scholarly journals Genetic slippage after sex maintains diversity for parasite resistance in a natural host population

2021 ◽  
Author(s):  
Camille Ameline ◽  
Felix Voegtli ◽  
Jason Andras ◽  
Eric Dexter ◽  
Jan Engelstaedter ◽  
...  
Keyword(s):  
Genetic Model ◽  
Large Population ◽  
Bacterial Pathogen ◽  
Host Population ◽  
Natural Host ◽  
Parasite Resistance ◽  
Resting Stages ◽  
Resistance Evolution ◽  
Multiple Loci ◽  
Cyclical Pattern

Although parasite-mediated selection is thought to be a major driver of host evolution, its influence on genetic variation for parasite resistance is not yet well understood. We monitored a large population of the planktonic crustacean Daphnia magna over eight years, as it underwent yearly epidemics of the bacterial pathogen Pasteuria ramosa. We observed a cyclical pattern of resistance evolution: resistant phenotypes increased in frequency throughout the epidemics, but susceptibility was restored each spring when hosts hatched from sexual resting stages, a phenomenon described as genetic slippage in response to sex. Collecting and hatching D. magna resting stages across multiple seasons showed that largely resistant host populations can produce susceptible offspring through recombination. Resting stages produced throughout the planktonic season accurately represent the hatching population cohort of the following spring. A genetic model of resistance developed for this host-parasite system, based on multiple loci and strong epistasis, is in partial agreement with these findings. Our results reveal that, despite strong selection for resistance in a natural host population, genetic slippage after sexual reproduction has the potential to maintain genetic diversity of host resistance.

scholarly journals A two-locus system with strong epistasis underlies rapid parasite-mediated evolution of host resistance

2020 ◽  
Author(s):  
Camille Ameline ◽  
Yann Bourgeois ◽  
Felix Vögtli ◽  
Eevi Savola ◽  
Jason Andras ◽  
...  
Keyword(s):  
Genome Wide Association Study ◽  
Genetic Model ◽  
Genetic Recombination ◽  
Bacterial Pathogen ◽  
Host Population ◽  
Strong Increase ◽  
Adaptive Responses ◽  
A Genome ◽  
Frequency Changes ◽  
Locus System

Abstract Parasites are a major evolutionary force, driving adaptive responses in host populations. Although the link between phenotypic response to parasite-mediated natural selection and the underlying genetic architecture often remains obscure, this link is crucial for understanding the evolution of resistance and predicting associated allele frequency changes in the population. To close this gap, we monitored the response to selection during epidemics of a virulent bacterial pathogen, Pasteuria ramosa, in a natural host population of Daphnia magna. Across two epidemics, we observed a strong increase in the proportion of resistant phenotypes as the epidemics progressed. Field and laboratory experiments confirmed that this increase in resistance was caused by selection from the local parasite. Using a genome wide association study (GWAS), we built a genetic model in which two genomic regions with dominance and epistasis control resistance polymorphism in the host. We verified this model by selfing host genotypes with different resistance phenotypes and scoring their F1 for segregation of resistance and associated genetic markers. Such epistatic effects with strong fitness consequences in host-parasite coevolution are believed to be crucial in the Red Queen model for the evolution of genetic recombination.

scholarly journals A two-locus system with strong epistasis underlies rapid parasite-mediated evolution of host resistance

2020 ◽  
Author(s):  
Camille Ameline ◽  
Yann Bourgeois ◽  
Felix Vögtli ◽  
Eevi Savola ◽  
Jason Andras ◽  
...  
Keyword(s):  
Genome Wide Association Study ◽  
Genetic Model ◽  
Genetic Recombination ◽  
Bacterial Pathogen ◽  
Host Population ◽  
Strong Increase ◽  
Adaptive Responses ◽  
A Genome ◽  
Frequency Changes ◽  
Locus System

