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Disease resistance (defined as the host capacity to limit systemic infection intensity) and disease tolerance (defined as the host capacity to limit infection-induced damage) are 2 complementary defense strategies that help the hosts maximize their survival and fitness when infected with pathogens and parasites. In addition to the underlying physiological mechanisms, the existing theory postulates that these 2 strategies differ in terms of the conditions under which each strategy evolves in the host populations, their evolutionary dynamics, and the ecological and epidemiological consequences of their evolution. Here, we explored if one or both of these strategies evolve when host populations are subjected to selection for increased postinfection survival. We experimentally evolved Drosophila melanogaster populations, selecting for the flies that survived an infection with the entomopathogen Enterococcus faecalis. We found that the host populations evolved increased disease resistance in response to selection for increased survival. This was despite the physiological costs associated with increased resistance, the expression of which varied with the phase of infection. We did not find evidence of any change in disease tolerance in the evolved host populations. [ABSTRACT FROM AUTHOR]

BACKGROUND AND OBJECTIVES: The yield of soybeans is affected by the performance of agronomic traits and the presence of abiotic and biotic environmental stresses. The utilization of pesticides to alleviate biotic environmental stressors results in environmental deterioration. One of the biotic environmental stresses is virus disease caused by Cowpea mild mottle virus. Identifying the main factors influencing yield and selecting traits resistant to virus infection can assist development programs in creating soybean varieties with enhanced Cowpea mild mottle virus tolerance. The soybean lines can face one of the biotic environmental stresses. Soybean varieties are susceptible to a range of biotic environmental challenges. This investigation sought to examine the diversity in agronomic traits and disease resistance, to identify the top-performing soybean varieties for controlling Cowpea mild mottle virus disease. METHODS: The plant materials were 1000 soybean lines originating from 26 crosses. Each line was planted in rows and inoculated with Cowpea mild mottle virus naturally using the Bemisia tabaci vector. To set up the experiment, a population of Bemisia tabaci carrying the Cowpea mild mottle virus was established in the field, enabling natural biotic environmental stress of the plants by the virus infection. The identification of the lines was conducted through an assessment of agronomic characteristics and an analysis of the relationship between these characteristics and their susceptibility to Cowpea mild mottle virus. The attributes that had a substantial impact on the principal component analysis biplot and their correlation with seed yield per plot were initially identified as selection criteria. FINDINGS: Soybean plants displayed diverse agronomic characteristics and disease ratings. Rather than relying on resistance, their defense mechanism against diseases involved tolerance. The variation in soybean characteristics can be attributed mainly to factors such as seed yield, the number of filled pods, and the number of productive pods per plant. Additionally, plant height showed the strongest correlation among these traits. The selected 100 soybean varieties displayed outstanding agronomic characteristics and resistance to diseases, leading to a decrease in the need for pesticides and contributing to environmental conservation. CONCLUSION: Soybean seed yield is influenced by agronomic traits and biotic environmental stress such as virus disease, with significant diversity observed among the tested lines. The attributes that had the most significant impact were the number of productive nodes, quantity of filled pods, and seed yield per plant. Plant height consistently showed a strong correlation with seed yield. Seed yield per plant had a positive correlation with the disease score, making it unsuitable as a selection criterion. This positive correlation has been observed, indicating that soybeans possess a mechanism of tolerance that enables them to sustain optimal seed yields even when infected by a virus. The criteria for selecting 100 superior soybean lines included the number of filled pods, number of nodes, and plant height, which were deemed suitable for the evaluation process. The use of 100 selected soybean lines can reduce pesticide usage while maintaining environmental quality and supporting sustainable agriculture. [ABSTRACT FROM AUTHOR]

BACKGROUND AND OBJECTIVES: The yield of soybeans is affected by the performance of agronomic traits and the presence of abiotic and biotic environmental stresses. The utilization of pesticides to alleviate biotic environmental stressors results in environmental deterioration. One of the biotic environmental stresses is virus disease caused by Cowpea mild mottle virus. Identifying the main factors influencing yield and selecting traits resistant to virus infection can assist development programs in creating soybean varieties with enhanced Cowpea mild mottle virus tolerance. The soybean lines can face one of the biotic environmental stresses. Soybean varieties are susceptible to a range of biotic environmental challenges. This investigation sought to examine the diversity in agronomic traits and disease resistance, with the goal of identifying the top-performing soybean varieties for controlling Cowpea mild mottle virus disease.METHODS: The plant materials were 1000 soybean lines originating from 26 crosses. Each line was planted in rows and inoculated with Cowpea mild mottle virus naturally using the Bemisia tabaci vector. To set up the experiment, a population of Bemisia tabaci carrying the Cowpea mild mottle virus was established in the field, enabling natural biotic environmental stress of the plants by the virus infection. The identification of the lines was conducted through an assessment of agronomic characteristics and an analysis of the relationship between these characteristics and their susceptibility to Cowpea mild mottle virus. The attributes that had a substantial impact on the principal component analysis biplot and their correlation with seed yield per plot were initially identified as selection criteria.FINDINGS: Soybean plants displayed diverse agronomic characteristics and disease ratings. Rather than relying on resistance, their defense mechanism against diseases involved tolerance. The variation in soybean characteristics can be attributed mainly to factors such as seed yield, the quantity of filled pods, and the number of productive pods per plant. Additionally, plant height showed the strongest correlation among these traits. The selected 100 soybean varieties displayed outstanding agronomic characteristics and resistance to diseases, leading to a decrease in the need for pesticides and contributing to environmental conservation.CONCLUSION: Soybean seed yield is influenced by agronomic traits and biotic environmental stress such as virus disease, with significant diversity observed among the tested lines. The attributes that had the most significant impact were the amount of productive nodes, quantity of filled pods, and seed yield per plant. Plant height consistently showed a strong correlation with seed yield. Seed yield per plant had a positive correlation with the disease score, making it unsuitable as a selection criterion. This positive correlation has been observed, indicating that soybeans possess a mechanism of tolerance that enables them to sustain optimal seed yields even when infected by a virus. The criteria for selecting 100 superior soybean lines included the number of filled pods, number of nodes, and plant height, which were deemed suitable for the evaluation process. The use of 100 selected soybean lines can reduce pesticide usage while maintaining environmental quality and supporting sustainable agriculture.

Disease tolerance is an infection phenotype where hosts show relatively high health despite harbouring elevated pathogen loads. Variation in the ability to reduce immunopathology may explain why some hosts can tolerate higher pathogen burdens with reduced pathology. Negative immune regulation would therefore appear to be a clear candidate for a mechanism underlying disease tolerance. Here, we examined how the negative regulation of the immune deficiency (IMD) pathway affects disease tolerance in Drosophila melanogaster when infected with four doses of the gram‐negative bacterial pathogen Pseudomonas entomophila. We find that while flies unable to regulate the IMD response exhibited higher expression of antimicrobial peptides and lower bacterial loads as expected, this was not accompanied by a proportional reduction in mortality. Instead, ubiquitous UAS‐RNAi knockdown of negative regulators of IMD (pirk and caudal) substantially increased the per‐pathogen‐mortality in both males and females across all tested infectious doses. Our results therefore highlight that in addition to regulating an efficient pathogen clearance response, negative regulators of IMD also contribute to disease tolerance. [ABSTRACT FROM AUTHOR]

Peanut stem rot disease, caused by the necrotrophic soil-borne fungus Sclerotium rolfsii, has a significant negative impact on crop yields. Chemical fungicides can mitigate the loss incurred by fungus, however, their usage raises environmental and human health concern. Seaweeds extracts are getting importance as bio-stimulant for improving growth and disease resistance in different plants. In the present study, we investigated the potential of Sargassum tenerrimum extract (S-extract) in controlling stem rot disease in peanuts. The foliar application of S-extract was applied at vegetative and reproductive stages on peanut plants to study plant growth and reduction of S. rolfsii-induced disease. Plant height, number of branches and branch length increased in S-extract treated plants (S) as compared to S-extract + S. rolfsii treated plants (S + F). Similarly, the activity of anti-oxidative enzymes such as catalase (CAT), guaiacol peroxidase (GPOX), polyphenol oxidase (PPO), and superoxide dismutase (SOD) increased by application of S-extract. Pigments such as chlorophyll a, chlorophyll b, and carotenoids showed higher accumulation in S-extract treated plants. The increased membrane stability index and reduced electrolyte leakage in S and S + F plants, positively affected the health and biotic stress tolerance of the plants. S-extract reduced the reactive oxygen species (ROS) such as O2•− and H2O2. Total phenol, soluble sugars and total amino acid accumulation were higher in S and S + F plants compared to C and F at vegetative stage. The mitigation of disease can be attributed to the application of S-extract leading to the elevated activity of antioxidant enzymes and the accumulation of non-enzymatic antioxidants, osmolytes, and pigments. Therefore, S-extract represents an environmentally friendly resource that can be employed in sustainable agriculture practices to boost plant growth and enhance disease tolerance. [ABSTRACT FROM AUTHOR]

