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

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.

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.

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 Borrelia afzelii alters reproductive success in a rodent host

2018 ◽  
Vol 285 (1884) ◽  
pp. 20181056 ◽  
Author(s):  
Claire Cayol ◽  
Anna Giermek ◽  
Andrea Gomez-Chamorro ◽  
Jukka Hytönen ◽  
Eva Riikka Kallio ◽  
...  
Keyword(s):  
Reproductive Success ◽  
Host Population ◽  
Natural Host ◽  
Myodes Glareolus ◽  
Offspring Size ◽  
Rodent Host ◽  
Mating Partner ◽  
Borrelia Afzelii ◽  
Bank Voles ◽  
The Impact

The impact of a pathogen on the fitness and behaviour of its natural host depends upon the host–parasite relationship in a given set of environmental conditions. Here, we experimentally investigated the effects of Borrelia afzelii, one of the aetiological agents of Lyme disease in humans, on the fitness of its natural rodent host, the bank vole ( Myodes glareolus ), in semi-natural conditions with two contrasting host population densities. Our results show that B. afzelii can modify the reproductive success and spacing behaviour of its rodent host, whereas host survival was not affected. Infection impaired the breeding probability of large bank voles. Reproduction was hastened in infected females without alteration of the offspring size at birth. At low density, infected males produced fewer offspring, fertilized fewer females and had lower mobility than uninfected individuals. Meanwhile, the infection did not affect the proportion of offspring produced or the proportion of mating partner in female bank voles. Our study is the first to show that B. afzelii infection alters the reproductive success of the natural host. The effects observed could reflect the sickness behaviour due to the infection or they could be a consequence of a manipulation of the host behaviour by the bacteria.

scholarly journals Transcriptome Sequencing Reveals Novel Candidate Genes for Cardinium hertigii-Caused Cytoplasmic Incompatibility and Host-Cell Interaction

mSystems ◽  
2017 ◽  
Vol 2 (6) ◽  
Author(s):  
Evelyne Mann ◽  
Corinne M. Stouthamer ◽  
Suzanne E. Kelly ◽  
Monika Dzieciol ◽  
Martha S. Hunter ◽  
...  
Keyword(s):  
Cytoplasmic Incompatibility ◽  
Parasitoid Wasp ◽  
Host Population ◽  
Reproductive Failure ◽  
Natural Host ◽  
Intracellular Bacteria ◽  
Bacterial Symbionts ◽  
Insect Host ◽  
Bacterial Lineage ◽  
Insight Into

ABSTRACT The majority of insects carry maternally inherited intracellular bacteria that are important in their hosts’ biology, ecology, and evolution. Some of these bacterial symbionts cause a reproductive failure known as cytoplasmic incompatibility (CI). In CI, the mating of symbiont-infected males and uninfected females produces few or no daughters. The CI symbiont then spreads and can have a significant impact on the insect host population. Cardinium, a bacterial endosymbiont of the parasitoid wasp Encarsia in the Bacteroidetes, is the only bacterial lineage known to cause CI outside the Alphaproteobacteria, where Wolbachia and another recently discovered CI symbiont reside. Here, we sought insight into the gene expression of a CI-inducing Cardinium strain in its natural host, Encarsia suzannae. Our study provides the first insights into the Cardinium transcriptome and provides support for the hypothesis that Wolbachia and Cardinium target similar host pathways with distinct and largely unrelated sets of genes. Cytoplasmic incompatibility (CI) is an intriguing, widespread, symbiont-induced reproductive failure that decreases offspring production of arthropods through crossing incompatibility of infected males with uninfected females or with females infected with a distinct symbiont genotype. For years, the molecular mechanism of CI remained unknown. Recent genomic, proteomic, biochemical, and cell biological studies have contributed to understanding of CI in the alphaproteobacterium Wolbachia and implicate genes associated with the WO prophage. Besides a recently discovered additional lineage of alphaproteobacterial symbionts only moderately related to Wolbachia, Cardinium (Bacteroidetes) is the only other symbiont known to cause CI, and genomic evidence suggests that it has very little homology with Wolbachia and evolved this phenotype independently. Here, we present the first transcriptomic study of the CI Cardinium strain cEper1, in its natural host, Encarsia suzannae, to detect important CI candidates and genes involved in the insect-Cardinium symbiosis. Highly expressed transcripts included genes involved in manipulating ubiquitination, apoptosis, and host DNA. Female-biased genes encoding ribosomal proteins suggest an increase in general translational activity of Cardinium in female wasps. The results confirm previous genomic analyses that indicated that Wolbachia and Cardinium utilize different genes to induce CI, and transcriptome patterns further highlight expression of some common pathways that these bacteria use to interact with the host and potentially cause this enigmatic and fundamental manipulation of host reproduction. IMPORTANCE The majority of insects carry maternally inherited intracellular bacteria that are important in their hosts’ biology, ecology, and evolution. Some of these bacterial symbionts cause a reproductive failure known as cytoplasmic incompatibility (CI). In CI, the mating of symbiont-infected males and uninfected females produces few or no daughters. The CI symbiont then spreads and can have a significant impact on the insect host population. Cardinium, a bacterial endosymbiont of the parasitoid wasp Encarsia in the Bacteroidetes, is the only bacterial lineage known to cause CI outside the Alphaproteobacteria, where Wolbachia and another recently discovered CI symbiont reside. Here, we sought insight into the gene expression of a CI-inducing Cardinium strain in its natural host, Encarsia suzannae. Our study provides the first insights into the Cardinium transcriptome and provides support for the hypothesis that Wolbachia and Cardinium target similar host pathways with distinct and largely unrelated sets of genes.

Sign in / Sign up

Export Citation Format

Share Document