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168 results for “susceptibility to infection”
Fig. 3 in Effects of cold-acclimation, pathogen infection, and varying temperatures on insecticide susceptibility, feeding, and detoxifying enzyme levels in Diaphorina citri (Hemiptera: Liviidae)
Fig. 3. Correlations between mean percentage mortality of Diaphorina citri and temperature for field-collected and uninfected D. citri and field-collected and 'Candidatus' Liberibacter asiaticus–infected D. citri, when exposed to chlorpyriphos (A), fenpropathrin (B), imidacloprid (C), thiamethoxam (D), and spinetoram (E).
Fig. 1 in Effects of cold-acclimation, pathogen infection, and varying temperatures on insecticide susceptibility, feeding, and detoxifying enzyme levels in Diaphorina citri (Hemiptera: Liviidae)
Fig. 1. Comparison of cytochrome P450 (A), general esterase (B), and glutathione S-transferase (C) activity levels in laboratory susceptible Diaphorina citri adults at 5 temperatures. For glutathione S-transferase, means with the same uppercase letters are not significantly different from one another for imidacloprid-treated D. citri. Means with the same lowercase letters are not significantly different from one another for spinetoram-treated D. citri.
MHC class II genes mediate susceptibility and resistance to coronavirus infections in bats
<p>Understanding the immunogenetic basis of coronavirus (CoV) susceptibility in major pathogen reservoirs, such as bats, is central to infer their zoonotic potential. Members of the cryptic <em>Hipposideros</em> bat species complex differ in CoV susceptibility, but the underlying mechanisms remain unclear. The genes of the major histocompatibility complex (MHC) are the best understood genetic basis of pathogen resistance, and differences in MHC diversity are one possible reason for asymmetrical infection patterns among closely related species. Here, we aimed to link asymmetries in observed CoV (CoV-229E, CoV-2B, and CoV-2Bbasal) susceptibility to immunogenetic differences amongst four <em>Hipposideros</em> bat species. From the 2,072 bats assigned to their respective species using the mtDNA cytochrome b gene, members of the most numerous and ubiquitous species, <em>Hipposideros caffer</em> D, were most infected with CoV-229E and SARS-related CoV-2B. Using a subset of 569 bats we determined that much of the existent allelic and functional (i.e., supertype) MHC DRB class II diversity originated from common ancestry. One MHC supertype shared amongst all species, ST12, was consistently linked to susceptibility with CoV-229E, which is closely related to the common cold agent HCoV-229E, and infected bats with ST12 had a lower body condition. The same MHC supertype was connected to resistance to CoV-2B, and bats with ST12 were less likely be co-infected with CoV-229E and CoV-2B. Our work suggests a role of immunogenetics in determining CoV susceptibility in bats. We advocate for the preservation of functional genetic and species diversity in reservoirs as means of mitigating the risk of disease spillover.</p>
Akkermansia muciniphila reduces diet-induced susceptibility to Listeria monocytogenes infection
<p>A high fat (HF) diet decreases levels of <em>Akkermansia muciniphila</em> in the gut and reduces resistance to the foodborne pathogen <em>Listeria monocytogenes</em>. We demonstrate that short-term gavage with <em>A. muciniphila</em> increases resistance to oral and systemic <em>L. monocytogenes</em> infection in mice fed a HF diet. <em>A. muciniphila</em> normalized diet-induced inflammation in the gut and liver prior to infection and reduced inflammatory cell infiltration in the ileum to levels similar to mice fed a low fat diet. <em>A. muciniphila</em> administration had minimal impact upon the microbiota and microbial metabolites and did not affect individual taxa or impact the Bacteroidetes to Firmicutes ratio. In summary, <em>A. muciniphila</em> increased resistance to <em>L. monocytogenes</em> infection in mice fed a HF diet, through normalising immune/physiological effects that more closely resembled mice fed a LF diet. The findings suggest an interaction between <em>A. muciniphila</em> and the host to reverse the effects of a westernized diet in this model.</p>
MHC class II genes mediate susceptibility and resistance to coronavirus infections in bats
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Prior exposure to long day photoperiods alters immune responses and increases susceptibility to parasitic infection in stickleback
<p>Seasonal disease and parasitic infection are common across organisms, including humans, and there is increasing evidence for intrinsic seasonal variation in immune systems. Changes are orchestrated through organisms' physiological clocks using cues such as day length. Ample research in diverse taxa has demonstrated multiple immune responses are modulated by photoperiod, but to date, there have been few experimental demonstrations that photoperiod cues alter susceptibility to infection. We investigated the interactions among photoperiod history, immunity, and susceptibility in laboratory-bred three-spined stickleback, a long-day breeding fish, and its external, directly-reproducing, monogenean parasite <i>Gyrodactylus gasterostei</i>. We demonstrate that previous exposure to long day photoperiods (PLD) increases susceptibility to infection relative to previous exposure to short days (PSD), and modifies the response to infection for the mucin gene <i>muc2</i> and Treg cytokine <i>foxp3a</i> in skin tissues in an intermediate 12L:12D photoperiod experimental trial. Expression of skin <i>muc2</i> is reduced in PLD fish, and negatively associated with parasite abundance. We also observe inflammatory gene expression variation associated with natural inter-population variation in resistance, but find that photoperiod modulation of susceptibility is consistent across host populations. Thus, photoperiod-modulation of the response to infection is important for host susceptibility, highlighting new mechanisms affecting seasonality of host-parasite interactions.</p>
