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The precise regulation of energy homeostasis is essential for sustainable poultry production. Dysregulation of the avian gut-brain axis (GBA) contributes to metabolic disorders such as ascites and sudden death syndrome, impaired feed efficiency, and welfare problems in high-yield broilers. The avian GBA is a specialized bidirectional network that integrates hormonal, neural, and microbial signals to match feeding behavior with acute nutrient availability and long-term metabolic demands. Unique avian traits include a simplified gustatory system, lack of a functional T1R2 sweet receptor, a divergent leptin system, and distinct microbiota composition; these traits necessitate a species-specific framework for appetite control. This narrative review synthesizes current knowledge on how peripheral signals from the gastrointestinal tract, pancreas, liver, adipose tissue, and microbiota are encoded and conveyed to central command centers to regulate feed intake in poultry. We first outline nutrient sensing and gut-derived hormones with complex or divergent actions in birds (ghrelin, peptide YY, somatostatin), then summarize canonical satiety peptides (cholecystokinin, proglucagon-derived peptides, amylin, bombesin-like peptides, and neuromedin U) and long-term metabolic cues (leptin, insulin, insulin-like growth factors, liver-expressed antimicrobial peptide-2). At the central level, we describe how arcuate neuropeptide Y/agouti-related peptide (NPY/AgRP) and pro-opiomelanocortin/cocaine- and amphetamine-regulated transcript (POMC/CART) neurons, downstream hypothalamic nuclei, and brainstem relays integrate these inputs into a dynamic balance between opposing orexigenic and anorexigenic neurochemical effector pathways. Finally, we link these mechanistic insights to potential practical strategies for improving feed conversion, reducing metabolic disease, and enhancing resilience to environmental stressors. These strategies include dietary and microbiota-targeted interventions, receptor-level modulation, and the use of divergent genetic lines.

Pegiviruses are generally regarded as non-pathogenic viruses with controversial clinical significance. Here, we describe an avian pegivirus (partridge pegivirus, ParPgV) associated with field outbreaks of encephalitis in red-legged partridges (Alectoris rufa). Next-generation sequencing identified ParPgV in brain tissues, revealing two distinct avian-origin pegiviruses. Histopathology and electron microscopy revealed encephalitic lesions, neuronal degeneration, and viral particles within neurons. Field surveillance demonstrated widespread vertical transmission across multiple partridge flocks. Experimental inoculation of red-legged partridges, grey partridges, and specific-pathogen-free chickens demonstrated viral neurotropism and systemic distribution with differences in humoral immune response. Infected red-legged partridges developed cerebellar atrophy detectable by MRI. Detection of negative-strand RNA replication intermediates confirmed active viral replication across different experimental hosts, and RNAscope in situ hybridization and immunohistochemistry further confirmed viral RNA and antigen in neural and lymphoid tissues. Here, we show experimental evidence supporting an association between a pegivirus and encephalitis, and suggest underappreciated neuropathogenic potential.

Urban expansion threatens avian biodiversity in high-density cities globally, requiring strategies to enhance habitat connectivity through small-scale interventions. However, conventional ecological network planning often prioritizes biophysical metrics, overlooking the social values and public preferences that shape the long-term acceptance and success of conservation measures. To address this gap, this study integrates public bird preference data with ecological network modeling. Beijing, a megacity characterized by intense urbanization and active biodiversity governance, was selected as a representative case to test this socio-ecological approach. Citizen science observations (2015-2025) of 15 resident-favored bird species were combined with 35 environmental factors to assess habitat suitability for six functional avian groups using Maximum Entropy modeling (AUC: 0.756-0.897). Circuit theory analysis delineated an ecological network of 127 core sources, 260 stepping stones, and 1009 corridors, demonstrating substantial spatial overlap with the existing protected zones of the Beijing Garden City Nature Belts. Multi-scenario simulations showed that compared to random or patch-size-prioritized removal, conserving high-centrality stepping stones delayed connectivity decline and fragmentation by over 60% and preserved 68.6% of post-collapse connectivity. Building on these findings, we propose a three-tiered protection strategy for popular species, ranging from strict protection to adaptive management. In conclusion, by fundamentally shifting public preference from a peripheral to a central input in network analysis, this study establishes a novel, socially informed conservation framework. This integration enables precise identification of critical stepping stones and yields an actionable, prioritized conservation blueprint, thereby enhancing the practical relevance and implementability of ecological network designs for advancing bird-friendly cities worldwide.