Rough lemon is indigenous and has wide adaptability in Indian citriculture. Rough lemon and Volkamer lemon are comparable in horticultural performance and their resistance against biotic and abiotic stresses are almost similar but Volkamer lemon has better adaptability in different agroclimatic conditions. To improve Volkamer lemon hybridization has been attempted with Kinkoji (citrus greening tolerance), Swingle citrumelo (Phytophthora resistance), and Cleopatra (salinity tolerance). Polyembryony in Volkamer lemon and absence of the heritable morphological markers (Cleopatra) are limiting factors for hybrid identification and morphological characters are not being segregated in Kinkoji and Swingle citrumelo at early stage, then molecular markers are employed for detection of putative zygotic seedlings. We performed hybridization between Volkamer lemon (♀), Kinkoji (B cross) (58 F1) (♂), Swingle citrumelo (D cross) (71 F1) (♂), Cleopatra (N cross) (83 F1) (♂) and discriminate the hybrids by using 25 SSR markers. The fifteen markers were found efficient for hybrid identification (> 71% hybrids detected). CCSME23 (88.21%) marker has detected 187 hybrids in all crosses thereafter, 184 hybrids detected each by HvSSRCS-2, HvSSRCS-135, HvSSRCS-237, HvSSRCM-92 and HvSSRCM-466 with 86.79%. A total of 44 qualitative and 18 quantitative characters were analysed. Fifteen qualitative and six quantitative characters were found significant variability in leaf, spine, branch, and stem. Sufficient amount of genetic variability was detected through phylogenetic analysis and population structure analysis showed two subpopulations in B and N cross but in D cross five subpopulations were detected. After primary screening, nine F1 hybrids for citrus greening tolerance and twelve F1 hybrids for Phytophthora tolerance were identified. The newly developed F1 hybrids exhibited phenotypic and genetic diversity along with disease tolerance. These potential hybrids may be recommended for commercial citriculture after thorough horticultural evaluation. [ABSTRACT FROM AUTHOR]

Effective responses against severe systemic infection require coordination between two complementary defense strategies that minimize the negative impact of infection on the host: resistance, aimed at pathogen elimination, and disease tolerance, which limits tissue damage and preserves organ function. Resistance and disease tolerance mostly rely on divergent metabolic programs that may not operate simultaneously in time and space. Due to evolutionary reasons, the host initially prioritizes the elimination of the pathogen, leading to dominant resistance mechanisms at the potential expense of disease tolerance, which can contribute to organ failure. Here, we summarize our current understanding of the role of physiological perturbations resulting from infection in immune response dynamics and the metabolic program requirements associated with resistance and disease tolerance mechanisms. We then discuss how insight into the interplay of these mechanisms could inform future research aimed at improving sepsis outcomes and the potential for therapeutic interventions. Responses to severe infection involve resistance, aimed at pathogen elimination, and disease tolerance, that limit tissue damage. These defense strategies are both essential but rely on distinct metabolic programs. Willmann and Moita review how physiology is disrupted by infection, and how this knowledge may inspire novel therapies for sepsis. [ABSTRACT FROM AUTHOR]

This article, titled "Editorial: Immune tolerance and human malaria," explores the relationship between immune tolerance and malaria. The authors discuss how exposure to malaria parasites can affect susceptibility to malaria and other pathogens. They also examine the mechanisms underlying immune tolerance to blood-stage infection and the role of immunoregulatory cells in limiting immunopathology. The article highlights the potential impact of malaria-induced immune tolerance on vaccine efficacy and suggests strategies to overcome immune tolerance to improve vaccine effectiveness. The authors present several studies that investigate the modulation of immune responses during malaria infection and its implications for host protection and vaccine development. [Extracted from the article]

• IFN-γ is necessary and sufficient to increase systemic GDF-15 levels. • GDF-15 plays an important role in infection-induced weight loss. • GDF-15 is required for infection-induced FGF21 expression in the liver. Infections are often accompanied by weight loss caused by alterations in host behavior and metabolism, also known as sickness behaviors. Recent studies have revealed that sickness behaviors can either promote or impede survival during infections depending on factors such as the type of infectious pathogen. Nevertheless, we have an incomplete understanding of the underlying mechanisms of sickness behaviors. Furthermore, although the host immune responses to infections have long been known to contribute to the induction of sickness behaviors, recent studies have identified emerging cytokines that are also key regulators of host metabolism during infection and inflammation, such as growth differentiation factor 15 (GDF-15). GDF-15 is a distant member of the TGF-β superfamily that causes weight loss by suppressing appetite and food consumption and causing emesis. These effects require activation of neurons that express the only known GDF-15 receptor, the GFRAL receptor. GDF-15 also functions in the periphery including the induction of ketogenesis and immunoregulation. Nevertheless, the functions and regulation of GDF-15 during live infections is not yet known. Murine infection with avirulent Toxoplasma gondii is an established model to understand infection-induced weight loss. Past studies have determined that acute T. gondii infection causes weight loss due to diminished food consumption and increased energy expenditure through unknown mechanisms. Additionally, our lab previously demonstrated that T. gondii causes upregulation in serum GDF-15 in an IFN-γ-dependent manner during the post-acute phase of the infection. In this study, we interrogated the in-vivo functions and immune regulation of GDF-15 during Toxoplasma gondii infection. First, we found that in wild-type mice, acute T. gondii infection caused a significant weight loss that is preceded by elevation of serum levels of IFN-γ and GDF-15. To determine whether IFN-γ regulates GDF-15, we neutralized IFN-γ on days 5 and 6 and measured GDF-15 on day 7 and found that serum but not tissue levels of GDF-15 decreased after IFN-γ neutralization. Additionally, exogenous IFN-γ was sufficient to elevate serum GDF-15 in the absence of infection. Next, we compared the outcomes of T. gondii infection between WT and Gdf15−/− mice. We observed that the weight trajectories were declining in WT mice while they were increasing in Gdf15−/− mice during the acute phase of the infection. This difference in trajectories extended throughout the chronic infection resulting to an overall weight loss relative to initial weights in WT mice but not Gdf15−/− mice. Then, we determined that GDF-15 is not essential for survival and immunoregulation during T. gondii infection. We also demonstrated that GDF-15 is required for the induction of FGF21, stress-induced cytokine with prominent roles in regulating host metabolism. Finally, we discovered a cytokine cascade IFN-γ-GDF-15-FGF21 that is likely involved in the regulation of host metabolism. Overall, our study provides evidence that IFN-γ contributes to the regulation of host metabolism during infection by inducing GDF-15 and FGF21. GDF-15 orchestrates changes in host metabolism that supports the host immune response in clearing the infection. These physiological alterations induce FGF21, which in turn, orchestrates the adaptive responses to the effects of GDF-15, which can be detrimental when protracted. [ABSTRACT FROM AUTHOR]

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Simple Summary: Diseases pose a significant challenge for aquaculture, exacerbated by changing weather conditions. The sector has explored various strategies, including maintaining a clean environment and employing vaccines, to combat these diseases. However, these solutions are effective only against specific diseases and species. In our recent research, we investigated the use of genetics to enhance disease resistance in three crucial species: white leg shrimp, striped catfish, and yellowtail kingfish. Our findings indicate that the studied populations of these species possess genes that can be inherited, imparting greater resistance to diseases such as White Spot Syndrome Virus, Bacterial Necrotic Pancreatitis, and skin fluke. By selectively breeding animals with these resistant genes, we successfully increased resistance within the population, promoting overall fish health and boosting production. Additionally, we examined these genes and utilized computer models to predict the most resistant individuals for breeding to combat diseases. Looking ahead, our focus is on omics technologies, precision farming systems, and advanced algorithms to further enhance the disease resistance of these species, thereby making aquaculture more sustainable and resilient against threats. Diseases pose a significant and pressing concern for the sustainable development of the aquaculture sector, particularly as their impact continues to grow due to climatic shifts such as rising water temperatures. While various approaches, ranging from biosecurity measures to vaccines, have been devised to combat infectious diseases, their efficacy is disease and species specific and contingent upon a multitude of factors. The fields of genetics and genomics offer effective tools to control and prevent disease outbreaks in aquatic animal species. In this study, we present the key findings from our recent research, focusing on the genetic resistance to three specific diseases: White Spot Syndrome Virus (WSSV) in white shrimp, Bacterial Necrotic Pancreatitis (BNP) in striped catfish, and skin fluke (a parasitic ailment) in yellowtail kingfish. Our investigations reveal that all three species possess substantial heritable genetic components for disease-resistant traits, indicating their potential responsiveness to artificial selection in genetic improvement programs tailored to combat these diseases. Also, we observed a high genetic association between disease traits and survival rates. Through selective breeding aimed at enhancing resistance to these pathogens, we achieved substantial genetic gains, averaging 10% per generation. These selection programs also contributed positively to the overall production performance and productivity of these species. Although the effects of selection on immunological traits or immune responses were not significant in white shrimp, they yielded favorable results in striped catfish. Furthermore, our genomic analyses, including shallow genome sequencing of pedigreed populations, enriched our understanding of the genomic architecture underlying disease resistance traits. These traits are primarily governed by a polygenic nature, with numerous genes or genetic variants, each with small effects. Leveraging a range of advanced statistical methods, from mixed models to machine and deep learning, we developed prediction models that demonstrated moderate-to-high levels of accuracy in forecasting these disease-related traits. In addition to genomics, our RNA-seq experiments identified several genes that undergo upregulation in response to infection or viral loads within the populations. Preliminary microbiome data, while offering limited predictive accuracy for disease traits in one of our studied species, underscore the potential for combining such data with genome sequence information to enhance predictive power for disease traits in our populations. Lastly, this paper briefly discusses the roles of precision agriculture systems and AI algorithms and outlines the path for future research to expedite the development of disease-resistant genetic lines tailored to our target species. In conclusion, our study underscores the critical role of genetics and genomics in fortifying the aquaculture sector against the threats posed by diseases, paving the way for more sustainable and resilient aquaculture development. [ABSTRACT FROM AUTHOR]

