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13,569
result(s) for
"host–parasite interactions"
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Host and parasite thermal ecology jointly determine the effect of climate warming on epidemic dynamics
Host–parasite systems have intricately coupled life cycles, but each interactor can respond differently to changes in environmental variables like temperature. Although vital to predicting how parasitism will respond to climate change, thermal responses of both host and parasite in key traits affecting infection dynamics have rarely been quantified. Through temperature-controlled experiments on an ectothermic host–parasite system, we demonstrate an offset in the thermal optima for survival of infected and uninfected hosts and parasite production. We combine experimentally derived thermal performance curves with field data on seasonal host abundance and parasite prevalence to parameterize an epidemiological model and forecast the dynamical responses to plausible future climate-warming scenarios. In warming scenarios within the coastal southeastern United States, the model predicts sharp declines in parasite prevalence, with local parasite extinction occurring with as little as 2 °C warming. The northern portion of the parasite’s current range could experience local increases in transmission, but assuming no thermal adaptation of the parasite, we find no evidence that the parasite will expand its range northward under warming. This work exemplifies that some host populations may experience reduced parasitism in a warming world and highlights the need to measure host and parasite thermal performance to predict infection responses to climate change.
Journal Article
Extracellular Vesicle-Mediated Communication Within Host-Parasite Interactions
Extracellular vesicles (EVs) are small membrane-surrounded structures released by different kinds of cells (normal, diseased, and transformed cells)
and
that contain large amounts of important substances (such as lipids, proteins, metabolites, DNA, RNA, and non-coding RNA (ncRNA), including miRNA, lncRNA, tRNA, rRNA, snoRNA, and scaRNA) in an evolutionarily conserved manner. EVs, including exosomes, play a role in the transmission of information, and substances between cells that is increasingly being recognized as important. In some infectious diseases such as parasitic diseases, EVs have emerged as a ubiquitous mechanism for mediating communication during host-parasite interactions. EVs can enable multiple modes to transfer virulence factors and effector molecules from parasites to hosts, thereby regulating host gene expression, and immune responses and, consequently, mediating the pathogenic process, which has made us rethink our understanding of the host-parasite interface. Thus, here, we review the present findings regarding EVs (especially exosomes) and recognize the role of EVs in host-parasite interactions. We hope that a better understanding of the mechanisms of parasite-derived EVs may provide new insights for further diagnostic biomarker, vaccine, and therapeutic development.
Journal Article
Parasites in bloom: flowers aid dispersal and transmission of pollinator parasites within and between bee species
The dispersal of parasites is critical for epidemiology, and the interspecific vectoring of parasites when species share resources may play an underappreciated role in parasite dispersal. One of the best examples of such a situation is the shared use of flowers by pollinators, but the importance of flowers and interspecific vectoring in the dispersal of pollinator parasites is poorly understood and frequently overlooked. Here, we use an experimental approach to show that during even short foraging periods of 3 h, three bumblebee parasites and two honeybee parasites were dispersed effectively onto flowers by their hosts, and then vectored readily between flowers by non-host pollinator species. The results suggest that flowers are likely to be hotspots for the transmission of pollinator parasites and that considering potential vector, as well as host, species will be of general importance for understanding the distribution and transmission of parasites in the environment and between pollinators.
Journal Article
Role of microorganisms in the evolution of animals and plants: the hologenome theory of evolution
Abstract
We present here the hologenome theory of evolution, which considers the holobiont (the animal or plant with all of its associated microorganisms) as a unit of selection in evolution. The hologenome is defined as the sum of the genetic information of the host and its microbiota. The theory is based on four generalizations: (1) All animals and plants establish symbiotic relationships with microorganisms. (2) Symbiotic microorganisms are transmitted between generations. (3) The association between host and symbionts affects the fitness of the holobiont within its environment. (4) Variation in the hologenome can be brought about by changes in either the host or the microbiota genomes; under environmental stress, the symbiotic microbial community can change rapidly. These points taken together suggest that the genetic wealth of diverse microbial symbionts can play an important role both in adaptation and in evolution of higher organisms. During periods of rapid changes in the environment, the diverse microbial symbiont community can aid the holobiont in surviving, multiplying and buying the time necessary for the host genome to evolve. The distinguishing feature of the hologenome theory is that it considers all of the diverse microbiota associated with the animal or the plant as part of the evolving holobiont. Thus, the hologenome theory fits within the framework of the ‘superorganism’ proposed by Wilson and Sober.
Journal Article
Genetic diversity and disease
Why do infectious diseases erupt in some host populations and not others? This question has spawned independent fields of research in evolution, ecology, public health, agriculture, and conservation. In the search for environmental and genetic factors that predict variation in parasitism, one hypothesis stands out for its generality and longevity: genetically homogeneous host populations are more likely to experience severe parasitism than genetically diverse populations. In this perspective piece, I draw on overlapping ideas from evolutionary biology, agriculture, and conservation to capture the far-reaching implications of the link between genetic diversity and disease. I first summarize the development of this hypothesis and the results of experimental tests. Given the convincing support for the protective effect of genetic diversity, I then address the following questions: (1) Where has this idea been put to use, in a basic and applied sense, and how can we better use genetic diversity to limit disease spread? (2) What new hypotheses does the established disease-diversity relationship compel us to test? I conclude that monitoring, preserving, and augmenting genetic diversity is one of our most promising evolutionarily informed strategies for buffering wild, domesticated, and human populations against future outbreaks.
