Search Results (29,687)

Measles virus infection couples nonlinear processes across biological scales, including within-host viral amplification, immune-cell depletion, delayed adaptive control, persistent viral RNA, heterogeneous host severity and vaccination-dependent population spread. A multiscale mathematical framework is developed by coupling a seven-variable within-host ordinary differential equation model to a stochastic cellular automaton. The within-host system extends a four-variable measles immunodynamics core by including IFN-$\gamma$-dominant and IL-17-associated immune responses, persistent viral RNA and neutralizing antibodies. Six host archetypes are represented as structured parameter perturbations of this common dynamical core. The principal novelty is an explicit cross-scale coupling operator that separates genuinely ODE-derived host descriptors from hybrid epidemiological mapping rules and independently specified population-level contact and susceptibility assumptions, allowing within-host heterogeneity to propagate transparently into a spatial stochastic epidemic model. An explicit ODE-to-cellular-automaton map translates within-host trajectories into infectious timing, daily infectivity profiles and an illustrative ODE-informed severity-to-death transition mapping used internally by the cellular automaton. The mortality map depends on viral burden, infectious duration, IFN-$\gamma$ deficit, cumulative infectivity and an immune-deficit–infectivity interaction term. Population simulations show a nonlinear reduction in attack rate with increasing vaccination coverage, reduced modeled death burden under targeted high-risk in silico perturbations and additional suppression under reactive vaccination campaigns. A direct local cellular-automaton secondary-infection estimate is reported instead of interpreting cumulative infectivity burden as a reproduction number. A targeted contact-structure sensitivity further shows that matching the expected local direct-secondary-infection potential does not imply equivalent population-level attack rates, emphasizing that the quantitative CA outcomes are geometry specific. Sobol sensitivity analysis with convergence up to $N_{\mathrm{base}}=4096$ identifies core viral and immune parameters as dominant drivers of within-host and multiscale outputs. The framework provides an explicit dynamical-systems approach for coupling differential-equation immunodynamics to spatial stochastic population models in mathematical biology. Full article

The functions of most proteins encoded by the African swine fever virus (ASFV) remain largely unknown, although several have been reported to possess immunomodulatory properties. Among these, we identified that the DP71L protein exerts an inhibitory effect on inflammatory bowel disease. To investigate its protective role in murine colitis, we constructed and expressed a recombinant DP71L protein. Colitis was induced in mice using DSS, and the effects of DP71L treatment were evaluated by assessing histopathological changes, inflammatory cytokine profiles, oxidative stress markers, colonic tissue pathology, and the expression of tight-junction proteins (claudin-1, occludin, and ZO-1). Our results showed that DP71L intervention significantly attenuated body weight loss and organ damage and ameliorated DSS-induced colonic histopathological injury. Moreover, DP71L treatment markedly increased superoxide dismutase (SOD) activity and reduced malondialdehyde (MDA) content in colonic tissues. Mechanistically, DP71L suppressed both DSS-induced NF-κB and JAK-STAT activation and concurrently inhibited DSS-induced epithelial cell apoptosis. These events likely underlie the observed reduction in pro-inflammatory cytokines (IL-1β, IL-6, IFN-γ, and TNF-α) and the restoration of tight-junction protein expression, as DP71L treatment effectively prevented DSS-induced downregulation of claudin-1, occludin, and ZO-1, while also promoting the anti-inflammatory cytokines IL-10 and TGF-β. Collectively, our findings demonstrate that DP71L effectively inhibits the progression of murine colitis through coordinated anti-inflammatory and anti-apoptotic mechanisms. This study suggests that DP71L may function as a potential immunosuppressant, opening new avenues for the application of viral proteins in the treatment of immune-related disorders. Full article

Background: Amikacin is an effective aminoglycoside antibiotic, but its clinical use is limited by nephrotoxicity, hepatotoxicity, and neurotoxicity. N-acetylcysteine (NAC), a glutathione precursor and antioxidant, may help reduce these side effects. This study evaluated whether NAC attenuated selected amikacin-induced biochemical, inflammatory, and histopathological alterations in mice. Methods: Male Swiss albino mice were divided into four groups: control, amikacin, NAC, and amikacin−NAC, and the behavioral performance was assessed using the light–dark box test. Serum samples were collected for measurements of kidney and liver biomarkers, metabolic markers, and electrolytes (calcium, inorganic phosphate, and uric acid). A multiplex cytokine/chemokine panel was used to assess the effects of amikacin with/without NAC on systemic inflammation. Results: Amikacin-treated mice showed a reduction in the time spent in the light area, and this effect was improved by NAC. Amikacin also altered certain biochemistry parameters, increasing levels of aspartate transferase and albumin; these changes were attenuated by NAC. Amikacin caused marked increases in certain inflammatory cytokines and chemokines, including IL-6, IL-12p70, IL-22, IL-18, CXCL10, and CCL11. Treatment with NAC lowered IL-6, IL-12p70, IL-22, IL-18, CXCL10, and CCL11. The sparse partial least squares discriminant and heatmap analysis of the serum inflammatory profile revealed segregation of the amikacin group from the other three groups. Importantly, the histopathological assays on renal and cerebral cortex showed NAC caused improvements, with well-shaped tissues, attenuating the cortical histopathological alterations observed in animals treated with amikacin. Conclusions: These findings suggest that NAC may have the potential to attenuate certain biochemical, inflammatory, and histopathological alterations associated with high-dose amikacin exposure. Full article

