Latest recommendations
Id | Title * | Authors * ▲ | Abstract * | Picture * | Thematic fields * | Recommender | Reviewers | Submission date | |
---|---|---|---|---|---|---|---|---|---|
23 Jan 2020
![]() A novel workflow to improve multi-locus genotyping of wildlife species: an experimental set-up with a known model systemGillingham, Mark A. F., Montero, B. Karina, Wilhelm, Kerstin, Grudzus, Kara, Sommer, Simone and Santos, Pablo S. C. https://doi.org/10.1101/638288Improving the reliability of genotyping of multigene families in non-model organismsRecommended by François Rousset based on reviews by Sebastian Ernesto Ramos-Onsins, Helena Westerdahl and Thomas BigotThe reliability of published scientific papers has been the topic of much recent discussion, notably in the biomedical sciences [1]. Although small sample size is regularly pointed as one of the culprits, big data can also be a concern. The advent of high-throughput sequencing, and the processing of sequence data by opaque bioinformatics workflows, mean that sequences with often high error rates are produced, and that exact but slow analyses are not feasible. References [1] Ioannidis, J. P. A, Greenland, S., Hlatky, M. A., Khoury, M. J., Macleod, M. R., Moher, D., Schulz, K. F. and Tibshirani, R. (2014) Increasing value and reducing waste in research design, conduct, and analysis. The Lancet, 383, 166-175. doi: 10.1016/S0140-6736(13)62227-8 | A novel workflow to improve multi-locus genotyping of wildlife species: an experimental set-up with a known model system | Gillingham, Mark A. F., Montero, B. Karina, Wilhelm, Kerstin, Grudzus, Kara, Sommer, Simone and Santos, Pablo S. C. | <p>Genotyping novel complex multigene systems is particularly challenging in non-model organisms. Target primers frequently amplify simultaneously multiple loci leading to high PCR and sequencing artefacts such as chimeras and allele amplification... | ![]() | Bioinformatics & Computational Biology, Evolutionary Ecology, Genome Evolution, Molecular Evolution | François Rousset | Helena Westerdahl, Sebastian Ernesto Ramos-Onsins, Paul J. McMurdie , Arnaud Estoup, Vincent Segura, Jacek Radwan , Torbjørn Rognes , William Stutz , Kevin Vanneste , Thomas Bigot, Jill A. Hollenbach , Wieslaw Babik , Marie-Christin... | 2019-05-15 17:30:44 | View |
12 Jul 2017
![]() Assortment of flowering time and defense alleles in natural Arabidopsis thaliana populations suggests co-evolution between defense and vegetative lifespan strategiesGlander S, He F, Schmitz G, Witten A, Telschow A, de Meaux J 10.1101/131136Towards an integrated scenario to understand evolutionary patterns in A. thalianaRecommended by Xavier Picó based on reviews by Rafa Rubio de Casas and Xavier PicóNobody can ignore that a full understanding of evolution requires an integrated approach from both conceptual and methodological viewpoints. Although some life-history traits, e.g. flowering time, have long been receiving more attention than others, in many cases because the former are more workable than the latter, we must acknowledge that our comprehension about how evolution works is strongly biased and limited. In the Arabidopsis community, such an integration is making good progress as an increasing number of research groups worldwide are changing the way in which evolution is put to the test. This manuscript [1] is a good example of that as the authors raise an important issue in evolutionary biology by combining gene expression and flowering time data from different sources. In particular, the authors explore how variation in flowering time, which determines lifespan, and host immunity defenses co-vary, which is interpreted in terms of co-evolution between the two traits. Interestingly, the authors go beyond that pattern by separating lifespan-dependent from lifespan–independent defense genes, and by showing that defense genes with variants known to impact fitness in the field are among the genes whose expression co-varies most strongly with flowering time. Finally, these results are supported by a simple mathematical model indicating that such a relationship can also be expected theoretically. Overall, the readers will find many conceptual and methodological elements of interest in this manuscript. The idea that