting on the bones during growth affect their final shape and strength. Mechanoregulation of bone growth may be recognized in embryogenesis, and also in the adaptation of the adult skeleton to changes in mechanical loading. Mechanoregulatory responses for tissues have arisen during evolution, but does evolution give rise to responses that produce optimal skeletal phenotypes? In this paper, we investigate the emergence of an optimal mechanoregulation response in a population. By combining equations describing long bone growth with a genetic algorithm to describe evolutionary change, we created a computational model to simulate the evolution of mechanoregulation in bone growth. A population of individuals is created where each individual is assigned a diploid gene set which controls the growth and remodelling of the bone. At maturity, each bone is assessed and its 'fitness' calculated; fitness is quantified as bone strength relative to bone mass. The simulation continues for many generations, and includes mutations and a varying environment. The genes present in the population are tracked and the evolution of parameters governing mechanoregulation is calculated. The results indicate that a population may converge to one bone growth algorithm but, more usually, a range of mechanoregulation algorithms for different individuals will persist after many generations. Even if the population converges to one mechanoregulation law, convergence to the 'optimum' bone was never found. Although many researchers propose that natural selection has pushed skeletal structure towards an optimum, our computational model suggests that this is unlikely to be the case.

Adaptation, Physiological↗

PubMed2005

The standard genetic code enhances adaptive evolution of proteins.

The standard genetic code, by which most organisms translate genetic material into protein metabolism, is non-randomly organized. The Error Minimization hypothesis interprets this non-randomness as an adaptation, proposing that natural selection produced a pattern of codon assignments that buffers genomes against the impact of mutations. Indeed, on the average any given point mutation has a lesser effect on the chemical properties of the utilized amino acid than expected by chance. Might it also, however, be the case that the non-random nature of the code effects the rate of adaptive evolution? To investigate this, here we develop population genetic simulations to test the rate of adaptive gene evolution under different genetic codes. We identify two independent properties of a genetic code that profoundly influence the speed of adaptive evolution. Noting that the standard genetic code exhibits both, we offer a new insight into the effects of the "error minimizing" code: such a code enhances the efficacy of adaptive sequence evolution.

Evolution, Molecular↗

PubMed2006

Within-host evolution and virulence in microparasites.

An important aspect of microparasite biology is the fact that infections are populations of thousands of microbes. As any population, infections are hence subject to two main types of changes: demographic and evolutionary. Here we analyse the consequences of within-host evolutionary changes. We build an epidemiological model where infections are regularly invaded by locally favored mutations affecting various infectious traits (virulence, transmissibility and clearance). Our results are the following. In durable infections, where within-host evolution is an important matter, a drop of transmissibility is only slightly deleterious to the infection, while a reduction of infection lifespan is very costly. In consequence, locally favored mutations reducing transmissibility reach a larger frequency, or even the complete fixation, and the suboptimality accumulated in infections owing to within-host evolution affects more their transmission than their duration. Conversely, taking an infection at random and observing the events of within-host evolution, one is more likely to observe reductions of infection length than reductions of transmissibility, because the mutations affecting transmissibility are often already present in infections. We then discuss the interpretation of these results in terms of deleterious mutations, and we also emphasize that the management of within-host evolution could be used as a novel therapeutic approach to the treatment of infection.

Animals↗

PubMed2006

Evolution of the maturation rate collapses competitive coexistence.

Most theoretical studies on character displacement and the coexistence of competing species have focused attention on the evolution of competitive traits driven by inter-specific competition. We investigated the evolution of the maturation rate which is not directly related to competition and trades off with the birth rate and how it influences competitive outcomes. Evolution may result in the superior competitor becoming extinct if, initially, the inferior competitor has a lower, and the superior one a higher, maturation rate at the coexistence equilibrium. This counterintuitive result is explained by an explosive increase in the adult population of the inferior competitor as a result of the more rapid evolution of its maturation rate, which is caused by differences in the intensity and direction of selection on the maturation rates of the two species and in their adult densities, which are related to differences in their life histories. Thus, a life history trait trade-off with a competitive trait may cause a competitive ecological coexistence to collapse.

Animals↗

PubMed2006

Optimality models of phage life history and parallels in disease evolution.

Optimality models constitute one of the simplest approaches to understanding phenotypic evolution. Yet they have shortcomings that are not easily evaluated in most organisms. Most importantly, the genetic basis of phenotype evolution is almost never understood, and phenotypic selection experiments are rarely possible. Both limitations can be overcome with bacteriophages. However, phages have such elementary life histories that few phenotypes seem appropriate for optimality approaches. Here we develop optimality models of two phage life history traits, lysis time and host range. The lysis time models show that the optimum is less sensitive to differences in host density than suggested by earlier analytical work. Host range evolution is approached from the perspective of whether the virus should avoid particular hosts, and the results match optimal foraging theory: there is an optimal "diet" in which host types are either strictly included or excluded, depending on their infection qualities. Experimental tests of both models are feasible, and phages provide concrete illustrations of many ways that optimality models can guide understanding and explanation. Phage genetic systems already support the perspective that lysis time and host range can evolve readily and evolve without greatly affecting other traits, one of the main tenets of optimality theory. The models can be extended to more general properties of infection, such as the evolution of virulence and tissue tropism.