In a large portion of the tropics, there is a demand for the development of hybrid chilies (Capsicum annuum L.) with high pungency, antioxidant vitamins, and tolerance to chili leaf curl virus, and anthracnose. Six genetically diverse parents were crossed in half-diallel fashion to develop 15 F1 hybrids to assess the level of heterosis, combining ability and gene action for 17 quantitative traits. The inheritance of most traits was apparently controlled by non-additive gene action. "Bidhan Chili 4" recorded the maximum, significant, GCA effects in a desired direction for PDIs of leaf curl virus and anthracnose along with commercially important traits. The maximum extent of heterobeltiosis was for oleoresin content followed by ascorbic acid and capsaicin contents, PDIs of chili leaf curl virus and anthracnose, and fruit yield per plant. The hybrids "Bidhan Chili 4 × Chili 38-Ragi" and "Pant C 1 × Bidhan Chili 4" could be isolated on the basis of their average performance, heterosis manifested in them, and SCA effects. Such hybrids could make a difference by meeting the horticultural requirements, high yield, disease tolerance and pungency, of commercial chili growing zones in the tropics. Hybrid vigor is available for commercial production of chili hybrids. A different approach from hybrid vigor is to isolate pure lines from segregating generations of potential heterotic F1s to increase fruit yield, quality attributes, and resistance to the chili leaf curl virus and anthracnose disease. [ABSTRACT FROM AUTHOR]

Summary: The opportunistic pathogen Pseudomonas viridiflava colonizes > 50 agricultural crop species and is the most common Pseudomonas in the phyllosphere of European Arabidopsis thaliana populations. Belonging to the P. syringae complex, it is genetically and phenotypically distinct from well‐characterized P. syringae sensu stricto. Despite its prevalence, we lack knowledge of how A. thaliana responds to its native isolates at the molecular level. Here, we characterize the host response in an A. thaliana – P. viridiflava pathosystem.We measured host and pathogen growth in axenic infections and used immune mutants, transcriptomics, and metabolomics to determine defense pathways influencing susceptibility to P. viridiflava infection.Infection with P. viridiflava increased jasmonic acid (JA) levels and the expression of ethylene defense pathway marker genes. The immune response in a susceptible host accession was delayed compared with a tolerant one. Mechanical injury rescued susceptibility, consistent with an involvement of JA.The JA/ethylene pathway is important for suppression of P. viridiflava, yet suppression capacity varies between accessions. Our results shed light on how A. thaliana can suppress the ever‐present P. viridiflava, but further studies are needed to understand how P. viridiflava evades this suppression to spread broadly across A. thaliana populations. [ABSTRACT FROM AUTHOR]

ABSTRACTChlamydiae are obligate intracellular bacterial pathogens that may cause genital pathology via induction of destructive host immune responses. Human-adapted Chlamydia trachomatis causes inflammatory disease in human hosts but is easily cleared in mice, and mouse-adapted Chlamydia muridarum establishes a productive and pathogenic infection in murine hosts. While numerous anti-chlamydial host resistance factors have been discovered in mice and humans alike, little is known about host factors promoting host fitness independent of host resistance. Here, we show that interferon-inducible immunity-related GTPase M (Irgm) proteins function as such host factors ameliorating infection-associated sequalae in the murine female genital tract, thus characterizing Irgm proteins as mediators of disease tolerance. Specifically, we demonstrate that mice deficient for all three murine Irgm paralogs (pan-Irgm−/−) are defective for cell-autonomous immunity to C. trachomatis, which correlates with an early and transient increase in bacterial burden and sustained hyperinflammation in vivo. In contrast, upon infection of pan-Irgm−/− mice with C. muridarum, bacterial burden is unaffected, yet genital inflammation and scarring pathology are nonetheless increased, demonstrating that Irgm proteins can promote host fitness without altering bacterial burden. Additionally, pan-Irgm−/− mice display increased granulomatous inflammation in genital Chlamydia infection, implicating Irgm proteins in the regulation of granuloma formation and maintenance. These findings demonstrate that Irgm proteins regulate pathogenic immune responses to Chlamydia infection in vivo, establishing an effective infection model to examine the immunoregulatory functions and mechanisms of Irgm proteins.IMPORTANCEIn response to genital Chlamydia infection, the immune system mounts a proinflammatory response to resist the pathogen, yet inflammation must be tightly controlled to avoid collateral damage and scarring to host genital tissue. Variation in the human IRGM gene is associated with susceptibility to autoinflammatory diseases but its role in ameliorating inflammatory diseases caused by infections is poorly defined. Here, we use mice deficient for all three murine Irgm paralogs to demonstrate that Irgm proteins not only provide host resistance to Chlamydia infections but also limit associated inflammation in the female genital tract. In particular, we find that murine Irgm expression prevents granulomatous inflammation, which parallels inflammatory diseases associated with variants in human IRGM. Our findings therefore establish genital Chlamydia infection as a useful model to study the roles for Irgm proteins in both promoting protective immunity and limiting pathogenic inflammation.

Regulation of immune responses during viral infection is critical to preventing the development immunopathology that impairs host survival. Natural killer (NK) cells are well known for their antiviral functions that promote viral clearance; however, their roles in limiting immune-mediated pathology are still unclear. Using a mouse model for genital herpes simplex virus type 2 infection, we find that NK cell-derived interferon-γ directly counteracts interleukin-6-mediated matrix metalloproteases (MMPs) activity in macrophages to limit MMP-mediated tissue damage. Our findings uncover a key immunoregulatory function of NK cells during host-pathogen interactions that highlight the potential of NK cell therapy for treatment of severe viral infections. [ABSTRACT FROM AUTHOR]

Simple Summary: To combat infections, hosts employ a combination of antagonistic and cooperative host defense strategies. The former refers to pathogen killing mediated by host immunity (disease resistance), while the latter refers to physiological defense mechanisms that promote host health during infection independent of pathogen killing, leading to a cooperation between the host and the pathogen (diseases tolerance). In chickens, the paratyphoid Salmonella evolved the capacity to survive the initial robust immune response and persist in the avian ceca for months without triggering clinical signs. The persistent or carrier phase of a Salmonella infection in the avian host involves a complex balance of antagonistic and cooperative host defense strategies. Initially, the host reacts with a normal inflammatory response that controls bacterial invasion. After 3–4 days of inflammation, the host response changes to a more anti-inflammatory response characterized by changes in the local intestinal physiology that is no longer antagonistic to the bacterial pathogen, but instead 'tolerates' its presence. Thus, the chicken becomes a carrier of the pathogen allowing it to survive in the intestine without causing disease. It is hoped that understanding these mechanisms of pathogen survival in the chicken will allow future research to exploit these novel disease tolerance mechanisms to impact poultry health and reduced foodborne infections of Salmonella. The gastrointestinal ecosystem involves interactions between the host, gut microbiota, and external environment. To colonize the gut of poultry, Salmonella must surmount barriers levied by the intestine including mucosal innate immune responses and microbiota-mediated niche restrictions. Accordingly, comprehending Salmonella intestinal colonization in poultry requires an understanding of how the pathogen interacts with the intestinal ecosystem. In chickens, the paratyphoid Salmonella have evolved the capacity to survive the initial immune response and persist in the avian ceca for months without triggering clinical signs. The persistence of a Salmonella infection in the avian host involves both host defenses and tolerogenic defense strategies. The initial phase of the Salmonella–gut ecosystem interaction is characteristically an innate pro-inflammatory response that controls bacterial invasion. The second phase is initiated by an expansion of the T regulatory cell population in the cecum of Salmonella-infected chickens accompanied by well-defined shifts in the enteric neuro-immunometabolic pathways that changes the local phenotype from pro-inflammatory to an anti-inflammatory environment. Thus, paratyphoid Salmonella in chickens have evolved a unique survival strategy that minimizes the inflammatory response (disease resistance) during the initial infection and then induces an immunometabolic reprogramming in the cecum that alters the host defense to disease tolerance that provides an environment conducive to drive asymptomatic carriage of the bacterial pathogen. [ABSTRACT FROM AUTHOR]