evolution is better understood under the scope of life history variation is really exciting and challenging, and in my opinion on the right track for disentangling the inherent complexities of evolutionary research. However, only when we face complexity, we also face its costs and burdens. In this particular case, the well-known co-variation between seed dormancy and flowering time is a missing piece, as well as the identification of (variation in) putative selective pressures accounting for the co-evolution between defense mechanisms and life history (seed dormancy vs. flowering time) along environmental gradients. More intellectual, technical and methodological challenges that with no doubt are totally worth it. Reference [1] Glander S, He F, Schmitz G, Witten A, Telschow A, de Meaux J. 2017. Assortment of flowering time and defense alleles in natural Arabidopsis thaliana populations suggests co-evolution between defense and vegetative lifespan strategies. bioRxiv ver.1 of June 19, 2017. doi: 10.1101/131136 | Assortment of flowering time and defense alleles in natural Arabidopsis thaliana populations suggests co-evolution between defense and vegetative lifespan strategies | Glander S, He F, Schmitz G, Witten A, Telschow A, de Meaux J | The selective impact of pathogen epidemics on host defenses can be strong but remains transient. By contrast, life-history shifts can durably and continuously modify the balance between costs and benefits of immunity, which arbitrates the evolutio... | ![]() | Adaptation, Evolutionary Ecology, Expression Studies, Life History, Phenotypic Plasticity, Quantitative Genetics, Species interactions | Xavier Picó | Sophie Karrenberg, Rafa Rubio de Casas, Xavier Picó | 2017-06-21 10:57:14 | View |
18 Aug 2020
![]() Early phylodynamics analysis of the COVID-19 epidemics in FranceGonché Danesh, Baptiste Elie,Yannis Michalakis, Mircea T. Sofonea, Antonin Bal, Sylvie Behillil, Grégory Destras, David Boutolleau, Sonia Burrel, Anne-Geneviève Marcelin, Jean-Christophe Plantier, Vincent Thibault, Etienne Simon-Loriere, Sylvie van der Werf, Bruno Lina, Laurence Josset, Vincent Enouf, Samuel Alizon and the COVID SMIT PSL group https://doi.org/10.1101/2020.06.03.20119925SARS-Cov-2 genome sequence analysis suggests rapid spread followed by epidemic slowdown in FranceRecommended by B. Jesse Shapiro based on reviews by Luca Ferretti and 2 anonymous reviewersSequencing and analyzing SARS-Cov-2 genomes in nearly real time has the potential to quickly confirm (and inform) our knowledge of, and response to, the current pandemic [1,2]. In this manuscript [3], Danesh and colleagues use the earliest set of available SARS-Cov-2 genome sequences available from France to make inferences about the timing of the major epidemic wave, the duration of infections, and the efficacy of lockdown measures. Their phylodynamic estimates -- based on fitting genomic data to molecular clock and transmission models -- are reassuringly close to estimates based on 'traditional' epidemiological methods: the French epidemic likely began in mid-January or early February 2020, and spread relatively rapidly (doubling every 3-5 days), with people remaining infectious for a median of 5 days [4,5]. These transmission parameters are broadly in line with estimates from China [6,7], but are currently unknown in France (in the absence of contact tracing data). By estimating the temporal reproductive number (Rt), the authors detected a slowing down of the epidemic in the most recent period of the study, after mid-March, supporting the efficacy of lockdown measures. References [1] Grubaugh, N. D., Ladner, J. T., Lemey, P., Pybus, O. G., Rambaut, A., Holmes, E. C., & Andersen, K. G. (2019). Tracking virus outbreaks in the twenty-first century. Nature microbiology, 4(1), 10-19. doi: 10.1038/s41564-018-0296-2 | Early phylodynamics analysis of the COVID-19 epidemics in France | Gonché Danesh, Baptiste Elie,Yannis Michalakis, Mircea T. Sofonea, Antonin Bal, Sylvie Behillil, Grégory Destras, David Boutolleau, Sonia Burrel, Anne-Geneviève Marcelin, Jean-Christophe Plantier, Vincent Thibault, Etienne Simon-Loriere, Sylvie va... | <p>France was one of the first countries to be reached by the COVID-19 pandemic. Here, we analyse 196 SARS-Cov-2 genomes collected between Jan 24 and Mar 24 2020, and perform a phylodynamics analysis. In particular, we analyse the doubling time, r... | ![]() | Evolutionary Epidemiology, Molecular Evolution, Phylogenetics / Phylogenomics | B. Jesse Shapiro | 2020-06-04 13:13:57 | View | |