AbstractParasites are a major evolutionary force, driving adaptive responses in host populations. Although the link between phenotypic response to parasite-mediated natural selection and the underlying genetic architecture often remains obscure, this link is crucial for understanding the evolution of resistance and predicting associated allele frequency changes in the population. To close this gap, we monitored the response to selection during epidemics of a virulent bacterial pathogen, Pasteuria ramosa, in a natural host population of Daphnia magna. Across two epidemics, we observed a strong increase in the proportion of resistant phenotypes as the epidemics progressed. Field and laboratory experiments confirmed that this increase in resistance was caused by selection from the local parasite. Using a genome wide association study (GWAS), we obtained a genetic model in which two genomic regions with dominance and epistasis control resistance polymorphism in the host. We verified this model by selfing host genotypes with different resistance phenotypes and scoring their F1 for segregation of resistance and associated genetic markers. Applying the model to the dynamics of the field population revealed moderate changes in allele frequencies at the two resistance loci relative to the profound changes observed at the phenotypic level. This apparent discrepancy is explained by strong epistasis and dominance at the two resistance loci, which reduces the effect of selection on alleles at both loci. Such epistatic effects with strong fitness consequences in host-parasite coevolution are believed to be crucial in the Red Queen model for the evolution of genetic recombination.

scholarly journals Experimental Morogoro Virus Infection in Its Natural Host, Mastomys natalensis

Viruses ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 851
Author(s):  
Chris Hoffmann ◽  
Stephanie Wurr ◽  
Elisa Pallasch ◽  
Sabrina Bockholt ◽  
Toni Rieger ◽  
...  
Keyword(s):  
Persistent Infection ◽  
Virus Transmission ◽  
Host Population ◽  
Natural Host ◽  
Lassa Virus ◽  
Mastomys Natalensis ◽  
Natural Hosts ◽  
History Of ◽  
Morogoro Virus ◽  
The Impact

Natural hosts of most arenaviruses are rodents. The human-pathogenic Lassa virus and several non-pathogenic arenaviruses such as Morogoro virus (MORV) share the same host species, namely Mastomys natalensis (M. natalensis). In this study, we investigated the history of infection and virus transmission within the natural host population. To this end, we infected M. natalensis at different ages with MORV and measured the health status of the animals, virus load in blood and organs, the development of virus-specific antibodies, and the ability of the infected individuals to transmit the virus. To explore the impact of the lack of evolutionary virus–host adaptation, experiments were also conducted with Mobala virus (MOBV), which does not share M. natalensis as a natural host. Animals infected with MORV up to two weeks after birth developed persistent infection, seroconverted and were able to transmit the virus horizontally. Animals older than two weeks at the time of infection rapidly cleared the virus. In contrast, MOBV-infected neonates neither developed persistent infection nor were able to transmit the virus. In conclusion, we demonstrate that MORV is able to develop persistent infection in its natural host, but only after inoculation shortly after birth. A related arenavirus that is not evolutionarily adapted to M. natalensis is not able to establish persistent infection. Persistently infected animals appear to be important to maintain virus transmission within the host population.

scholarly journals A genetic locus for paranoia

2018 ◽  
Vol 14 (1) ◽  
pp. 20170694 ◽  
Author(s):  
Bernard Crespi ◽  
Silven Read ◽  
Iiro Salminen ◽  
Peter Hurd
Keyword(s):  
Genetic Model ◽  
Genetic Locus ◽  
Large Population ◽  
Autism Spectrum ◽  
Psychological Effects ◽  
Imprinted Genes ◽  
Nucleotide Polymorphism ◽  
Single Nucleotide ◽  
Altered Expression ◽  
Schizophrenia Spectrum

The psychological effects of brain-expressed imprinted genes in humans are virtually unknown. Prader–Willi syndrome (PWS) is a neurogenetic condition mediated by genomic imprinting, which involves high rates of psychosis characterized by hallucinations and paranoia, as well as autism. Altered expression of two brain-expressed imprinted genes, MAGEL2 and NDN , mediates a suite of PWS-related phenotypes, including behaviour, in mice. We phenotyped a large population of typical individuals for schizophrenia-spectrum and autism-spectrum traits, and genotyped them for the single-nucleotide polymorphism rs850807, which is putatively functional and linked with MAGEL2 and NDN . Genetic variation in rs850807 was strongly and exclusively associated with the ideas of reference subscale of the schizophrenia spectrum, which is best typified as paranoia. These findings provide a single-locus genetic model for analysing the neurological and psychological bases of paranoid thinking, and implicate imprinted genes, and genomic conflicts, in human mentalistic thought.

scholarly journals Spatial and temporal evolution of Lassa virus in the natural host population in Upper Guinea