Data from: Disentangling the steps of the infection process responsible for juvenile disease susceptibility
<p>1. Juveniles of diverse host taxa, including vertebrates, invertebrates and plants, are more susceptible to parasitic infections than adults, a phenomenon still poorly understood.</p> <p>2. To shed light on the mechanisms underlying this host age effect, we investigated its expression during different steps of the infection process of a bacterial parasite of the planktonic crustacean <i>Daphnia</i>. To do so, we infected juvenile and adult <i>Daphnia magna</i> with the bacterium <i>Pasteuria ramosa</i> and monitored parasite development in experiments specific to different steps of the infection process.</p> <p>3. We did not find an effect of host age on parasite attachment, but found a strong increase in the penetration time of the parasite into hosts with increasing age. Host age at exposure also affected within-host parasite development, which was delayed in old adult <i>D. magna</i> in comparison to young adults and juveniles. Furthermore, parasite clearance was observed only in old adults, suggesting that old hosts have a better immune response than young adults and juveniles.</p> <p>4. Our results reveal a step-specific effect of host age on disease progression, giving support for different hypotheses explaining high juvenile disease susceptibility. While these mechanisms are likely to work independently from each other, earlier steps of the infection process influence later steps, and thus may respond more readily to selection than later steps.</p> <p>5. Our results also highlight that clearance can occur both during early parasite establishment and surprisingly at progressed infection phases, an undocumented phenomenon in invertebrates, where late infections are often considered chronic, lasting until host death.</p>
High prevalence of lipopolysaccharide mutants and R2-Pyocin susceptible variants in Pseudomonas aeruginosa populations sourced from cystic fibrosis lung infections
<p>Chronic, highly antibiotic-resistant infections in cystic fibrosis (CF) lungs contribute to increasing morbidity and mortality. <em>Pseudomonas</em> <em>aeruginosa</em>, a common CF pathogen, exhibits resistance to multiple antibiotics, contributing to antimicrobial resistance (AMR). These bacterial populations display genetic and phenotypic diversity, but it is unclear how this diversity affects susceptibility to bacteriocins. R-pyocins, i.e. bacteriocins produced by <em>P. aeruginosa</em>, are phage-tail-like antimicrobials. R-pyocins have potential as antimicrobials, however, recent research suggests the diversity of <em>P. aeruginosa</em> variants within CF lung infections leads to varying susceptibility to R-pyocins. This variation may be linked to changes in lipopolysaccharide (LPS), acting as the R-pyocin receptor. Currently, it is unknown how frequently R-pyocin-susceptible strains are in chronic CF lung infection, particularly when considering the heterogeneity within these strains. In this study, we tested R2-pyocin susceptibility of 139 <em>P. aeruginosa</em> variants from 17 sputum samples of seven CF patients and analyzed LPS phenotypes. We found that 83% of sputum samples did not have R2-pyocin-resistant variants, while nearly all samples contained susceptible variants. There was no correlation between LPS phenotype and R2-pyocin susceptibility, though we estimate that about 76% of sputum-derived variants lack an O-specific antigen, 40% lack a common antigen, and 24% have altered LPS cores. The absence of a correlation between LPS phenotype and R-pyocin susceptibility suggests LPS packing density may play a significant role in R-pyocin susceptibility among CF variants. Our research supports the potential of R-pyocins as therapeutic agents, as many infectious CF variants are susceptible to R2-pyocins, even within diverse bacterial populations.</p>
Prior exposure to long day photoperiods alters immune responses and increases susceptibility to parasitic infection in stickleback
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Effects of sleep deprivation on susceptibility to parasitic infection
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Data from: Disentangling the steps of the infection process responsible for juvenile disease susceptibility
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Starvation increases susceptibility to bacterial infection and promotes systemic pathogen proliferation in Drosophila melanogaster females
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Impacts of selective predation on infection prevalence and host susceptibility
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High prevalence of lipopolysaccharide mutants and R2-Pyocin susceptible variants in Pseudomonas aeruginosa populations sourced from cystic fibrosis lung infections
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Data from: Impact of field-realistic doses of glyphosate and nutritional stress on mosquito life history-traits and susceptibility to malaria parasite infection
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Data from: Subsets of tissue CD4 T cells display different susceptibilities to HIV infection and death: Analysis by CyTOF and single cell RNA-seq
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Data from: Inter- and intra-specific variation of spider mite susceptibility to fungal infections: implications for the long-term success of biological control