Normally, the host immunological response to viral infection is coordinated to restore homeostasis and protect the individual from possible tissue damage. The two major approaches are adopted by the host to deal with the pathogen: resistance or tolerance. The nature of the responses often differs between species and between individuals of the same species. Resistance includes innate and adaptive immune responses to control virus replication. Disease tolerance relies on the immune response allowing the coexistence of infections in the host with minimal or no clinical signs, while maintaining sufficient viral replication for transmission. Here, we compared the virome of bats, rodents and migratory birds and the molecular mechanisms underlying symptomatic and asymptomatic disease progression. We also explore the influence of the host physiology and environmental influences on RNA virus expression and how it impacts on the whole brain transcriptome of seemingly healthy semipalmated sandpiper (Calidris pusilla) and spotted sandpiper (Actitis macularius). Three time points throughout the year were selected to understand the importance of longitudinal surveys in the characterization of the virome. We finally revisited evidence that upstream and downstream regulation of the inflammatory response is, respectively, associated with resistance and tolerance to viral infections. [ABSTRACT FROM AUTHOR]

The northward expansion of Bursaphelenchus xylophilus has caused devastating disasters in the northeastern region, posing a significant threat to Pinus koraiensis, which is the major component species of the top ecological community of the Northeast China forest area. This study aims to enrich the molecular mechanism of the interaction between P. koraiensis and B. xylophilus, thus laying a theoretical foundation for the breeding of disease-tolerant P. koraiensis. The disease tolerance of 20 families of P. koraiensis to B. xylophilus was identified by artificial inoculation and different families of P. koraiensis were divided into three categories: tolerant, susceptible and high-susceptible. The RNA of tolerant and high-susceptible P. koraiensis was extracted for transcriptome sequencing. The α-terpineol synthase gene (Pk-αts) related to disease tolerance was screened and cloned. The expression level of Pk-αts in 4 tolerant, 2 susceptible, and 4 high-susceptible P. koraiensis was randomly detected by RT-qPCR, and the relative tolerance index of these 10 P. koraiensis families was calculated. The correlation between Pk-αts expression level and the relative tolerance index of P. koraiensis was analyzed. The results showed that after inoculating B. xylophilus for 20 days, only a few needles of tolerant P. koraiensis turned yellow, with an average relative tolerance index of 0. 88, while high-susceptible P. koraiensis showed partial needle redness, with an average relative tolerance index of 0. 09. Transcriptome sequencing identified 1 770 genes that were up-regulated in tolerant P. koraiensis and had no change or down-regulated in high-susceptible P. koraiensis. The relative expression of Pk-αts in tolerant P. koraiensis was 2. 83, which was extremely significant, but the relative expression in high-susceptible P. koraiensis was -1. 27. The cloned Pk-αts gene was 1 230 bp in length, encoding a protein composed of 409 amino acids, with an isoelectric point of 5. 55 and a relative molecular weight of 47. 60 ku. After comparison, it had the highest homology with the α-terpineol synthase gene and contained conserved motifs such as DDxxD and RRx8W of plant monoterpene synthases and Terpene_synth domain, which were consistent with the structural characteristics of monoterpene synthases. RT-qPCR detection showed that the expression of the Pk-αts gene was upregulated (the average expression level is 1. 39) in tolerant P. koraiensis, while it was unchanged or downregulated in susceptible and high -susceptible P. koraiensis, indicating that the upregulation of the Pk-αts gene expression was synchronized with the temporal and spatial of P. koraiensis tolerance to in the early stage of B. xylophilus infection. The expression level of Pk-αts was positively correlated with the relative tolerance index of P. koraiensis (Pearson's coefficient was 0. 911, P< 0. 01), indicating that the up-regulated expression of the Pk-αts gene improved the disease tolerance of P. koraiensis. In summary, different families of P. koraiensis have different tolerance to B. xylophilus, and some P. koraiensis have certain disease tolerance. The up-regulated expression of Pk-αts gene alleviates disease symptoms and helps to improve the disease tolerance of P. koraiensis to B. xylophilus. The Pk-αts gene can be used as a detection target for identifying tolerance of P. koraiensis to B. xylophilus, which is helpful for the breeding of tolerant P. koraiensis. [ABSTRACT FROM AUTHOR]

Holm oaks (Quercus ilex L.) can suffer severe infection by the oomycete Phytophthora cinnamomi Rands; the production of more tolerant plants is, therefore, required. Embryo formation is a key period in the establishment of epigenetic memory. Somatic embryos from three holm oak genotypes were elicited, either over 3 days or 60 days, with methyl-jasmonate, salicylic acid (SA), β-aminobutyric acid (BABA), or benzothiadiazole (all at 50 μM and 100 μM), or 10% and 30% of a filtered oomycete extract (FILT10 and FILT30) to activate plant immune responses. The number of embryos produced and conversion rate under all conditions were recorded. Some elicited embryos were then exposed to P. cinnamomi in dual culture, and differential mycelial growth and the progression of necrosis were measured. The same was performed with the roots of germinated embryos. Within genotypes, significant differences were seen among the elicitation treatments in terms of both variables. Embryos and roots of 60-day BABA, SA, or FILT10 treatments inhibited mycelium growth. The 3-day BABA (either concentration) and 60-day FILT10 induced the greatest inhibition of necrosis. Mycelium and necrosis inhibition were compared with those of tolerant trees. Both inhibitions might be a defense response maintained after primed embryo germination, thus increasing the likelihood of tolerance to infection. [ABSTRACT FROM AUTHOR]

Massive propagation of cork oak (Quercus suber) individuals tolerant to Phytophthora cinnamomi (Pc) is probably the most important challenge for cork production. Screening for resistance to Pc of ca. 200 seedlings obtained from a single cork oak tree that has survived the epidemic was performed by soil infestation. Twenty months after Pc inoculation, 33 seedlings survived from Pc infection and the four most vigorous seedlings were selected. The plants were forced to produce new shoots under controlled climatic conditions, and the new shoots were used to establish the plants in vitro by axillary budding. High axillary shoot proliferation rates were achieved by culturing the new shoots on Lloyd and McCown (WPM) medium, followed by subculturing for 2 weeks on 0.22 µM benzyladenine (BA) and for 2 weeks further on 0.04 µM BA. Addition of 20 µM silver thiosulphate (STS) increased the proliferation rates and improved the appearance and development of shoots. Rooting rates of 80–100% were obtained by culturing the shoots for 24 or 48 h on Gresshoff and Doy medium with ⅓ macronutrients plus 122.5 µM indole-3-butyric acid and subsequent transfer to root expression medium containing 20 µM STS. The results of this study optimize the micropropagation of a relevant and recalcitrant tree species in forestry. [ABSTRACT FROM AUTHOR]

Resistance and tolerance are two important strategies employed by the host immune response to defend against pathogens. Multidrug-resistant bacteria affect the resistance mechanisms involved in pathogen clearance. Disease tolerance, defined as the ability to reduce the negative impact of infection on the host, might be a new research direction for the treatment of infections. The lungs are highly susceptible to infections and thus are important for understanding host tolerance and its precise mechanisms. This review focuses on the factors that induce lung disease tolerance, cell and molecular mechanisms involved in tissue damage control, and the relationship between disease tolerance and sepsis immunoparalysis. Understanding the exact mechanism of lung disease tolerance could allow better assessment of the immune status of patients and provide new ideas for the treatment of infections. [ABSTRACT FROM AUTHOR]

Normally, the host immunological response to viral infection is coordinated to restore homeostasis and protect the individual from possible tissue damage. The two major approaches are adopted by the host to deal with the pathogen: resistance or tolerance. The nature of the responses often differs between species and between individuals of the same species. Resistance includes innate and adaptive immune responses to control virus replication. Disease tolerance relies on the immune response allowing the coexistence of infections in the host with minimal or no clinical signs, while maintaining sufficient viral replication for transmission. Here, we compared the virome of bats, rodents and migratory birds and the molecular mechanisms underlying symptomatic and asymptomatic disease progression. We also explore the influence of the host physiology and environmental influences on RNA virus expression and how it impacts on the whole brain transcriptome of seemingly healthy semipalmated sandpiper (Calidris pusilla) and spotted sandpiper (Actitis macularius). Three time points throughout the year were selected to understand the importance of longitudinal surveys in the characterization of the virome. We finally revisited evidence that upstream and downstream regulation of the inflammatory response is, respectively, associated with resistance and tolerance to viral infections.