Avian influenza virus (AIV) poses a persistent threat to poultry health and food security, with conventional control measures offering limited protection. A promising alternative is the use of gene editing to generate host resistance by ablating viral entry receptors or cellular proteins that are required for completion of the viral life cycle. The solute carrier family 35 member A1 (SLC35A1) gene encodes a Golgi-localized CMP-sialic acid transporter that is a key step in the sialylation of glycoproteins. In this study, we used the CRISPR/Cas9 system to disrupt SLC35A1 in chicken DF-1 fibroblasts and evaluated the effect on sialic acid expression and susceptibility to different strains of AIV. Lectin staining and flow cytometry confirmed a significant reduction in α2,3-linked sialic acids in SLC35A1 knockout cells, while α2,6-linked sialic acids were absent in the cells regardless of genotype. Infection experiments with three avian influenza virus strains (H5N1/PR8, H5N2, and H7N1) revealed that SLC35A1 knockout reduced viral replication in a strain-specific manner. Knockout cells infected with H5N1/PR8 showed the greatest dependence on SLC35A1-mediated sialylation with decreased viral load at 24 hours post-infection (hpi) and 48 hpi compared to wildtype cells and no observable viral growth between the timepoints. Infection of knockout cells with H5N2 resulted in a modest decrease in viral load at both timepoints as well as absence of viral growth. On the other hand, infection of knockout cells with H7N1 resulted in decreased viral load only at 48 hpi compared to wildtype cells, but the amount of virus in knockout cultures increased from 24 hpi to 48 hpi. These results demonstrate that SLC35A1 is a key host factor that supports AIV entry via α2,3-linked sialic acids; however, viral dependency on this host factor may be confounded by strain.

Avian infectious bronchitis virus (IBV) infection causes growth suppression in broilers, which has been hypothesized to involve a diversion of metabolic resources from growth toward immune defense. This study evaluated the efficacy and molecular mechanisms of Qingfei Huatan Formula (QHF) in IBV-challenged broilers. A total of 180 Yellow-feathered broilers were randomly assigned to a blank control, IBV-challenged (M41 strain), Ribavirin, and QHF dose-gradient groups. High-dose QHF intervention significantly increased body weight gain (BWG) at 14 days post-infection compared with the IBV model group (P < 0.05), reaching a level comparable to the blank control. This growth recovery was associated with reduced viral copy numbers in the trachea and lungs at 3 dpi. Mechanistically, high-dose QHF reduced serum IL-1&#x3b2; (P < 0.05) and increased total antioxidant capacity (T-AOC) (P < 0.05). Systems pharmacology identified quercetin, baicalein, and nobiletin as core active components, with predicted binding affinities of -8.53 kcal/mol for quercetin with TP53 and -6.38 kcal/mol for quercetin with IBV Mpro. Pearson correlation analysis showed a negative correlation between viral load/inflammatory markers and BWG. These findings indicate that QHF alleviates IBV-induced growth suppression, likely by reducing the metabolic demand of immune activation.

The global outbreak of highly pathogenic avian influenza (HPAI) A(H5N1) among birds and the spillover to mammals increases the risk for humans. A recent case in British Columbia with a clade 2.3.4.4b H5 virus infection revealed a mixture of 226Q/H in the receptor-binding site of hemagglutinin. While significant changes in pre-existing immunity by H1 or H3 polyclonal sera are not evident, we show that the Q226H mutation enables binding to human-type a2-6 sialic acid receptors. High-resolution cryo-EM structures provide a basis for the alteration in receptor preference and show that a possible path towards human adaptation also requires a conformational change of the bound a2-6-sialylated glycan. Continued surveillance for additional mutations that could enhance this phenotype is warranted.