Animals↗

PubMed2025

SARS-CoV-2 genomic diversity and within-host evolution in individuals with persistent infection in the UK: an observational, longitudinal, population-based surveillance study.

BACKGROUND: Persistent SARS-CoV-2 infections in hospitalised immunocompromised individuals are known to facilitate accelerated within-host viral evolution, potentially contributing to the emergence of highly divergent variants. However, little is known about the evolutionary dynamics and transmission risks of persistent infections in the general population. We aimed to characterise the within-host evolution of SARS-CoV-2 during persistent infections identified through a large community surveillance study. METHODS: We used data from the Office for National Statistics COVID-19 Infection Survey (ONS-CIS), a large-scale, longitudinal, population-based surveillance study conducted in the UK from April, 2020, to March, 2023. For this analysis, we focused on infections with high viral load (cycle threshold ≤30) and available genome sequences, from seven major SARS-CoV-2 lineages (alpha, delta, BA.1, BA.2, BA.4, BA.5, and XBB). ONS-CIS participants were randomly selected from the general population and tested regularly by RT-PCR, regardless of symptoms. We defined persistent infections as those with sustained or rebounding high viral RNA titres for 26 days or longer. We examined associated host characteristics and used raw sequence data to identify de novo mutations and estimate within-host synonymous and non-synonymous evolutionary rates across the SARS-CoV-2 genome. FINDINGS: Between Nov 2, 2020, and March 21, 2023, we identified 576 persistent infections with at least two sequences, including 11 alpha, 106 delta, 102 BA.1, 204 BA.2, 16 BA.4, 133 BA.5, and 4 XBB. Persistent infections were more common in males than females (p<0·0001) and individuals older than 60 years (p=0·0027). The median within-host genome-wide evolutionary rate was 7·9 × 10-4 substitutions per site per year (IQR 7·0-9·0 × 10-4), with high inter-individual variability driven largely by non-synonymous mutations, particularly in the N-terminal and receptor-binding domains of the spike protein. Longer infection duration was associated with higher evolutionary rates, while no associations were found with age, sex, vaccination status, previous infection, or virus lineage. We found no clear evidence of transmission beyond the first month of infection in any of the 84 persistent infections lasting 56 days or longer. In total, we identified 379 recurrent mutations, including many with known or predicted negative fitness effects and low prevalence at the population level, as well as de novo reversions to the Wuhan-Hu-1 reference sequence, which were likely under positive selection within those individuals. INTERPRETATION: This study highlights the heterogeneous nature of within-host SARS-CoV-2 evolution in individuals with persistent infection in the community. Notably, a small subset of persistent infections with high viral loads underwent accelerated viral evolution or recurrently acquired hallmark mutations found in novel variants. In addition, onward transmission from a persistent infection during the later stages of infection is likely to be rare. These insights have important implications for prioritising genomic surveillance and managing patients with persistent infections. FUNDING: Department of Health and Social Care.

Humans↗

PubMed2005

A general theory of evolution based on energy efficiency: its implications for diseases.

We propose a general theory of evolution based on energy efficiency. Life represents an emergent property of energy. The earth receives energy from cosmic sources such as the sun. Biologic life can be characterized by the conversion of available energy into complex systems. Direct energy converters such as photosynthetic microorganisms and plants transform light energy into high-energy phosphate bonds that fuel biochemical work. Indirect converters such as herbivores and carnivores predominantly feed off the food chain supplied by these direct converters. Improving energy efficiency confers competitive advantage in the contest among organisms for energy. We introduce a term, return on energy (ROE), as a measure of energy efficiency. We define ROE as a ratio of the amount of energy acquired by a system to the amount of energy consumed to generate that gain. Life-death cycling represents a tactic to sample the environment for innovations that allow increases in ROE to develop over generations rather than an individual lifespan. However, the variation-selection strategem of Darwinian evolution may define a particular tactic rather than an overarching biological paradigm. A theory of evolution based on competition for energy and driven by improvements in ROE both encompasses prior notions of evolution and portends post-Darwinian mechanisms. Such processes may involve the exchange of non-genetic traits that improve ROE, as exemplified by cognitive adaptations or memes. Under these circumstances, indefinite persistence may become favored over life-death cycling, as increases in ROE may then occur more efficiently within a single lifespan rather than over multiple generations. The key to this transition may involve novel methods to address the promotion of health and cognitive plasticity. We describe the implications of this theory for human diseases.