Edwardsiellosis caused by Edwardsiella tarda resulted in significant economic losses in aquaculture operations worldwide. This disease could infect a wide range of hosts, including freshwater, brackish water, and marine aquatic animals. Currently, antibiotics and vaccines are being used as prophylactic agents to overcome Edwardsiellosis in aquaculture. However, application of antibiotics has led to antibiotic resistance among pathogenic bacteria, and the antibiotic residues pose a threat to public health. Meanwhile, the use of vaccines to combat Edwardsiellosis requires intensive labor work and high costs. Thus, phytobiotics were attempted to be used as antimicrobial agents to minimize the impact of Edwardsiellosis in aquaculture. These phytobiotics may also provide farmers with new options to manage aquaculture species' health. The impact of Edwardsiellosis in aquaculture worldwide was elaborated on and highlighted in this review study, as well as the recent application of phytobiotics in aquaculture and the status of vaccines to combat Edwardsiellosis. This review also focuses on the potential of phytobiotics in improving aquatic animal growth performance, enhancing immune system function, and stimulating disease resistance.

ABSTRACT Infected hosts possess two alternative strategies to protect themselves against the negative impact of virus infections: resistance, used to abrogate virus replication, and disease tolerance, used to avoid tissue damage without controlling viral burden. The principles governing pathogen resistance are well understood, while less is known about those involved in disease tolerance. Here, we studied bluetongue virus (BTV), the cause of bluetongue disease of ruminants, as a model system to investigate the mechanisms of virus-host interactions correlating with disease tolerance. BTV induces clinical disease mainly in sheep, while cattle are considered reservoirs of infection, rarely exhibiting clinical symptoms despite sustained viremia. Using primary cells from multiple donors, we show that BTV consistently reaches higher titers in ovine cells than cells from cattle. The variable replication kinetics of BTV in sheep and cow cells were mostly abolished by abrogating the cell type I interferon (IFN) response. We identified restriction factors blocking BTV replication, but both the sheep and cow orthologues of these antiviral genes possess anti-BTV properties. Importantly, we demonstrate that BTV induces a faster host cell protein synthesis shutoff in primary sheep cells than cow cells, which results in an earlier downregulation of antiviral proteins. Moreover, by using RNA sequencing (RNA-seq), we also show a more pronounced expression of interferon-stimulated genes (ISGs) in BTV-infected cow cells than sheep cells. Our data provide a new perspective on how the type I IFN response in reservoir species can have overall positive effects on both virus and host evolution. IMPORTANCE The host immune response usually aims to inhibit virus replication in order to avoid cell damage and disease. In some cases, however, the infected host avoids the deleterious effects of infection despite high levels of viral replication. This strategy is known as disease tolerance, and it is used by animal reservoirs of some zoonotic viruses. Here, using a virus of ruminants (bluetongue virus [BTV]) as an experimental system, we dissected virus-host interactions in cells collected from species that are susceptible (sheep) or tolerant (cow) to disease. We show that (i) virus modulation of the host antiviral type I interferon (IFN) responses, (ii) viral replication kinetics, and (iii) virus-induced cell damage differ in tolerant and susceptible BTV-infected cells. Understanding the complex virus-host interactions in disease tolerance can allow us to disentangle the critical balance between protective and damaging host immune responses.

Potato (Solanum tuberosum L.) cultivation is an important agricultural activity in the Andean region. The late blight Phytophthora infestans (Mont.) de Bary, considered one of the limiting diseases in production, represents a threat to food security and causes losses ranging from 30 to 100% of yield. This research evaluated the response to the disease in four commercial materials widely planted in the department of Nariño. The evaluation was carried out under field conditions, in the municipality of Pasto, at AGROSAVIA's Obonuco research center, with natural inoculum, under a randomized complete block design with four replications. The response variables evaluated were incidence, severity, leaf area index and yield in the commercial categories. The ICA Única variety, reported as highly resistant in 2001, presented damage levels close to 75%, with a yield reduction of 49.88%, caused mainly by low yields of first category tubers, indicating a loss of its level of resistance, with damage levels similar to the highly susceptible control Diacol Capiro, which presented 100% of the area with symptoms of the disease and a reduction of 89% in yield. The genotypes Pastusa Suprema with disease tolerance characteristics and Superior showed the best performance with a severity level of 30% in each case and yield reductions of 30.5% and 40.92%, respectively. The results highlight the importance of these genotypes and their role as pillars in the integrated management of the disease through the planting of varieties with favorable behavior against the disease.

Growing cassava in Africa requires resistance against the viruses causing cassava mosaic disease (CMD) and the viruses causing cassava brown streak disease (CBSD). A dominant CMD2 resistance gene from a West African cassava landrace provides strong resistance against the cassava mosaic viruses. However, resistance against cassava brown streak viruses is limited to cassava varieties that show tolerance to the disease. A recently identified cassava germplasm that cannot be infected with cassava brown streak viruses provides a new source of the resistance required to protect cassava from CBSD. We present a synopsis of the status of virus resistance in cassava and report on the research to combine resistance against CBSD and CMD. We improve the lengthy and erratic screening for CBSD resistance by proposing a virus infection and screening protocol for the viruses causing CBSD and CMD, which allows a rapid and precise assessment of cassava resistance under controlled conditions. Using this approach, we classified the virus responses of cassava lines from Africa and South America and identified truly virus-resistant clones that cannot be infected with any of the known viruses causing CBSD even under the most stringent virus infections. A modification of this protocol was used to test seedlings from cassava crosses for resistance against both diseases. A broad-spectrum resistance was identified in a workflow that lasted 9 months from seed germination to the identification of virus resistance. The workflow we propose dramatically reduces the evaluation and selection time required in a classical breeding workflow to reach the advanced field trial stage in only 9 months by conducting selections for virus resistance and plant multiplication in parallel. However, it does not bypass field evaluations; cassava resistance assessment prior to the field limits the evaluation to candidates with virus resistance defined as the absence of symptoms and the absence of the virus. The transfer of our virus screening workflow to cassava breeding programs enhances the efficiency by which resistance against viruses can be selected. It provides a precise definition of the plant’s resistance response and can be used as a model system to tackle resistance in cassava against other diseases. [ABSTRACT FROM AUTHOR]

Native (flat) oyster (Ostrea edulis) beds, once a major component of the North Sea, largely disappeared from the region in the late 19th century. Flat oyster restoration is taking place at a number of locations in the North Sea. When flat oyster beds are restored in areas where O. edulis is functionally extinct it is advised to treat these as disease-free areas. Adult oysters were collected in the Dutch Delta area which is infected with the pathogenic parasite Bonamia ostreae. The aim of this research was to obtain Bonamia-free seed from parents collected in a Bonamia-infected area. In addition, the oysters were analysed to identify candidate genomic regions related to bonamiosis tolerance and exposed to Bonamia in the field to assess survival compared to a naïve control group. With the aid of a non-destructive screening method, Bonamia-free broodstock were selected. These oysters produced Bonamia-free larvae and seed. For comparison, broodstock oysters were collected in the Dutch Wadden Sea, an area free of Bonamia. These oysters also produced Bonamia-free larvae and seed. To study if the Delta area oysters had developed a degree of resistance to the disease, while the naïve Wadden Sea oysters had not, seed of both groups was challenged in Lake Grevelingen where Bonamia occurs. Survival of the pre-selected Bonamia-free oysters was significantly higher than the naïve group. Samples of seed were analysed for association of candidate genetic markers related to bonamiosis tolerance. A higher percentage of individuals with tolerance-associated marker genotypes was found in the screened group compared to the naïve one. However, mortality of the naïve group could not be related to Bonamia presence. Further challenge tests are needed before firm conclusions regarding the genetic markers can be made. The results show that hatchery production of Bonamia-free and potentially Bonamia-tolerant flat oysters is possible. [ABSTRACT FROM AUTHOR]