Mycotoxin contamination in poultry feed, particularly aflatoxin B1 (AFB1) and ochratoxin-A (OTA), induces immunosuppression and compromises vaccine efficacy, leading to substantial economic losses in broiler production. Avian influenza (AI) remains endemic in several poultry-producing regions, where vaccination is the primary control strategy. However, impaired immune responses due to mycotoxin exposure frequently result in vaccination failure. This study aimed to evaluate the efficacy of a combined mycotoxin-detoxifier containing bentonite and Trichosporon mycotoxinivorans in restoring humoral immune responses to AI vaccination and mitigating histopathological lesions in broilers exposed to AFB1 and OTA. A total of 40 broiler chickens were randomly assigned to four groups: negative control (C-), positive control (C+), treatment 1 (T1; 1.1 g/kg detoxifier), and treatment 2 (T2; 1.6 g/kg detoxifier). Groups C+, T1, and T2 received feed contaminated with AFB1 and OTA (0.1 mg/kg each). Birds were vaccinated against AI at 7 days with a booster at 21 days. Antibody titers were measured by hemagglutination inhibition at 14, 21, 28, and 35 days. Histopathological evaluations of the proventriculus and bursa of Fabricius were conducted on day 35. Parametric and non-parametric statistical analyses were applied with significance set at p < 0.05. Antibody titers were significantly reduced in the mycotoxin-exposed group (C+) compared to the negative control (C-) at all post-vaccination time points. Supplementation with the detoxifier significantly improved antibody titers, particularly in T2, with values comparable to those of the negative control. Histopathological analysis revealed severe inflammatory cell infiltration, oxyntico-peptic cell necrosis, and degeneration in C+, whereas T1 and T2 groups demonstrated significant amelioration of lesions, with T2 showing the greatest protective effect. Similarly, lymphoid follicle depletion and necrosis in the bursa of Fabricius were markedly reduced in detoxifier-treated groups. Dietary supplementation with a mycotoxin-detoxifier, particularly at 1.6 g/kg, effectively mitigates the immunosuppressive effects of AFB1 and OTA, enhances humoral responses to AI vaccination, and reduces histopathological damage in broilers. This strategy represents a practical and effective approach to improving poultry health and vaccine performance under mycotoxin-contaminated conditions.

The nucleocapsid (N) protein of infectious bronchitis virus (IBV) is the most abundant viral protein in infected cells and is essential for virion assembly and for modulating host cellular processes. Although previous studies have reported nucleolar accumulation of IBV N, a comprehensive mapping of its nucleolar localization signals (NoLSs) is lacking. Here, we systematically mapped functional NoLSs within the IBV N protein and evaluated their contributions to viral replication. Under both infection and transient-transfection conditions, the N protein exhibited a dual cytoplasmic-nucleolar distribution. Analysis of EGFP-tagged N protein truncation mutants identified four candidate NoLSs (NoLS1-4) and a nuclear localization signal (NLS). Alanine-scanning mutagenesis established that NoLS3 (amino acids [aa] 330-349) and NoLS4 (aa 356-368) were the principal determinants of nucleolar targeting within the full-length protein, with this activity depending on basic residue clusters 2 and 3 in NoLS3 and cluster 1 in NoLS4. Recombinant virus rescue assays demonstrated that the double mutant strain (rYN-N-K356A/R359A) abolished nucleolar accumulation of N protein and showed significantly decreased replication levels at 24 and 36 h post-infection. Collectively, this study identifies specific basic residues in NoLS3 and NoLS4 as the molecular basis for IBV N nucleolar localization and demonstrates that nucleolar targeting is required for optimal IBV replication. Avian infectious bronchitis virus (IBV) is a highly contagious pathogen that causes severe economic losses to the global poultry industry. While the N protein is known to localize to the nucleolus, the precise sequences of its NoLSs and their impact on viral replication, remain unclear. This study systematically identified the functional NoLSs of the IBV N protein and the essential basic residues within them. Crucially, we demonstrated that the nucleolar localization of the N protein plays an important role in viral replication. Furthermore, elucidating the specific motifs required for N protein functionality may inform the rational design of live-attenuated vaccines or antiviral approaches against IBV.