11 Dec 2020
![]() Quantifying transmission dynamics of acute hepatitis C virus infections in a heterogeneous population using sequence dataGonche Danesh, Victor Virlogeux, Christophe Ramière, Caroline Charre, Laurent Cotte, Samuel Alizon https://doi.org/10.1101/689158Phylodynamics of hepatitis C virus reveals transmission dynamics within and between risk groups in LyonRecommended by David Rasmussen based on reviews by Chris Wymant and Louis DuPlessisGenomic epidemiology seeks to better understand the transmission dynamics of infectious pathogens using molecular sequence data. Phylodynamic methods have given genomic epidemiology new power to track the transmission dynamics of pathogens by combining phylogenetic analyses with epidemiological modeling. In recent year, applications of phylodynamics to chronic viral infections such as HIV and hepatitis C virus (HVC) have provided some of the best examples of how phylodynamic inference can provide valuable insights into transmission dynamics within and between different subpopulations or risk groups, allowing for more targeted interventions. References [1] Rasmussen, D. A., Volz, E. M., and Koelle, K. (2014). Phylodynamic inference for structured epidemiological models. PLoS Comput Biol, 10(4), e1003570. doi: https://doi.org/10.1371/journal.pcbi.1003570 | Quantifying transmission dynamics of acute hepatitis C virus infections in a heterogeneous population using sequence data | Gonche Danesh, Victor Virlogeux, Christophe Ramière, Caroline Charre, Laurent Cotte, Samuel Alizon | <p>Opioid substitution and syringes exchange programs have drastically reduced hepatitis C virus (HCV) spread in France but HCV sexual transmission in men having sex with men (MSM) has recently arisen as a significant public health concern. The fa... | ![]() | Evolutionary Epidemiology, Phylogenetics / Phylogenomics | David Rasmussen | 2019-07-11 13:37:23 | View | |
05 Feb 2019
![]() The quiescent X, the replicative Y and the AutosomesGuillaume Achaz, Serge Gangloff, Benoit Arcangioli https://doi.org/10.1101/351288Replication-independent mutations: a universal signature ?Recommended by Nicolas GaltierMutations are the primary source of genetic variation, and there is an obvious interest in characterizing and understanding the processes by which they appear. One particularly important question is the relative abundance, and nature, of replication-dependent and replication-independent mutations - the former arise as cells replicate due to DNA polymerization errors, whereas the latter are unrelated to the cell cycle. A recent experimental study in fission yeast identified a signature of mutations in quiescent (=non-replicating) cells: the spectrum of such mutations is characterized by an enrichment in insertions and deletions (indels) compared to point mutations, and an enrichment of deletions compared to insertions [2]. References [1] Achaz, G., Gangloff, S., and Arcangioli, B. (2019). The quiescent X, the replicative Y and the Autosomes. BioRxiv, 351288, ver. 3 peer-reviewed and recommended by PCI Evol Biol. doi: 10.1101/351288 | The quiescent X, the replicative Y and the Autosomes | Guillaume Achaz, Serge Gangloff, Benoit Arcangioli | <p>From the analysis of the mutation spectrum in the 2,504 sequenced human genomes from the 1000 genomes project (phase 3), we show that sexual chromosomes (X and Y) exhibit a different proportion of indel mutations than autosomes (A), ranking the... | ![]() | Bioinformatics & Computational Biology, Genome Evolution, Human Evolution, Molecular Evolution, Population Genetics / Genomics, Reproduction and Sex | Nicolas Galtier | 2018-07-25 10:37:48 | View | |
12 Feb 2024