Individual animals vary greatly in their responses to infection, either killing off the invading pathogen (resistance) or minimizing the per‐pathogen costs of infection on host fitness (tolerance). Though we understand little about the physiological drivers of tolerance in wild animals, phenotypically, it manifests as milder clinical signs of disease. Here, we use a well‐described disease system, finch mycoplasmosis, to evaluate the role of inflammation in disease tolerance. House finches (Haemorhous mexicanus) infected with the bacterial pathogen Mycoplasma gallisepticum (MG) develop conjunctival pathology that satisfies the cardinal signs of inflammation. We report on a captive trial performed in 2016 and replicated in 2018 that tested whether chemotherapeutics, specifically nonsteroidal anti‐inflammatory drugs (NSAIDs), can reduce lesion severity, thus pushing individuals toward more tolerant phenotypes. Though birds treated with NSAIDs in the first trial developed milder pathology per unit pathogen load, we found no effect of treatment in the second trial, perhaps due to natural variation in baseline tolerance within the source population across years. Second‐trial control birds developed markedly milder pathology than first‐year controls, suggesting that the effect of trial swamped the effect of treatment in this study. Moving forward, using birds from a population in which the disease is absent or only recently emerged—and so tolerance has not yet been selected for—may better elucidate the role of pro‐inflammatory mediators in disease tolerance. Research Highlights: An individual's disease phenotype reflects how its immune system responds to tissue injury caused by an infectious pathogen. Limiting the pro‐inflammatory response may be one‐way animals express milder clinical signs to disease consistent with disease tolerance. Exogenous treatment with nonsteroidal anti‐inflammatory drugs may similarly push individuals toward tolerant phenotypes, however, population‐level swings in baseline tolerance can mask treatment effects. [ABSTRACT FROM AUTHOR]

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Myalgic encephalomyelitis (ME) previously also known as chronic fatigue syndrome is a heterogeneous, debilitating syndrome of unknown etiology responsible for long-lasting disability in millions of patients worldwide. The most well-known symptom of ME is post-exertional malaise, but many patients also experience autonomic dysregulation, cranial nerve dysfunction and signs of immune system activation. Many patients also report a sudden onset of disease following an infection. The brainstem is a suspected focal point in ME pathogenesis and patients with structural impairment to the brainstem often show ME-like symptoms. The brainstem is also where the vagus nerve originates, a critical neuro-immune interface and mediator of the inflammatory reflex which regulate systemic inflammation. Here, we report the results of a randomized, placebo-controlled trial using intranasal mechanical stimulation targeting nerve endings in the nasal cavity, likely from the trigeminal nerve, possibly activating additional centers in the brainstem of ME patients and correlating with a ∼30% reduction in overall symptom scores after 8 weeks of treatment. By performing longitudinal, systems-level monitoring of the blood immune system in these patients, we uncover signs of chronic immune activation in ME, as well as immunological correlates of improvement that center around gut-homing immune cells and reduced inflammation. The mechanisms of symptom relief remain to be determined, but transcriptional analyses suggest an upregulation of disease tolerance mechanisms. We believe that these results are suggestive of ME as a condition explained by a maladaptive disease tolerance response following infection. [ABSTRACT FROM AUTHOR]

This study aimed to characterise and evaluate the probiotic properties of a newly isolated marine bacterium, strain S6031. The isolated strain was identified as Pseudoalteromonas ruthenica. In vivo experiments were conducted with P. ruthenica- immersed larvae and P. ruthenica -enriched Artemia fed to adult zebrafish. Disease tolerance of larval zebrafish against Edwardsiella piscicida was demonstrated by 66.34% cumulative per cent survival (CPS) in the P. ruthenica -exposed group, which was higher than the CPS of the control (46.67%) at 72 h post challenge (hpc). Heat-stressed larvae had 55% CPS in the P. ruthenica -immersed group, while the control had 30% CPS at 60 hpc. Immune-stress response gene transcripts (muc5.1 , muc5.2 , muc5.3 , alpi2 , alpi3 , hsp70 , and hsp90a) were induced, while pro-inflammatory genes (tnfα , il1b , and il6) were downregulated in P. ruthenica -immersed larvae compared to the control. This trend was confirmed by low pro-inflammatory and high stress-responsive protein expression levels in P. ruthenica -exposed larvae. Adult zebrafish had higher CPS (27.2%) in the P. ruthenica -fed group than the control (9.52%) upon E. piscicida challenge, suggesting increased disease tolerance. Histological analysis demonstrated modulation of goblet cell density and average villus height in the P. ruthenica -supplemented group. Metagenomics analysis clearly indicated modulation of alpha diversity indices and the relative abundance of Proteobacteria in the P. ruthenica -supplemented zebrafish gut. Furthermore, increased Firmicutes colonisation and reduced Bacteroidetes abundance in the gut were observed upon P. ruthenica supplementation. Additionally, this study confirmed the concentration-dependent increase of colony dispersion and macrophage uptake upon mucin treatment. In summary, P. ruthenica possesses remarkable functional properties as a probiotic that enhances host defence against diseases and thermal stress. [Display omitted] • Pseudoalteromonas ruthenica is a marine bacterium isolated from Jeju, Republic of Korea. • P. ruthenica facilitate the inhibition of the fish pathogenic bacterium, E. piscicida. • P. ruthenica enriched Artemia supplemented adult zebrafish developed disease resistance, modulation of immune responses and gut microbial composition. • P. ruthenica possess functional properties of probiotics which enhance the host defense against diseases and thermal stress. [ABSTRACT FROM AUTHOR]

Fusarium wilt disease is the most important disease of cumin (Cuminum cyminum L.) and causes great damage to it every year. The present study was conducted to evaluate the response of 13 cumin genotypes to Fusarium wilt disease as a factorial experiment in a completely randomized design (genotype as the first factor and absence and presence of the pathogen as the second one) with three replications in the greenhouse of Research and Technology Institute of Plant Production, Shahid Bahonar University of Kerman during growing season of 2020-2021. The results showed that the interaction of genotype and treatment was statistically significant on most of the traits. The highest traits correlation was observed between plant dry weight and number of umbrellas per plant (0.92) under the absence of pathogen conditions and between plant height and number of seeds per plant (0.76) under the presence of pathogen conditions. Cluster analysis (Ward method) regarding the studied traits divided the genotypes into three groups under the absence of pathogen conditions and two groups under the presence of pathogen. Principal component analysis showed that the first two components could explain 80.13% (absence of pathogen) and 84.55% (presence of pathogen) of the variations. Also, biplot analysis showed high diversity of the genotypes as well as confirming the clustering results. The genotype E7r1b1 had the highest plant mortality ratio (100%) under the presence of pathogen. Under the absence of pathogen, the genotype g8r2b2 had the highest yield (0.20 g) and number (75.66) of seeds per plant. Yield and number of seeds per plant decreased significantly under the presence of pathogen. The highest seed yield (0.14 g) under the presence of pathogen was observed in the genotype 2-14-3. Based on the studied traits, the genotypes g5r2B1 and F12r1b1 had the lowest potential compared to the others under the both conditions. In general, the genotypes reacted differently under the absence and presence of pathogen conditions. The genotypes that revealed tolerance to the disease conditions could be introduced as sources of tolerance in further breeding programs. [ABSTRACT FROM AUTHOR]

Among their many unique biological features, bats are increasingly recognized as a key reservoir of many emerging viruses that cause massive morbidity and mortality in humans. Bats are capable of harboring many of these deadly viruses without any apparent signs of pathology, in a mechanism known as viral disease tolerance. However, the immunological mechanisms behind viral tolerance remain poorly understood. As a non-model organism species, there are very limited research resources and tools available to study bat immunology. In the cave nectar bat Eonycteris spelaea , we have a panel of monoclonal antibodies (mAbs) against major immune markers. An immunophenotyping survey of major immune compartments and barrier sites using these mAbs reveals differences in the immunological landscape of bats. [Display omitted] • Development of a panel of monoclonal antibodies specific to E. spelaea • Flow cytometric phenotyping of multiple tissues to compare bats and mice • Bats have fewer B cells and a skewing of monocytes toward the non-classical lineage • CD4 and CD21 mAbs demonstrate cross-reactivity to two other bat species Bats are reservoir hosts of many viruses, harboring these viruses using unique mechanisms of viral tolerance. However, immunological study has been impaired by a lack of suitable tools. Chen et al. address this limitation by the usage of a panel of bat-specific monoclonal antibodies for flow cytometry. [ABSTRACT FROM AUTHOR]

Disease tolerance is an essential defense strategy against pathogens, alleviating tissue damage regardless of pathogen multiplication. However, its genetic and molecular basis remains largely unknown. Here, we discovered that protein condensation at the endoplasmic reticulum (ER) regulates disease tolerance in Arabidopsis against Pseudomonas syringae. During infection, Hematopoietic protein-1 (HEM1) and Bax-inhibitor 1 (BI-1) coalesce into ER-associated condensates facilitated by their phase-separation behaviors. While BI-1 aids in clearing these condensates via autophagy, it also sequesters lipid-metabolic enzymes within condensates, likely disturbing lipid homeostasis. Consequently, mutations in hem1 , which hinder condensate formation, or in bi-1 , which prevent enzyme entrapment, enhance tissue-damage resilience, and preserve overall plant health during infection. These findings suggest that the ER is a crucial hub for maintaining cellular homeostasis and establishing disease tolerance. They also highlight the potential of engineering disease tolerance as a defense strategy to complement established resistance mechanisms in combating plant diseases. [Display omitted] • Virulent pathogens trigger HEM1 condensation at the ER • HEM1 condensates are degraded by BI-1-promoted autophagy • HEM1 condensates trap lipid-metabolic enzymes interacting with BI-1 • Reducing damage by condensation boosts disease tolerance and preserves health Tang et al. report that pathogen infections trigger HEM1 condensate formation in plants, causing endoplasmic reticulum damage. Reducing this damage enhances disease tolerance, helping plants stay healthy regardless of pathogen proliferation. This immune strategy complements well-known disease resistance, boosting overall resilience against diseases. [ABSTRACT FROM AUTHOR]