Journal Article
Infection-induced plasmablasts are a nutrient sink that impairs humoral immunity to malaria
Plasmodium
parasite–specific antibodies are critical for protection against malaria, yet the development of long-lived and effective humoral immunity against
Plasmodium
takes many years and multiple rounds of infection and cure. Here, we report that the rapid development of short-lived plasmablasts during experimental malaria unexpectedly hindered parasite control by impeding germinal center responses. Metabolic hyperactivity of plasmablasts resulted in nutrient deprivation of the germinal center reaction, limiting the generation of memory B cell and long-lived plasma cell responses. Therapeutic administration of a single amino acid to experimentally infected mice was sufficient to overcome the metabolic constraints imposed by plasmablasts and enhanced parasite clearance and the formation of protective humoral immune memory responses. Thus, our studies not only challenge the current model describing the role and function of blood-stage
Plasmodium
-induced plasmablasts but they also reveal new targets and strategies to improve anti-
Plasmodium
humoral immunity.
Early humoral responses to malaria fail to induce durable protective antibodies. Butler and colleagues report that low-affinity, short-lived plasmablasts become nutrient sinks for glutamine and starve germinal center B and T cells, thereby reducing the generation of high-affinity B cells and long-lived plasma cells and memory B cells.
Journal Article
Inflammation and oxidative stress in vertebrate host-parasite systems
Innate, inflammation-based immunity is the first line of vertebrate defence against micro-organisms. Inflammation relies on a number of cellular and molecular effectors that can strike invading pathogens very shortly after the encounter between inflammatory cells and the intruder, but in a non-specific way. Owing to this non-specific response, inflammation can generate substantial costs for the host if the inflammatory response, and the associated oxygen-based damage, get out of control. This imposes strong selection pressure that acts to optimize two key features of the inflammatory response: the timing of activation and resolution (the process of downregulation of the response). In this paper, we review the benefits and costs of inflammation-driven immunity. Our aim is to emphasize the importance of resolution of inflammation as a way of maintaining homeostasis against oxidative stress and to prevent the 'horror autotoxicus' of chronic inflammation. Nevertheless, host immune regulation also opens the way to pathogens to subvert host defences. Therefore, quantifying inflammatory costs requires assessing (i) short-term negative effects, (ii) delayed inflammation-driven diseases, and (iii) parasitic strategies to subvert inflammation.
Journal Article
Comprehensive transcriptomic analysis reveals immune response modulation in Brontispa longissima Gestro larvae following parasitism by Asecodes hispinarum Bouček
The coconut leaf beetle,
, is a major pest of palm plants in China and is significantly affected by the parasitoid wasp
, which targets the beetle's larval stage.
Using single-molecule real-time (SMRT) sequencing, we constructed a high-quality transcriptome reference to assess gene expression associated with
parasitism in
. Differentially expressed genes (DEGs) were identified at 24, 48, 72, and 96 h post-parasitism compared with non-parasitized controls.
Based on 12,196 reference transcripts, a total of 2,120, 467, 500, and 5,749 DEGs were identified at 24, 48, 72, and 96 h post-parasitism, respectively. Over 75% of DEGs were upregulated across all time points. Gene Ontology (GO) enrichment analysis revealed significant enrichment of immune-related processes alongside hemocyte differentiation. Validation by quantitative PCR (qPCR) confirmed the consistency and reliability of the RNA-seq results.
The study identified immune-related genes differentially expressed in the fourth instar larvae of B. longissima. Overall, the results indicate that parasitism by
is associated with changes in the immune response of
larvae, offering preliminary insights into host-parasite interactions for potential biological control strategies.
Journal Article
Monoallelic expression and epigenetic inheritance sustained by a Trypanosoma brucei variant surface glycoprotein exclusion complex
The largest gene families in eukaryotes are subject to allelic exclusion, but mechanisms underpinning single allele selection and inheritance remain unclear. Here, we describe a protein complex sustaining variant surface glycoprotein (
VSG
) allelic exclusion and antigenic variation in
Trypanosoma brucei
parasites. The
VSG-
exclusion-1 (VEX1) protein binds both telomeric
VSG
-associated chromatin and VEX2, an ortholog of nonsense-mediated-decay helicase, UPF1. VEX1 and VEX2 assemble in an RNA polymerase-I transcription-dependent manner and sustain the active, subtelomeric
VSG
-associated transcription compartment.
VSG
transcripts and VSG coats become highly heterogeneous when VEX proteins are depleted. Further, the DNA replication-associated chromatin assembly factor, CAF-1, binds to and specifically maintains VEX1 compartmentalisation following DNA replication. Thus, the VEX-complex controls
VSG
-exclusion, while CAF-1 sustains VEX-complex inheritance in association with the active-
VSG
. Notably, the VEX2-orthologue and CAF-1 in mammals are also implicated in exclusion and inheritance functions. In trypanosomes, these factors sustain a highly effective and paradigmatic immune evasion strategy.
Monoallelic expression of variant surface glycoprotein genes (
VSGs
) is essential for immune evasion by
Trypanosoma brucei
. Here, Faria
et al
. show that the VEX protein complex controls
VSG
allelic exclusion, and that CAF‐1 sustains inheritance of the VEX‐complex in association with the active
VSG
.
Journal Article