Animals↗

PubMed2006

The evolution of myiasis in humans and other animals in the Old and New Worlds (part II): biological and life-history studies.

Myiasis, which is the dipteran parasitism of living vertebrates, occurs in several forms - ranging from benign to fatal, opportunistic to obligate - and seems to have evolved through two distinct routes: saprophagous and sanguinivorous. However, the convergent evolution of morphological and life-history traits seems to have had a major role in confusing the overall picture of how myiasis evolved and this simplistic division is further complicated by the existence of both ectoparasitic and endoparasitic species of myiasis-causing Diptera, the evolutionary affinities of which remain to be resolved. As discussed in part I of this review, if we are to elucidate how the different forms of parasitism arose, it is essential to separate the evolution of the various groups of myiasis-causing flies from the evolution of the myiasis habit per se. Accordingly, whereas we focused on recent landmark phylogenetics studies in part I, we use this framework to analyse relevant biochemical, immunological, behavioural, biogeographical and fossil evidence to elucidate the evolution of myiasis in part II.

Animals↗

PubMed2004

Evolution of the Fgf and Fgfr gene families.

Fibroblast growth factors (Fgfs) and Fgf receptors (Fgfrs) comprise a signaling system that is conserved throughout metazoan evolution. Twenty-two Fgfs and four Fgfrs have been identified in humans and mice. During evolution, the Fgf family appears to have expanded in two phases. In the first phase, during early metazoan evolution, Fgfs expanded from two or three to six genes by gene duplication. In the second phase, during the evolution of early vertebrates, the Fgf family expanded by two large-scale gen(om)e duplications. By contrast, the Fgfr family has expanded only in the second phase. However, the acquisition of alternative splicing by Fgfrs has increased their functional diversity. The mechanisms that regulate alternative splicing have been conserved since the divergences of echinoderms and vertebrates. The expansion of the Fgf and Fgfr gene families has enabled this signaling system to acquire functional diversity and, therefore, an almost ubiquitous involvement in developmental and physiological processes.

Animals↗

PubMed2003

Molecular evolution of myotoxic phospholipases A2 from snake venom.

After two decades of study, we draw the conclusion that venom-gland phospholipase A2 (PLA2) isozymes, including PLA2 myotoxins of Crotalinae snakes, have evolved in an accelerated manner to acquire their diverse physiological activities. In this review, we describe how accelerated evolution of venom PLA2 isozymes was discovered. This type of evolution is fundamental for other venom isozyme systems. Accelerated evolution of venom PLA2 isozyme genes is due to rapid change in exons, but not in introns and the flanking regions, being completely opposite to the case of the ordinary isozyme genes. The molecular mechanism by which proper base substitutions had occurred in the particular sites of venom isozyme genes is a puzzle to be solved in future studies. It should be noted that accelerated evolution occurred until the isozymes had acquired their particular function and, since then, they have evolved with less frequent mutation, possibly for functional conservation. We also found that interisland mutations occurred in venom PLA2 isozymes. The relationships between mutation and its driving force are speculative and the real mechanism remains a mystery.

Amino Acid Sequence↗

PubMed2006

Evolution of the vertebrate ABC gene family: analysis of gene birth and death.

Vertebrate evolution has been largely driven by the duplication of genes that allow for the acquisition of new functions. The ATP-binding cassette (ABC) proteins constitute a large and functionally diverse family of membrane transporters. The members of this multigene family are found in all cellular organisms, most often engaged in the translocation of a wide variety of substrates across lipid membranes. Because of the diverse function of these genes, their large size, and the large number of orthologs, ABC genes represent an excellent tool to study gene family evolution. We have identified ABC proteins from the sea squirt (Ciona intestinalis), zebrafish (Danio rerio), and chicken (Gallus gallus) and, using phylogenetic analysis, identified those genes with a one-to-one orthologous relationship to human ABC proteins. All ABC protein subfamilies found in Ciona and zebrafish correspond to the human subfamilies, with the exception of a single ABCH subfamily gene found only in zebrafish. Multiple gene duplication and deletion events were identified in different lineages, indicating an ongoing process of gene evolution. As many ABC genes are involved in human genetic diseases, and important drug transport phenotypes, the understanding of ABC gene evolution is important to the development of animal models and functional studies.

ATP-Binding Cassette Transporters↗

PubMed2006

Convergent evolution of gigantism in damselflies of Africa and South America? Evidence from nuclear and mitochondrial sequence data.