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Elisabeth Fichet-Calvet ◽  
Stephan Ölschläger ◽  
Thomas Strecker ◽  
Lamine Koivogui ◽  
Beate Becker-Ziaja ◽  
...  
Keyword(s):  
Temporal Evolution ◽  
Host Population ◽  
Natural Host ◽  
Lassa Virus

Acquired immunity protects against helminth infection in a natural host population: long-term field and laboratory evidence

2012 ◽  
Vol 42 (10) ◽  
pp. 931-938 ◽  
Author(s):  
Richard Tinsley ◽  
Lucy Stott ◽  
Jenny York ◽  
Amy Everard ◽  
Sara Chapple ◽  
...  
Keyword(s):  
Helminth Infection ◽  
Host Population ◽  
Natural Host ◽  
Acquired Immunity ◽  
Laboratory Evidence ◽  
Term Field

scholarly journals Activation of CCR2+ human proinflammatory monocytes by human herpesvirus-6B chemokine N-terminal peptide

2013 ◽  
Vol 94 (7) ◽  
pp. 1624-1635 ◽  
Author(s):  
D. J. Clark ◽  
J. Catusse ◽  
A. Stacey ◽  
P. Borrow ◽  
U. A. Gompels
Keyword(s):  
Ex Vivo ◽  
Shape Change ◽  
Human Herpesvirus ◽  
Host Population ◽  
Lytic Replication ◽  
Natural Host ◽  
Sub Saharan Africa ◽  
Cellular Interactions ◽  
Immune Effector ◽  
Effector Cells

Human monocytes expressing CCR2 with CD14 and CD16 can mediate antigen presentation, and promote inflammation, brain infiltration and immunosenescence. Recently identified roles are in human immunodeficiency virus infection, tuberculosis and parasitic disease. Human herpesvirus 6B (HHV-6B) encodes a chemokine, U83B, which is monospecific for CCR2, and is distinct from the related HHV-6A U83A, which activates CCR1, CCR4, CCR5, CCR6 and CCR8 on immune effector cells and dendritic cells. These differences could alter leukocyte-subset recruitment for latent/lytic replication and associated neuroinflammatory pathology. Therefore, cellular interactions between U83A and U83B could help dictate potential tropism differences between these viruses. U83A specificity is maintained in the 38-residue N-terminal spliced-truncated form. Here, we sought to determine the basis for the chemokine receptor specificity differences and identify possible applications. To do this we first analysed variation in a natural host population in sub-Saharan Africa where both viruses are equally prevalent and compared these to global strains. Analyses of U83 N-terminal variation in 112 HHV-6A and HHV-6B infections identified 6/38 U83A or U83B-specific residues. We also identified a unique single U83A-specific substitution in one U83B sequence, ‘U83BA’. Next, the variation effects were tested by deriving N-terminal (NT) 17-mer peptides and assaying activation of ex vivo human leukocytes, the natural host and cellular target. Chemotaxis of CCR2+ leukocytes was potently induced by U83B-NT, but not U83BA-NT or U83A-NT. Analyses of the U83B-NT activated population identified migrated CCR2+, but not CCR5+, leukocytes. The U83BA-NT asparagine-lysine14 substitution disrupted activity, thus defining CCR2 specificity and acting as a main determinant for HHV-6A/B differences in cellular interactions. A flow-cytometry-based shape-change assay was designed, and used to provide further evidence that U83B-NT could activate CCR2+CD14+CD16+ monocytes. This defines a potential antiviral target for HHV-6A/B disease and novel peptide immunomodulator for proinflammatory monocytes.