<p><span><span><span><span><span><span><span><span><span><span><span>Spider mites are severe pests of several annual and perennial crops worldwide, often causing important economic damages. As rapid evolution of pesticide resistance in this group hampers the efficiency of chemical control, alternative control strategies, such as the use of entomopathogenic fungi, are being developed. However, while several studies have focused on the evaluation of the control potential of different fungal species and/or isolates as well as their compatibility with other control methods (e.g. predators or chemical pesticides), knowledge on the extent of inter- and intraspecific variation in spider mite susceptibility to fungal infection is as yet incipient. Here, we measured the mortality induced by two generalist fungi, <i>Beauveria </i><i>bassiana </i>and <i>Metarhizium </i><i>brunneum</i>, in 12 spider mite populations belonging to different <i>Tetranychus </i>species: <i>T. evansi</i>, <i>T. ludeni</i>, the green form of <i>T. urticae </i>and the red form of <i>T. urticae</i>, within a full factorial experiment. We found that spider mite species differed in their susceptibility to infection by both fungal species. Moreover, we also found important intraspecific variation for this trait. These results draw caution on the development of single strains as biocontrol agents. Indeed, the high level of intraspecific variation suggests that (a) the one-size-fits-all strategy may fail to control spider-mite populations and (b) hosts resistance to infection may evolve at a rapid pace. Finally, we propose future directions to better understand this system and improve the long-term success of spider mite control strategies based on entomopathogenic fungi.</span></span></span></span></span></span></span></span></span></span></span></p>
Data from: Fine-scale spatial covariation between infection prevalence and susceptibility in a natural population
The prevalence of infection varies dramatically on a fine spatial scale. Many evolutionary hypotheses are founded on the assumption that this variation is due to host genetics, such that sites with a high frequency of alleles conferring susceptibility are associated with higher infection prevalence. This assumption is largely untested and may be compromised at finer spatial scales where gene flow between sites is high. We put this assumption to the test in a natural snail-trematode interaction in which host susceptibility is known to have a strong genetic basis. A decade of field sampling revealed substantial spatial variation in infection prevalence between 13 sites around a small lake. Laboratory assays replicated over 3 years demonstrate striking variation in host susceptibility among sites in spite of high levels of gene flow between sites. We find that mean susceptibility can explain more than one-third of the observed variation in mean infection prevalence among sites. We estimate that variation in susceptibility and exposure together can explain the majority of variation in prevalence. Overall, our findings in this natural host-parasite system argue that spatial variation in infection prevalence covaries strongly with variation in the distribution of genetically based susceptibility, even at a fine spatial scale.
Data from: Does hugging provide stress-buffering social support? A study of susceptibility to upper respiratory infection and illness
Perceived social support has been hypothesized to protect against the pathogenic effects of stress. How such protection might be conferred, however, is not well understood. Using a sample of 404 healthy adults, we examined the roles of perceived social support and received hugs in buffering against interpersonal stress-induced susceptibility to infectious disease. Perceived support was assessed by questionnaire, and daily interpersonal conflict and receipt of hugs were assessed by telephone interviews on 14 consecutive evenings. Subsequently, participants were exposed to a virus that causes a common cold and were monitored in quarantine to assess infection and illness signs. Perceived support protected against the rise in infection risk associated with increasing frequency of conflict. A similar stress-buffering effect emerged for hugging, which explained 32% of the attenuating effect of support. Among infected participants, greater perceived support and more-frequent hugs each predicted less-severe illness signs. These data suggest that hugging may effectively convey social support.
Data from: Genome-wide exon-capture approach identifies genetic variants of Norway spruce genes associated with susceptibility to Heterobasidion parviporum infection
Root and butt rot caused by members of the Heterobasidion annosum species complex is the most economically important disease of conifer trees in boreal forests. Wood decay in the infected trees dramatically decreases their value and causes considerable losses to forest owners. Trees vary in their susceptibility to Heterobasidion infection, but the genetic determinants underlying the variation in the susceptibility are not well-understood. We performed the identification of Norway spruce genes associated with the resistance to Heterobasidion parviporum infection using genome-wide exon-capture approach. Sixty-four clonal Norway spruce lines were phenotyped, and their responses to H. parviporum inoculation were determined by lesion length measurements. Afterwards, the spruce lines were genotyped by targeted resequencing and identification of genetic variants (SNPs). Genome-wide association analysis identified 10 SNPs located within 8 genes as significantly associated with the larger necrotic lesions in response to H. parviporum inoculation. The genetic variants identified in our analysis are potential marker candidates for future screening programs aiming at the differentiation of disease-susceptible and resistant trees.
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