Extreme large body size is rare in modern Zygoptera (damselflies). Only the South and Central American damselfly family Pseudostigmatidae and one African species, Coryphagrion grandis, share the morphological trait of gigantism. By means of phylogenetic analyses using two mitochondrial markers (16S rDNA and ND1) and one nuclear marker (EF1) in combination with an existing morphological data set, we trace the evolution of gigantism in damselflies. Individual and combined data sets were analyzed using the maximum parsimony, minimum evolution and maximum likelihood algorithms. Regardless of the algorithm used and the data set analyzed all principal tree topologies support a monophyly of the damselfly taxa displaying giant body size. This supports the view that the evolution of gigantism in damselflies from Africa and South America is not the result of convergent evolution due to strikingly similar habitat preferences, but rather the result of close genealogical relationship. Because modern odonates evolved before the split of Africa from Gondwanaland, the proposed phylogeny suggests that C. grandis represents a Gondwana relict.

Africa↗

PubMed2006

Phylogenetics of the woodrat genus Neotoma (Rodentia: Muridae): implications for the evolution of phenotypic variation in male external genitalia.

Interspecific morphological variation in animal genitalia has long attracted the attention of evolutionary biologists because of the role genital form may play in the generation and/or maintenance of species boundaries. Here we examine the origin and evolution of genital variation in rodents of the muroid genus Neotoma. We test the hypothesis that a relatively rare genital form has evolved only once in Neotoma. We use four mitochondrial and four nuclear markers to evaluate this hypothesis by establishing a phylogenetic framework in which to examine genital evolution. We find intron seven of the beta-fibrinogen gene to be a highly informative nuclear marker for the levels of differentiation that characterize Neotoma with this locus evolving at a rate slower than cytochrome b but faster than 12S. We estimate phylogenetic relationships within Neotoma using both maximum parsimony and maximum likelihood-based Bayesian methods. Our Bayesian and parsimony reconstructions differ in significant ways, but we show that our parsimony analysis may be influenced by long-branch attraction. Furthermore, our estimate of Neotoma phylogeny remains consistent across various data partitioning strategies in the Bayesian analyses. Using ancestral state reconstruction, we find support for the monophyly of taxa that possess the relatively rare genital form. However, we also find support for the independent evolution of the common genital form and discuss possible underlying developmental shifts that may have contributed to our observed patterns of morphological evolution.

Animals↗

PubMed2003

A cellular automaton model for the study of DNA sequence evolution.

Cellular automata are introduced as a model for DNA structure, function and evolution. DNA is modeled as a one-dimensional cellular automaton with four states per cell. These states are the four DNA bases A, C, T and G. The four states are represented by numbers of the quaternary number system. Linear evolution rules, represented by square matrices, are considered. Based on this model a simulator of DNA evolution is developed and simulation results are presented. This simulator has a user-friendly input interface and can be used for the study of DNA evolution.

Evolution, Molecular↗

PubMed2003

A comparison of directed evolution approaches using the beta-glucuronidase model system.

Protein engineers can alter the properties of enzymes by directing their evolution in vitro. Many methods to generate molecular diversity and to identify improved clones have been developed, but experimental evolution remains as much an art as a science. We previously used DNA shuffling (sexual recombination) and a histochemical screen to direct the evolution of Escherichia coli beta-glucuronidase (GUS) variants with improved beta-galactosidase (BGAL) activity. Here, we employ the same model evolutionary system to test the efficiencies of several other techniques: recursive random mutagenesis (asexual), combinatorial cassette mutagenesis (high-frequency recombination) and a versatile high-throughput microplate screen. GUS variants with altered specificity evolved in each trial, but different combinations of mutagenesis and screening techniques effected the fixation of different beneficial mutations. The new microplate screen identified a broader set of mutations than the previously employed X-gal colony screen. Recursive random mutagenesis produced essentially asexual populations, within which beneficial mutations drove each other into extinction (clonal interference); DNA shuffling and combinatorial cassette mutagenesis led instead to the accumulation of beneficial mutations within a single allele. These results explain why recombinational approaches generally increase the efficiency of laboratory evolution.

Directed Molecular Evolution↗

PubMed2003

Kin selection may inhibit the evolution of reciprocation.

Kin selection and reciprocal cooperation provide two candidate explanations for the evolution of cooperation. Models of the evolution of cooperation have typically focussed on one or the other mechanism, despite claims that kin selection could pave the way for the evolution of reciprocal cooperation. We describe a computer simulation model that explicitly supports both kin selection and reciprocal cooperation. The model simulates a viscous population of discrete individuals with social interaction taking the form of the Prisoner's Dilemma and selection acting on performance in these interactions. We recount how the analytical and empirical study of this model led to the conclusion that kin selection may actually inhibit the evolution of effective strategies for establishing reciprocal cooperation.

Altruism↗