The gastrointestinal ecosystem involves interactions between the host, gut microbiota, and external environment. To colonize the gut of poultry, Salmonella must surmount barriers levied by the intestine including mucosal innate immune responses and microbiota-mediated niche restrictions. Accordingly, comprehending Salmonella intestinal colonization in poultry requires an understanding of how the pathogen interacts with the intestinal ecosystem. In chickens, the paratyphoid Salmonella have evolved the capacity to survive the initial immune response and persist in the avian ceca for months without triggering clinical signs. The persistence of a Salmonella infection in the avian host involves both host defenses and tolerogenic defense strategies. The initial phase of the Salmonella–gut ecosystem interaction is characteristically an innate pro-inflammatory response that controls bacterial invasion. The second phase is initiated by an expansion of the T regulatory cell population in the cecum of Salmonella-infected chickens accompanied by well-defined shifts in the enteric neuro-immunometabolic pathways that changes the local phenotype from pro-inflammatory to an anti-inflammatory environment. Thus, paratyphoid Salmonella in chickens have evolved a unique survival strategy that minimizes the inflammatory response (disease resistance) during the initial infection and then induces an immunometabolic reprogramming in the cecum that alters the host defense to disease tolerance that provides an environment conducive to drive asymptomatic carriage of the bacterial pathogen.

Abstract Disease resilience, defined as an animal’s ability to maintain productive performance in the face of infection, provides opportunities to manage the polymicrobial challenge common in pig production. Disease resilience can deliver a number of benefits, including more sustainable production as well as improved animal health and the potential for reduced antimicrobial use. However, little progress has been made to date in the application of disease resilience in breeding programs due to a number of factors, including (1) confusion around definitions of disease resilience and its component traits disease resistance and tolerance, and (2) the difficulty in characterizing such a complex trait consisting of multiple biological functions and dynamic elements of rates of response and recovery from infection. Accordingly, this review refines the definitions of disease resistance, tolerance, and resilience based on previous studies to help improve the understanding and application of these breeding goals and traits under different scenarios. We also describe and summarize results from a “natural disease challenge model” designed to provide inputs for selection of disease resilience. The next steps for managing polymicrobial challenges faced by the pig industry will include the development of large-scale multi-omics data, new phenotyping technologies, and mathematical and statistical methods adapted to these data. Genome editing to produce pigs resistant to major diseases may complement selection for disease resilience along with continued efforts in the more traditional areas of biosecurity, vaccination and treatment. Altogether genomic approaches provide exciting opportunities for the pig industry to overcome the challenges provided by hard-to-manage diseases as well as new environmental challenges associated with climate change.

Growing cassava in Africa requires resistance against the viruses causing cassava mosaic disease (CMD) and the viruses causing cassava brown streak disease (CBSD). A dominant CMD2 resistance gene from a West African cassava landrace provides strong resistance against the cassava mosaic viruses. However, resistance against cassava brown streak viruses is limited to cassava varieties that show tolerance to the disease. A recently identified cassava germplasm that cannot be infected with cassava brown streak viruses provides a new source of the resistance required to protect cassava from CBSD. We present a synopsis of the status of virus resistance in cassava and report on the research to combine resistance against CBSD and CMD. We improve the lengthy and erratic screening for CBSD resistance by proposing a virus infection and screening protocol for the viruses causing CBSD and CMD, which allows a rapid and precise assessment of cassava resistance under controlled conditions. Using this approach, we classified the virus responses of cassava lines from Africa and South America and identified truly virus-resistant clones that cannot be infected with any of the known viruses causing CBSD even under the most stringent virus infections. A modification of this protocol was used to test seedlings from cassava crosses for resistance against both diseases. A broad-spectrum resistance was identified in a workflow that lasted 9 months from seed germination to the identification of virus resistance. The workflow we propose dramatically reduces the evaluation and selection time required in a classical breeding workflow to reach the advanced field trial stage in only 9 months by conducting selections for virus resistance and plant multiplication in parallel. However, it does not bypass field evaluations; cassava resistance assessment prior to the field limits the evaluation to candidates with virus resistance defined as the absence of symptoms and the absence of the virus. The transfer of our virus screening workflow to cassava breeding programs enhances the efficiency by which resistance against viruses can be selected. It provides a precise definition of the plant’s resistance response and can be used as a model system to tackle resistance in cassava against other diseases.

Over the past two decades, our appreciation of the gut mucus has moved from a static lubricant to a dynamic and essential component of the gut ecosystem that not only mediates the interface between host tissues and vast microbiota, but regulates how this ecosystem functions to promote mutualistic symbioses and protect from microbe-driven diseases. By delving into the complex chemistry and biology of the mucus, combined with innovative in vivo and ex vivo approaches, recent studies have revealed novel insights into the formation and function of the mucus system, the O-glycans that make up this system, and how they mediate two major host-defense strategies – resistance and tolerance – to reduce damage caused by indigenous microbes and opportunistic pathogens. This current review summarizes these findings by highlighting the emerging roles of mucus and mucin-type O-glycans in influencing host and microbial physiology with an emphasis on host defense strategies against bacteria in the gastrointestinal tract.

Host defense mechanisms are categorized into different strategies, namely, avoidance, resistance and tolerance. Resistance encompasses mechanisms that directly kill the pathogen while tolerance is mainly concerned with alleviating the harsh consequences of the infection regardless of the pathogen burden. Resistance is well‐known strategy in immunology while tolerance is relatively new. Studies addressed tolerance mainly using mouse models revealing a wide range of interesting tolerance mechanisms. Herein, we aim to emphasize on the interspecies comparative approaches to explore potential new mechanisms of disease tolerance. We will discuss mechanisms of tolerance with focus on those that were revealed using comparative study designs of mammals followed by summarizing the reasons for adopting comparative approaches on disease tolerance studies. Disease tolerance is a relatively new concept in immunology, we believe combining comparative studies with model organism study designs will enhance our understanding to tolerance and unveil new mechanisms of tolerance. [ABSTRACT FROM AUTHOR]

Background: Huanglongbing (HLB) is currently one of the most devasting diseases in citrus plants worldwide. Resistance against its causal agent, Candidatus Liberibacter asiaticus (CLas), in commercial Citrus species remains a challenge, even though they show differences in CLas multiplication. Methods: A total of 14 citrandarins and their parents (Sunki mandarin and Poncirus trifoliata cv. Rubidoux) were top-grafted onto the canopy of potted 'Valencia' sweet orange plants with high CLas titers. The grafted genotypes were tested for CLas infection and physiological effects of the disease (starch accumulation and callose deposition) for 12 months. Results: All tested genotypes were infected by CLas during the time frame of the experiment. However, a decrease in the infection rate ranging from 50% to 80% for the hybrids H109, H126, H157, and H222 was observed 360 days from the top-grafting. CLas was undetected by real-time PCR in H106 at the end of the experiment, which had low levels of starch and callose deposition. Conclusions: CLas infected all of the tested citrandarins, but a decrease in the infection rate over time was detected for some specific genotypes, which led to less starch accumulation and callose deposition. [ABSTRACT FROM AUTHOR]

Streptococcosis is the leading bacterial disease impacting Nile tilapia (Oreochromis niloticus) and causes substantial economic losses in China. This study assessed the resistance and tolerance of three Nile tilapia (88, 99, and NG) to Streptococcus agalactiae infection. Survival rates were monitored, and samples were collected from blood, liver, and spleen at 0, 1, 2, 5, 7, and 14 days post-infection. Serum biochemical parameters, hepatic antioxidant enzymes, and the expression of related antioxidant and immune genes were measured. Results showed that strain 88 had superior resistance, with the highest survival rate, reduced liver damage, and lower alanine aminotransferase and alkaline phosphatase levels at 1 and 5 days post-infection. This strain also had higher serum cholesterol and triglyceride levels between days 5 and 14. Antioxidant activities increased in all strains post-infection, with strain 88 showing significantly higher superoxide dismutase (SOD) activity and elevated catalase (CAT) and SOD gene expressions; this indicated enhanced control of reactive oxygen species and reduced tissue damage. Additionally, strain 88 exhibited lower levels of inflammatory markers (TNF-α, IL-1β, IL-10) with higher IgM levels and superior MHC-II expression during early infection, which demonstrated a strong immune response. These results indicate that strain 88 is a promising candidate for selective breeding to improve streptococcosis resistance in tilapia., Competing Interests: Declaration of Competing Interest All the authors do not have any possible conflicts of interest., (Copyright © 2024. Published by Elsevier Ltd.)