Avian pathogenic Escherichia coli (APEC) is a major cause of colibacillosis in broiler chickens, leading to systemic inflammation, organ dysfunction, disrupted lipid metabolism, and compromised meat quality. Growing concerns about antimicrobial resistance necessitate the development of sustainable alternatives to antibiotic growth promoters. Myrmecodia sp., a medicinal plant rich in bioactive flavonoids, tannins, and phenolics, has demonstrated antibacterial and antioxidant properties. However, limited information is available on the comparative effects of different preparation forms on organ function and lipid metabolism under APEC challenge conditions. This study aimed to evaluate the effects of Myrmecodia sp. extract and infusion on liver and kidney biomarkers, serum lipid profile, and meat lipid composition in APEC-infected broiler chickens. A total of 56 male Lohmann MB 202 broiler chickens were randomly assigned to seven groups: negative control, positive APEC-infected control, antibiotic control (zinc bacitracin), two extract treatments (15% and 30%), and two infusion treatments (1% and 2%). Treatments were administered from day 8 to day 35, and APEC infection was induced orally on day 21. Measured parameters included serum glutamate pyruvate transaminase (SGPT), serum glutamate oxaloacetate transaminase (SGOT), blood urea nitrogen (BUN), creatinine, low-density lipoprotein (LDL), high-density lipoprotein (HDL), and meat LDL and HDL. Data were analyzed using one-way analysis of variance followed by Duncan's multiple range test (p < 0.05). APEC infection significantly increased SGPT, SGOT, BUN, creatinine, and LDL levels while decreasing HDL levels (p < 0.05). Supplementation with Myrmecodia sp. extract and infusion significantly improved all evaluated parameters compared with the positive control (p < 0.05). Among treatments, the 1% infusion consistently produced the most favorable effects, including reduced liver enzyme activity, improved renal function, decreased LDL levels, and increased HDL levels in both serum and meat. Myrmecodia sp., particularly in infusion form, demonstrated protective effects on organ function and lipid metabolism in broilers infected with APEC. These findings support its potential as a phytogenic alternative to antibiotics in sustainable poultry production systems within a One Health framework.

In 2024, we identified and sequenced 52 avian influenza A (H9N2) virus strains in Laos. Using the established H9N2 genomic classification system, a novel HA gene clade of the A/chicken/Beijing/1/94-like (BJ/94-like) lineage, designated Clade 4.6.20, was identified. This new clade is phylogenetically distinct from the previously described clades, and the representative strains in this new Clade 4.6.20 presented a low cross reactivity to the antisera of other clades, suggesting antigenic drift of the viruses between the new Clade 4.6.20, and other clades in the dominant lineage of Clade 4.6. In addition, all the newly identified viruses in Clade 4.6.20 possessed HA-L226 and NP-N52 mutations, which are associated with human-type receptor binding and human MxA-related innate immunity escape, respectively. Our findings underscore the necessity of global surveillance network and cooperation to monitor the evolution of AIVs, update vaccine seed strains, and develop new vaccines with high effectiveness against H9N2 AIVs circulating globally, which threaten poultry and human health.

High pathogenicity avian influenza (HPAI) has caused widespread sickness and mortality in wildlife, especially since the emergence of a novel H5 virus belonging to clade 2.3.4.4b in 2021. The ongoing panzootic caused by this lineage has infected an unprecedented diversity of species across the globe, seeming capable of impacting all birds. Here, we analyse ecological and phylogenetic patterns in outbreak notifications of HPAI, and predict host susceptibility to HPAI disease for Australia as the only continent thus far unaffected by this panzootic. We found a significant family-level phylogenetic signal, showcasing that the panzootic is not impacting all birds equally, but ecological traits did not improve predictive power. Using the family-level phylogeny, we predict that families of Australian seabirds, shorebirds, and waterbirds will be most susceptible to HPAI once it arrives on the continent. Our results provide an empirical indication of species susceptible to HPAI H5N1, which can be used to direct monitoring efforts and disease management globally. With special reference to Australia, our predictions can be used alongside conservation status and species-specific information to inform preparedness activities, monitoring, and response upon incursion.

This study provides the first comprehensive PPP model for livestock disease surveillance in Korea. Highly pathogenic avian influenza (HPAI) outbreaks have increased globally, placing growing pressure on veterinary services. In the Republic of Korea, the proportion of unfilled public veterinary positions rose from 29.5% in 2019-41.4% in 2023. This study proposes a public-private partnership (PPP) framework for HPAI surveillance using the World Organisation for Animal Health (WOAH) PPP framework. We analyzed international PPP models from Australia's Emergency Animal Disease Response Agreement, Japan's focus-area system, and the European Union's SIGMA project. We also evaluated a 2024 pilot project conducted by three private testing facilities across four provinces and covering 267 farms, using WOAH's 44 evaluation criteria. The international comparison showed diverse PPP approaches emphasizing government-industry cost sharing, inter-ministerial coordination, and automated reporting systems. The Korean pilot project revealed major challenges, including farmer non-cooperation, regulatory constraints, and limited private facility capacity. Gap analysis identified major deficiencies in the legal framework, resource allocation, and information sharing domains. Based on these findings, we propose a phased Korean PPP model with clearly defined roles: MAFRA for policy coordination, APQA for technical support and confirmatory testing, provincial laboratories for supervision, and private facilities for M-gene screening. Successful implementation will require clear legal authority, sustainable funding, quality assurance through ISO 17025 certification, and improved information sharing via the Korea Animal Health Integrated System (KAHIS). This study provides the first comprehensive PPP model for livestock disease surveillance in Korea.