How do plant RNA viruses overcome the negative effect of Muller s ratchet despite strong transmission bottlenecks?Guillaume Lafforgue, Marie Lefebvre, Thierry Michon, Santiago F. Elena https://doi.org/10.1101/2023.08.01.550272How to survive the mutational meltdown: lessons from plant RNA virusesRecommended by Kavita Jain based on reviews by Brent Allman, Ana Morales-Arce and 1 anonymous reviewerAlthough most mutations are deleterious, the strongly deleterious ones do not spread in a very large population as their chance of fixation is very small. Another mechanism via which the deleterious mutations can be eliminated is via recombination or sexual reproduction. However, in a finite asexual population, the subpopulation without any deleterious mutation will eventually acquire a deleterious mutation resulting in the reduction of the population size or in other words, an increase in the genetic drift. This, in turn, will lead the population to acquire deleterious mutations at a faster rate eventually leading to a mutational meltdown. This irreversible (or, at least over some long time scales) accumulation of deleterious mutations is especially relevant to RNA viruses due to their high mutation rate, and while the prior work has dealt with bacteriophages and RNA viruses, the study by Lafforgue et al. [1] makes an interesting contribution to the existing literature by focusing on plants. In this study, the authors enquire how despite the repeated increase in the strength of genetic drift, how the RNA viruses manage to survive in plants. Following a series of experiments and some numerical simulations, the authors find that as expected, after severe bottlenecks, the fitness of the population decreases significantly. But if the bottlenecks are followed by population expansion, the Muller’s ratchet can be halted due to the genetic diversity generated during population growth. They hypothesize this mechanism as a potential way by which the RNA viruses can survive the mutational meltdown. As a theoretician, I find this investigation quite interesting and would like to see more studies addressing, e.g., the minimum population growth rate required to counter the potential extinction for a given bottleneck size and deleterious mutation rate. Of course, it would be interesting to see in future work if the hypothesis in this article can be tested in natural populations. References [1] Guillaume Lafforgue, Marie Lefebvre, Thierry Michon, Santiago F. Elena (2024) How do plant RNA viruses overcome the negative effect of Muller s ratchet despite strong transmission bottlenecks? bioRxiv, ver. 3 peer-reviewed and recommended by Peer Community In Evolutionary Biology | How do plant RNA viruses overcome the negative effect of Muller s ratchet despite strong transmission bottlenecks? | Guillaume Lafforgue, Marie Lefebvre, Thierry Michon, Santiago F. Elena | <p>Muller's ratchet refers to the irreversible accumulation of deleterious mutations in small populations, resulting in a decline in overall fitness. This phenomenon has been extensively observed in experiments involving microorganisms, including ... | Experimental Evolution, Genome Evolution | Kavita Jain | 2023-08-04 09:37:08 | View | ||
13 Apr 2023
![]() The landscape of nucleotide diversity in Drosophila melanogaster is shaped by mutation rate variationGustavo V Barroso, Julien Y Dutheil https://doi.org/10.1101/2021.09.16.460667An unusual suspect: the mutation landscape as a determinant of local variation in nucleotide diversityRecommended by Fernando Racimo based on reviews by David Castellano and 1 anonymous reviewerSometimes, important factors for explaining biological processes fall through the cracks, and it is only through careful modeling that their importance eventually comes out to light. In this study, Barroso and Dutheil introduce a new method based on the sequentially Markovian coalescent (SMC, Marjoran and Wall 2006) for jointly estimating local recombination and coalescent rates along a genome. Unlike previous SMC-based methods, however, their method can also co-estimate local patterns of variation in mutation rates. This is a powerful improvement which allows them to tackle questions about the reasons for the extensive variation in nucleotide diversity across the chromosomes of a species - a problem that has plagued the minds of population geneticists for decades (Begun and Aquadro 1992, Andolfatto 2007, McVicker et al., 2009, Pouyet and Gilbert 2021). The authors find that variation in de novo mutation rates appears to be the most important factor in determining nucleotide