Diplodia sapinea causes Diplodia tip blight (DTB) and is recognised as an opportunistic necrotrophic pathogen affecting conifers. While DTB is associated with abiotic stress, the impact of biotic stress in the host on D. sapinea's lifestyle shift is unknown. Observed co-occurrences of D. sapinea and Melampsora pinitorqua, causing pine twisting rust on Scots pine (Pinus sylvestris), instigated an investigation into their interaction with and influence on the defence mechanisms of the host. We hypothesised that M. pinitorqua infections predispose the trees to D. sapinea by stressing the host and altering the shoot metabolites. Pines in a plantation were sampled over time to study pathogen biomass and host metabolites. Symptoms of both pathogens were consistent over years, and the preceding season's symptoms affected the metabolic profiles pre-infection and M. pinitorqua's proliferation. Symptoms of M. pinitorqua altered shoot metabolites more than fungal biomass, with co-symptomatic trees exhibiting elevated M. pinitorqua biomass. Specific phenolic compounds had a strong positive association with the shoot symptom × D. sapinea interaction. D. sapinea's biomass presymptoms was independent of previous disease symptoms and infection by M. pinitorqua. Some trees showed disease tolerance, with delayed rust infections and minimal DTB symptoms. Further investigations on this trait are needed., (© 2024 The Author(s). Plant, Cell & Environment published by John Wiley & Sons Ltd.)

SUMMARYThe ability to overcome metabolic stress is a major determinant of outcomes during infections. Pathogens face nutrient and oxygen deprivation in host niches and during their encounter with immune cells. Immune cells require metabolic adaptations for producing antimicrobial compounds and mounting antifungal inflammation. Infection also triggers systemic changes in organ metabolism and energy expenditure that range from an enhanced metabolism to produce energy for a robust immune response to reduced metabolism as infection progresses, which coincides with immune and organ dysfunction. Competition for energy and nutrients between hosts and pathogens means that successful survival and recovery from an infection require a balance between elimination of the pathogen by the immune systems (resistance), and doing so with minimal damage to host tissues and organs (tolerance). Here, we discuss our current knowledge of pathogen, immune cell and systemic metabolism in fungal infections, and the impact of metabolic disorders, such as obesity and diabetes. We put forward the idea that, while our knowledge of the use of metabolic regulation for fungal proliferation and antifungal immune responses (i.e., resistance) has been growing over the years, we also need to study the metabolic mechanisms that control tolerance of fungal pathogens. A comprehensive understanding of how to balance resistance and tolerance by metabolic interventions may provide insights into therapeutic strategies that could be used adjunctly with antifungal drugs to improve patient outcomes., Competing Interests: A.R. receives funding from Boehringer-Ingelheim, a pharmaceutical company, for an unrelated research project.

The aim of the work was to study the growth, drought tolerance and biochemical characteristics of introduced cultivars (‘Jonkheer van Tets’, ‘Hollandische Rote’ and ‘Viksne’) and some selected Russian cultivars and red currant genotypes (‘Shchedraya’, ‘Natali’, 129-21-61, 111-19-81, 261-65-19 and 271-58-24). The studies were conducted between 2014 and 2018 under temperate continental climate conditions. The intensity of transpiration was determined by using a torsion balance. The soluble solid concentration (SSS – % Brix) of the fruits was determined by using a digital refractomer. The content of the sum of sugars was determined by the weight method according to Bertrand's method. Ascorbic acid content was then determined by the iodometric method. The total phenolic content was determined by a colourimetric method. Climatic conditions were found to have significant influence on the disease severity of the red currant genotypes, while the infections caused by Sphaerotheca mors-uvae increased in optimum seasons and damages caused by Pseudopeziza ribis increased in drought seasons. None of the selected genotypes was found to be resistant to any of the diseases/pests, but ‘Jonkheer van Tets’, ‘Hollandische Rote’ and 111-19-81 were less affected by these diseases/pests. Weight, yield and raceme length of berries and the number of berries in a raceme were found to be higher in optimum seasons, and different cultivars/genotypes had superior characteristics for different parameters. The highest berry weight was observed in the 261-65-19 genotype (0.65 g), while the highest yield was noted in ‘Hollandische Rote’ (15.6 t · ha−1). It was also found that the water content of leaves and transpiration have a strong positive relationship with soil moisture at a depth of 0–200 mm but a week correlation with soil moisture at a depth of 200–400 mm. Results also showed that the transpiration of leaves decreases in later developmental stages (July). Hierarchical clustering suggested four clusters: the introduced cultivars produced one cluster, Russian cultivars are another cluster, 261-65-19, 111-19-81 and 129-21-61 genotypes make up a third cluster and the 271-58-24 genotype (superior in terms of phenolic contents) forms the fourth cluster.

Mycobacterium avium subsp. paratuberculosis (MAP) causes Johne's disease or paratuberculosis (PTB), with important animal health and economic implications. There are no therapeutic strategies to control this disease, and vaccination with inactivated vaccines is limited in many countries because it can interfere with the intradermal test used for bovine tuberculosis detection. Thus, infected animals either get culled after a positive ELISA or fecal PCR result or die due to clinical disease. In this study, we review recent studies aimed to discover genetic markers which could help to identify and select cattle less susceptible and more resilient to PTB. In recent years, the genotyping and subsequent imputation to whole-genome sequence (WGS) has allowed the identification of single-nucleotide polymorphisms (SNPs), quantitative trait loci (QTL), and candidate genes in the Bos taurus genome associated with susceptibility to MAP infection. In most of these genome-wide association studies (GWAS), phenotypes were based on ante-mortem test results including serum ELISA, milk ELISA, and detection of MAP by fecal PCR and bacteriological culture. Cattle infected with MAP display lesions with distinct severity but the associations between host genetics and PTB-associated pathology had not been explored until very recently. On the contrary, the understanding of the mechanisms and genetic loci influencing pathogen resistance, and disease tolerance in asymptomatic individuals is currently very limited. The identification of long-time asymptomatic cattle that is able to resist the infection and/or tolerate the disease without having their health and milk production compromised is important for disease control and breeding purposes.

Holm oaks (Quercus ilex L.) can suffer severe infection by the oomycete Phytophthora cinnamomi Rands; the production of more tolerant plants is, therefore, required. Embryo formation is a key period in the establishment of epigenetic memory. Somatic embryos from three holm oak genotypes were elicited, either over 3 days or 60 days, with methyl-jasmonate, salicylic acid (SA), β-aminobutyric acid (BABA), or benzothiadiazole (all at 50 μM and 100 μM), or 10% and 30% of a filtered oomycete extract (FILT10 and FILT30) to activate plant immune responses. The number of embryos produced and conversion rate under all conditions were recorded. Some elicited embryos were then exposed to P. cinnamomi in dual culture, and differential mycelial growth and the progression of necrosis were measured. The same was performed with the roots of germinated embryos. Within genotypes, significant differences were seen among the elicitation treatments in terms of both variables. Embryos and roots of 60-day BABA, SA, or FILT10 treatments inhibited mycelium growth. The 3-day BABA (either concentration) and 60-day FILT10 induced the greatest inhibition of necrosis. Mycelium and necrosis inhibition were compared with those of tolerant trees. Both inhibitions might be a defense response maintained after primed embryo germination, thus increasing the likelihood of tolerance to infection.

Massive propagation of cork oak (Quercus suber) individuals tolerant to Phytophthora cinnamomi (Pc) is probably the most important challenge for cork production. Screening for resistance to Pc of ca. 200 seedlings obtained from a single cork oak tree that has survived the epidemic was performed by soil infestation. Twenty months after Pc inoculation, 33 seedlings survived from Pc infection and the four most vigorous seedlings were selected. The plants were forced to produce new shoots under controlled climatic conditions, and the new shoots were used to establish the plants in vitro by axillary budding. High axillary shoot proliferation rates were achieved by culturing the new shoots on Lloyd and McCown (WPM) medium, followed by subculturing for 2 weeks on 0.22 µM benzyladenine (BA) and for 2 weeks further on 0.04 µM BA. Addition of 20 µM silver thiosulphate (STS) increased the proliferation rates and improved the appearance and development of shoots. Rooting rates of 80–100% were obtained by culturing the shoots for 24 or 48 h on Gresshoff and Doy medium with ⅓ macronutrients plus 122.5 µM indole-3-butyric acid and subsequent transfer to root expression medium containing 20 µM STS. The results of this study optimize the micropropagation of a relevant and recalcitrant tree species in forestry.