This study investigated the chemical composition and antibacterial and antibiofilm activities of Cymbopogon flexuosus essential oil (CFEO) against multidrug-resistant (MDR) bacteria within a One Health framework. The bacterial panel comprised four clinical isolates (n&#x2009;=&#x2009;1 per source): a methicillin-resistant Mammaliicoccus sciuri (MR-M. sciuri) from bovine mastitis, a colistin-resistant ESBL-producing Escherichia coli (E. coli) from avian colibacillosis, and MR-Staphylococcus haemolyticus (MR-S. haemolyticus) and MDR Staphylococcus aureus (MDR S. aureus) from healthy farm personnel in contact with diseased animals. GC-MS analysis was performed to study the chemical composition of the CFEO. Antibacterial activities were evaluated via disk diffusion and broth microdilution assays. Disk diffusion was used exclusively as a qualitative screening tool to identify potential interactions; synergy was assessed definitively through the checkerboard assay by calculating the Fractional Inhibitory Concentration Index (FICI). The antibiofilm activity of CFEO was quantified via Congo red agar, crystal violet staining, and light microscopy. Molecular docking simulation was performed to assess the binding interactions of the CFEO constituents with key bacterial proteins. The major constituents of CFEO were geranial (&#x3b1;-citral; 32.98%), neral (&#x3b2;-citral; 28.62%), &#x3b2;-terpinene (11.50%), geraniol (5.42%), nerol acetate (3.40%), and linalool (2.31%). The inhibition zones ranged from 38&#x2009;&#xb1;&#x2009;2.00 to 56&#x2009;&#xb1;&#x2009;1.00&#xa0;mm, while the MIC values spanned from 8 to 8192&#xa0;&#xb5;g/mL. CFEO demonstrated a synergistic effect with oxacillin against MR-M. sciuri (FICI&#x2009;=&#x2009;0.28). Sub-MIC concentrations of CFEO significantly disrupted the biofilms of M. sciuri and E. coli. Bioinformatics analysis via molecular docking revealed favorable binding affinities between major compounds of CFEO and key bacterial proteins, including PBP2a, SarA, and AgrA. This study highlights the in vitro efficacy of CFEO against MDR, MR and biofilm-forming bacteria circulating at the animal-human interface, as well as its synergistic potential when combined with oxacillin against MR-M. sciuri. Molecular docking analyses suggest that the major compounds of CFEO may act as promising adjuvants in the development of new therapeutic strategies against MDR bacteria within a One Health framework.

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Social interactions are ubiquitous in nature and have the potential to affect trait evolution, particularly in group-living animals such as cooperative breeders. Interactions among conspecific individuals can affect the amount of additive genetic variation for a trait when the phenotype of an individual is also affected by the genotype of its social partner(s) via indirect genetic effects. Thus, quantifying both direct and indirect genetic effects of social partners is critical for understanding and predicting evolutionary trajectories. While much is known about maternal indirect genetic effects, empirical estimates of indirect genetic effects from other social partners remain limited, particularly in wild populations. Here, we use animal models to assess the contribution of indirect genetic effects from all social partners in a family group (mothers, fathers, and helpers) on juvenile morphometric traits across ontogeny in the cooperatively-breeding Florida scrub-jay ( Aphelocoma coerulescens ). We found indirect genetic effects of helpers and fathers on nestling weight, but no indirect genetic effect of mothers. Across ontogeny, we found increasing additive genetic variation in both weight and tarsus length. Our study provides a comprehensive assessment of within-group indirect genetic effects in a cooperative breeder and highlights the importance of considering indirect genetic effects beyond maternal effects.