diversity in Drosophila melanogaster. Though seemingly contradicting previous attempts at addressing this problem (Comeron 2014), they take care to investigate and explain why that might be the case. Barroso and Dutheil have also taken care to carefully explain the details of their new approach and have carried a very thorough set of analyses comparing competing explanations for patterns of nucleotide variation via causal modeling. The reviewers raised several issues involving choices made by the authors in their analysis of variance partitioning, the proper evaluation of the role of linked selection and the recombination rate estimates emerging from their model. These issues have all been extensively addressed by the authors, and their conclusions seem to remain robust. The study illustrates why the mutation landscape should not be ignored as an important determinant of local variation in genetic diversity, and opens up questions about the generalizability of these results to other organisms. REFERENCES Andolfatto, P. (2007). Hitchhiking effects of recurrent beneficial amino acid substitutions in the Drosophila melanogaster genome. Genome research, 17(12), 1755-1762. https://doi.org/10.1101/gr.6691007 Barroso, G. V., & Dutheil, J. Y. (2021). The landscape of nucleotide diversity in Drosophila melanogaster is shaped by mutation rate variation. bioRxiv, 2021.09.16.460667, ver. 3 peer-reviewed and recommended by Peer Community in Evolutionary Biology. https://doi.org/10.1101/2021.09.16.460667 Begun, D. J., & Aquadro, C. F. (1992). Levels of naturally occurring DNA polymorphism correlate with recombination rates in D. melanogaster. Nature, 356(6369), 519-520. https://doi.org/10.1038/356519a0 Comeron, J. M. (2014). Background selection as baseline for nucleotide variation across the Drosophila genome. PLoS Genetics, 10(6), e1004434. https://doi.org/10.1371/journal.pgen.1004434 Marjoram, P., & Wall, J. D. (2006). Fast" coalescent" simulation. BMC genetics, 7, 1-9. https://doi.org/10.1186/1471-2156-7-16 McVicker, G., Gordon, D., Davis, C., & Green, P. (2009). Widespread genomic signatures of natural selection in hominid evolution. PLoS genetics, 5(5), e1000471. https://doi.org/10.1371/journal.pgen.1000471 Pouyet, F., & Gilbert, K. J. (2021). Towards an improved understanding of molecular evolution: the relative roles of selection, drift, and everything in between. Peer Community Journal, 1, e27. https://doi.org/10.24072/pcjournal.16 | The landscape of nucleotide diversity in Drosophila melanogaster is shaped by mutation rate variation | Gustavo V Barroso, Julien Y Dutheil | <p style="text-align: justify;">What shapes the distribution of nucleotide diversity along the genome? Attempts to answer this question have sparked debate about the roles of neutral stochastic processes and natural selection in molecular evolutio... | ![]() | Bioinformatics & Computational Biology, Population Genetics / Genomics | Fernando Racimo | 2022-10-30 07:52:07 | View | |
19 Jul 2021
![]() Host phenology can drive the evolution of intermediate virulence strategies in some obligate-killer parasitesHannelore MacDonald, Erol Akçay, Dustin Brisson https://doi.org/10.1101/2021.03.13.435259Modelling parasitoid virulence evolution with seasonalityRecommended by Samuel AlizonThe harm most parasites cause to their host, i.e. the virulence, is a mystery because host death often means the end of the infectious period. For obligate killer parasites, or “parasitoids”, that need to kill their host to transmit to other hosts the question is reversed. Indeed, more rapid host death means shorter generation intervals between two infections and mathematical models show that, in the simplest settings, natural selection should always favour more virulent strains (Levin and Lenski, 1983). Adding biological details to the model modifies this conclusion and, for instance, if the relationship between the infection duration and the number of parasites transmission stages produced in a host is non-linear, strains with intermediate levels of virulence can be favoured (Ebert and Weisser 1997). Other effects, such as spatial structure, could yield similar effects (Lion and van Baalen, 2007). In their study, MacDonald et al. (2021) explore another type of