Take a Walk to the Wild Side of Caenorhabditis elegans-Pathogen Interactions

2021 ◽  
Vol 85 (2) ◽  
Author(s):  
Leah J. Radeke ◽  
Michael A. Herman
Keyword(s):  
Innate Immunity ◽  
Caenorhabditis Elegans ◽  
Recent Work ◽  
Genetic Model ◽  
Model Organism ◽  
Bacterial Pathogen ◽  
Content Type ◽  
Microbiome Composition ◽  
C Elegans ◽  
Functional Studies

SUMMARY Microbiomes form intimate functional associations with their hosts. Much has been learned from correlating changes in microbiome composition to host organismal functions. However, in-depth functional studies require the manipulation of microbiome composition coupled with the precise interrogation of organismal physiology—features available in few host study systems. Caenorhabditis elegans has proven to be an excellent genetic model organism to study innate immunity and, more recently, microbiome interactions. The study of C. elegans-pathogen interactions has provided in depth understanding of innate immune pathways, many of which are conserved in other animals. However, many bacteria were chosen for these studies because of their convenience in the lab setting or their implication in human health rather than their native interactions with C. elegans. In their natural environment, C. elegans feed on a variety of bacteria found in rotting organic matter, such as rotting fruits, flowers, and stems. Recent work has begun to characterize the native microbiome and has identified a common set of bacteria found in the microbiome of C. elegans. While some of these bacteria are beneficial to C. elegans health, others are detrimental, leading to a complex, multifaceted understanding of bacterium-nematode interactions. Current research on nematode-bacterium interactions is focused on these native microbiome components, both their interactions with each other and with C. elegans. We will summarize our knowledge of bacterial pathogen-host interactions in C. elegans, as well as recent work on the native microbiome, and explore the incorporation of these bacterium-nematode interactions into studies of innate immunity and pathogenesis.

scholarly journals Recurrent evolution of cross-resistance in response to selection for improved post-infection survival in Drosophila melanogaster

2021 ◽  
Author(s):  
Aparajita Singh ◽  
Aabeer Basu ◽  
Biswajit Shit ◽  
Tejashwini Hegde ◽  
Nitin Bansal ◽  
...  
Keyword(s):  
Drosophila Melanogaster ◽  
Genetic Variation ◽  
Bacterial Pathogen ◽  
Host Population ◽  
Host Susceptibility ◽  
Cross Resistance ◽  
Response To Selection ◽  
Host Sex ◽  
Determining Factors ◽  
Selection For

The host susceptibility to one pathogen can decrease, increase, or remain unaffected by virtue of the host evolving resistance towards a second pathogen. Negative correlations between a host susceptibility to different pathogens is an often-cited explanation for maintenance of genetic variation in immune function determining traits in a host population. In this study, we investigated the change in susceptibility of Drosophila melanogaster flies to various novel bacterial pathogens after being experimentally selected for increased resistance to one particular bacterial pathogen. We independently selected flies to become more resistant towards Enterococcus faecalis and Pseudomonas entomophila, and baring a few exceptions the evolved populations exhibited cross-resistance against the range of pathogens tested in the study. Neither the identity of the native pathogen nor the host sex was major determining factors in predicting the pattern of cross-resistance exhibited by the selected populations. We therefore report that a generalized cross-resistance to novel pathogens can repeatedly evolve in response to selection for resistance against a single pathogen.

scholarly journals Hygiene Hampers Competitive Release of Resistant Bacteria in the Commensal Microbiota

2019 ◽  
Author(s):  
Magnus Aspenberg ◽  
Sara Maad Sasane ◽  
Fredrik Nilsson ◽  
Sam P. Brown ◽  
Kristofer Wollein Waldetoft
Keyword(s):  
Antibiotic Resistance ◽  
Antibiotic Use ◽  
Host Population ◽  
Resistant Bacteria ◽  
Term Care ◽  
Resistance Evolution ◽  
Commensal Microbiota ◽  
Competitive Release ◽  
Antibiotic Selection Pressure ◽  
Metacommunity Dynamics

AbstractGood hygiene, in both health care and the community, is central to containing the rise of antibiotic resistance, as well as to infection control more generally. But despite the well-known importance, the ecological mechanisms by which hygiene affects resistance evolution remain obscure. Using metacommunity ecology theory, we here propose that hygiene attenuates the effect of antibiotic selection pressure. Specifically, we predict that hygiene limits the scope for antibiotics to induce competitive release of resistant bacteria within treated hosts, and that this is due to a modulating effect of hygiene on the distribution of resistant and sensitive strains in the host population. We show this in a mathematical model of bacterial metacommunity dynamics, and test the results against data on antibiotic resistance, antibiotic treatment, and the use of alcohol-based hand rub in long-term care facilities. Our results underscore the importance of hygiene, and point to a concrete way to weaken the link between antibiotic use and increasing resistance.

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