constraint, which is seasonality. Earlier studies, such as that by Donnelly et al. (2013) showed that this constraint can affect virulence evolution but they had focused on directly transmitted parasites. Using a mathematical model capturing the dynamics of a parasitoid, MacDonald et al. (2021) show if two main assumptions are met, namely that at the end of the season only transmission stages (or “propagules”) survive and that there is a constant decay of these propagules with time, then strains with intermediate levels of virulence are favoured. Practically, the authors use delay differential equations and an adaptive dynamics approach to identify evolutionary stable strategies. As expected, the longer the short the season length, the higher the virulence (because propagule decay matters less). The authors also identify a non-linear relationship between the variation in host development time and virulence. Generally, the larger the variation, the higher the virulence because the parasitoid has to kill its host before the end of the season. However, if the variation is too wide, some hosts become physically impossible to use for the parasite, whence a decrease in virulence. Finally, MacDonald et ali. (2021) show that the consequence of adding trade-offs between infection duration and the number of propagules produced is in line with earlier studies (Ebert and Weisser 1997). These mathematical modelling results provide testable predictions for using well-described systems in evolutionary ecology such as daphnia parasitoids, baculoviruses, or lytic phages. Reference Donnelly R, Best A, White A, Boots M (2013) Seasonality selects for more acutely virulent parasites when virulence is density dependent. Proc R Soc B, 280, 20122464. https://doi.org/10.1098/rspb.2012.2464 Ebert D, Weisser WW (1997) Optimal killing for obligate killers: the evolution of life histories and virulence of semelparous parasites. Proc R Soc B, 264, 985–991. https://doi.org/10.1098/rspb.1997.0136 Levin BR, Lenski RE (1983) Coevolution in bacteria and their viruses and plasmids. In: Futuyma DJ, Slatkin M eds. Coevolution. Sunderland, MA, USA: Sinauer Associates, Inc., 99–127. Lion S, van Baalen M (2008) Self-structuring in spatial evolutionary ecology. Ecol. Lett., 11, 277–295. https://doi.org/10.1111/j.1461-0248.2007.01132.x MacDonald H, Akçay E, Brisson D (2021) Host phenology can drive the evolution of intermediate virulence strategies in some obligate-killer parasites. bioRxiv, 2021.03.13.435259, ver. 8 peer-reviewed and recommended by Peer Community in Evolutionary Biology. https://doi.org/10.1101/2021.03.13.435259 | Host phenology can drive the evolution of intermediate virulence strategies in some obligate-killer parasites | Hannelore MacDonald, Erol Akçay, Dustin Brisson | <p style="text-align: justify;">The traditional mechanistic trade-offs resulting in a negative correlation between transmission and virulence are the foundation of nearly all current theory on the evolution of parasite virulence. Several ecologica... | ![]() | Evolutionary Dynamics, Evolutionary Ecology, Evolutionary Epidemiology, Evolutionary Theory | Samuel Alizon | 2021-03-14 13:47:33 | View | |
15 Sep 2022
![]() Bimodal breeding phenology in the Parsley Frog Pelodytes punctatus as a bet-hedging strategy in an unpredictable environment despite strong priority effectsHelene Jourdan-Pineau, Pierre-Andre Crochet, Patrice David https://doi.org/10.1101/2022.02.24.481784Spreading the risk of reproductive failure when the environment is unpredictable and ephemeralRecommended by Gabriele Sorci based on reviews by Thomas Haaland and Zoltan RadaiMany species breed in environments that are unpredictable, for instance in terms of the availability of resources needed to raise the offspring. Organisms might respond to such spatial and temporal unpredictability by adopting plastic responses to adjust their reproductive investment according to perceived cues of environmental quality. Some species such as the amphibians might also face the problem of ephemeral habitats, when the ponds where they breed have a chance of drying up before metamorphosis has occurred. In this case, maximizing long-term fitness might involve a strategy of spreading the risk, even though the reproductive success of a single reproductive bout might be lower. Understanding how animals (and plants) get adapted to stochastic environments is particularly crucial in the current context of rapid environmental changes. In this article, Jourdan-Pineau et al. report the results of field surveys of the Parsley Frog (Pelodytes punctatus) in Southern France. This frog has peculiar breeding phenology with females breeding in autumn and spring. The authors provide quite an extensive amount of information on the reproductive success of eggs laid in each season and the possible ecological factors accounting for differences between seasons. Although the presence of interspecific competitors and predators does not seem to account for pond-specific reproductive success, the survival of tadpoles hatching from eggs laid in spring is severely impaired when tadpoles from the autumn cohort have managed to survive. This intraspecific competition takes the form of a “priority” effect where tadpoles from the autumn cohort outcompete the smaller larvae from the spring cohort. Given this strong priority effect, one might tentatively predict that females laying in spring should avoid ponds with tadpoles from the autumn cohort. Surprisingly, however, the authors did not find any evidence for such avoidance, which might indicate strong constraints on the availability of ponds where females might possibly lay. Assuming that each female can indeed lay both in autumn and spring, how is this bimodal phenology maintained? Would not be worthier to allocate all the eggs to the autumn (or the spring) laying season? Eggs laid in autumn and spring have to face different environmental hazards, reducing their hatching success and the probability to produce metamorphs (for instance, tadpoles hatching from eggs laid in autumn have to overwinter which might be a particularly risky phase). Jourdan-Pineau and coworkers addressed this question by adapting a bet-hedging model that was initially developed to investigate the strategy of allocation into seed dormancy of annual plants (Cohen 1966) to the case of the bimodal phenology of the Parsley Frog. By feeding the model with the parameter values obtained from the field surveys, they found that the two breeding strategies (laying in autumn and in spring) can coexist as long as the probability of breeding success in the autumn cohort is between 20% and 80% (the range of values allowing the coexistence of a bimodal phenology shrinking a little bit when considering that frogs can reproduce 5 times during their lifespan instead of three times). This paper provides a very nice illustration of the importance of combining approaches (here field monitoring to gather data that can be used to feed models) to understand the evolution of peculiar breeding strategies. Although future work should attempt to gather individual-based data (in addition to population data), this work shows that spreading the risk can be an adaptive strategy in environments characterized by strong stochastic variation. References Cohen D (1966) Optimizing reproduction in a randomly varying environment. Journal of Theoretical Biology, 12, 119–129. https://doi.org/10.1016/0022-5193(66)90188-3 Jourdan-Pineau H., Crochet P.-A., David P. (2022) Bimodal breeding phenology in the Parsley Frog Pelodytes punctatus as a bet-hedging strategy in an unpredictable environment despite strong priority effects. bioRxiv, 2022.02.24.481784, ver. 5 peer-reviewed and recommended by Peer Community in Evolutionary Biology. https://doi.org/10.1101/2022.02.24.481784 | Bimodal breeding phenology in the Parsley Frog Pelodytes punctatus as a bet-hedging strategy in an unpredictable environment despite strong priority effects | Helene Jourdan-Pineau, Pierre-Andre Crochet, Patrice David | <p style="text-align: justify;">When environmental conditions are unpredictable, expressing alternative phenotypes spreads the risk of failure, a mixed strategy called bet-hedging. In the southern part of its range, the Parsley Frog <em>Pelodytes ... | ![]() | Adaptation, Evolutionary Ecology, Life History | Gabriele Sorci | 2022-02-28 11:53:00 | View | |
17 Dec 2016
![]()
POSTPRINT
Evolution of HIV virulence in response to widespread scale up of antiretroviral therapy: a modeling studyHerbeck JT, Mittler JE, Gottlieb GS, Goodreau SM, Murphy JT, Cori A, Pickles M, Fraser C https://doi.org/10.1093/ve/vew028Predicting HIV virulence evolution in response to widespread treatmentRecommended by Samuel AlizonIt is a classical result in the virulence evolution literature that treatments decreasing parasite replication within the host should select for higher replication rates, thus driving increased levels of virulence if the two are correlated. There is some evidence for this in vitro but very little in the field. HIV infections in humans offer a unique opportunity to go beyond the simple predictions that treatments should favour more virulent strains because many details of this host-parasite system are known, especially the link between set-point virus load, transmission rate and virulence. To tackle this question, Herbeck et al. [1] used a detailed individual-based model. This is original because it allows them to integrate existing knowledge from the epidemiology and evolution of HIV (e.g. recent estimates of the ‘heritability’ of set-point virus load from one infection to the next). This detailed model allows them to formulate predictions regarding the effect of different treatment policies; especially regarding the current policy switch away from treatment initiation based on CD4 counts towards universal treatment. The results show that, perhaps as expected from the theory, treatments based on the level of remaining host target cells (CD4 T cells) do not affect virulence evolution because they do not strongly affect the virulence level that maximizes HIV’s transmission potential. However, early treatments can lead to moderate increase in virulence within several years if coverage is high enough. These results seem quite robust to variation of all the parameters in realistic ranges. The great step forward in this model is the ability to obtain quantitative prediction regarding how a virus may evolve in response to public health policies. Here the main conclusion is that given our current knowledge in HIV biology, the risk of virulence evolution is perhaps more limited than expected from a direct application of virulence evolution model. Interestingly, the authors also conclude that recently observed increased in HIV virulence [2-3] cannot be explained by the impact of antiretroviral therapy alone; which raises the question about the main mechanism behind this increase. Finally, the authors make the interesting suggestion that “changing virulence is amenable to being monitored alongside transmitted drug resistance in sentinel surveillance”. References [1] Herbeck JT, Mittler JE, Gottlieb GS, Goodreau SM, Murphy JT, Cori A, Pickles M, Fraser C. 2016. Evolution of HIV virulence in response to widespread scale up of antiretroviral therapy: a modeling study. Virus Evolution 2:vew028. doi: 10.1093/ve/vew028 [2] Herbeck JT, Müller V, Maust BS, Ledergerber B, Torti C, et al. 2012. Is the virulence of HIV changing? A meta-analysis of trends in prognostic markers of HIV disease progression and transmission. AIDS 26:193-205. doi: 10.1097/QAD.0b013e32834db418 [3] Pantazis N, Porter K, Costagliola D, De Luca A, Ghosn J, et al. 2014. Temporal trends in prognostic markers of HIV-1 virulence and transmissibility: an observational cohort study. Lancet HIV 1:e119-26. doi: 10.1016/s2352-3018(14)00002-2 | Evolution of HIV virulence in response to widespread scale up of antiretroviral therapy: a modeling study | Herbeck JT, Mittler JE, Gottlieb GS, Goodreau SM, Murphy JT, Cori A, Pickles M, Fraser C | <p>There are global increases in the use of HIV antiretroviral therapy (ART), guided by clinical benefits of early ART initiation and the efficacy of treatment as prevention of transmission. Separately, it has been shown theoretically and empirica... | ![]() | Bioinformatics & Computational Biology, Evolutionary Applications, Evolutionary Epidemiology | Samuel Alizon | 2016-12-16 20:54:08 | View |
FOLLOW US
MANAGING BOARD
Guillaume Achaz
Juan Arroyo
Trine Bilde
Dustin Brisson
Julien Dutheil
Marianne Elias
Inês Fragata
Matteo Fumagalli
Tatiana Giraud
Frédéric Guillaume
Ruth Hufbauer
Sara Magalhaes
Caroline Nieberding
Michael David Pirie
Tanja Pyhäjärvi
François Rousset
Tanja Schwander
Alejandro Gonzalez Voyer