Urbanisation is a major driver of environmental contamination, yet its physiological consequences for amphibians in rapidly developing regions remain poorly understood. This study investigated spatial variation in heavy-metal bioaccumulation and associated physiological stress biomarkers in Bufo regularis along an urban–rural gradient in Southwestern Nigeria. Adult toads were sampled from Osogbo, Ile-Ife, and Modakeke sites, and concentrations of selected heavy metals (including Pb, Cd, Zn, Cu, and Cr) were quantified in liver and muscle tissues. To assess sublethal biological effects, oxidative stress biomarkers superoxide dismutase (SOD), catalase (CAT), glutathione-S-transferase (GST), reduced glutathione (GSH), and lipid peroxidation (malondialdehyde, MDA) were analysed alongside body condition indices. Heavy-metal concentrations were significantly higher in individuals from Osogbo sites than in those from Ile-Ife and Modakeke locations, with Pb and Cd showing the strongest spatial gradients. Correspondingly, Osogbo populations exhibited elevated antioxidant enzyme activities and MDA levels, indicating heightened oxidative stress, while GSH levels and body condition indices were reduced. These findings demonstrate that B. regularis effectively reflects spatial patterns of metal pollution and associated biological effects across land-use gradients. The study highlights the utility of amphibians as bioindicators of urban environmental health and underscores the potential long-term ecological consequences of metal contamination in tropical urbanising landscapes. Full article

Background/Objectives: Persistent neuroinflammation, oxidative imbalance, and neuronal apoptosis are key mechanisms underlying memory loss and working-memory impairment in many neurodegenerative conditions. LTG, an established anticonvulsant recognized for its glutamate-modulating and immune-dampening actions, has been reported to exert neuroprotective actions beyond seizure control. This study investigated whether LTG can counteract LPS-induced deficits in cognition and neuroinflammatory responses in rats by modulating oxidative stress- and apoptosis-related markers. Methods: A total of twenty-four rats were allocated into four different groups: Control, LPS, LTG, and LTG + LPS. LTG (30 mg/kg, orally) was administered for 15 days, whereas LPS (1 mg/kg, intraperitoneally) was administered during the final four days to provoke neuroinflammation. Working memory abilities were assessed utilizing the Y-maze spontaneous alternation test. Subsequently, brain tissues were analyzed for inflammatory mediators (COX-2, TNF-α, IL-6), apoptotic markers (Caspase-3, Bcl-2, BAX), and oxidative stress indicators (MDA, GSH, catalase). Results: LPS exposure produced significant memory deterioration, accompanied by elevated COX-2, TNF-α, IL-6, and MDA levels, along with reduced GSH and catalase activity, indicating oxidative and inflammatory stress. BAX and Caspase-3 expression were markedly enhanced, whereas Bcl-2 expression was significantly reduced. Pretreatment with LTG markedly attenuated the LPS-induced decline in Y-maze performance, cytokine elevation, and alterations in redox and apoptotic parameters. Conclusions: LTG effectively attenuated LPS-induced cognitive impairment and neuroinflammatory responses, accompanied by improvements in oxidative stress- and apoptosis-related markers. These findings support further investigation of the potential preventive or neuroprotective effects of LTG against neuroinflammation-associated working-memory impairment. Full article

Persistent inflammation driven by excessive AKR1B1 activation contributes to the progression of multiple chronic inflammatory diseases. Natural chlorogenic acid (CGA) exhibits anti-inflammatory activity but suffers from poor membrane permeability, while its laurate ester derivative (CGL) shows clear dose-dependent cytotoxicity in macrophages. Here, we synthesized a novel chlorogenic acid amide derivative (CGAA) by selective amidation of the aliphatic carboxyl group on the quinic acid moiety of CGA, fully preserving the chiral polyphenol scaffold. Structural identity was confirmed by HSQC, HMBC, FTIR and HR-ESI-MS. CCK-8 assays demonstrated that CGAA maintained > 95% viability of RAW264.7 cells at 100 μM, displaying markedly superior cellular safety relative to CGL. In LPS-stimulated RAW264.7 macrophages, CGAA dose-dependently suppressed NO, TNF-α and IL-6 production and exhibited stronger antioxidant activity than both CGA and CGL. Temperature-gradient CETSA, DARTS and enzymatic assays established direct binding and potent inhibition of AKR1B1 by CGAA (IC₅₀ = 7.85 μM). Molecular docking revealed that the newly introduced amide forms an additional hydrogen bond with ILE-260, enhancing ligand–target affinity. This carboxyl-amidation strategy simultaneously improves the cellular safety and AKR1B1 inhibitory potency of CGA, providing a rational approach for developing low-toxicity polyphenol-based anti-inflammatory leads. Full article

Objectives: We tested whether a database-derived phthalate ester (PAE)–ankylosing spondylitis (AS) candidate panel identifies an inflammatory transcriptional program and characterized its transcription-factor (TF) architecture. Methods: Machine learning prioritization and repeated nested cross-validation were followed by locked-model transfer from GSE73754 to GSE25101. Donor-level single-cell analyses included 96,746 peripheral blood mononuclear cells from 10 AS and 29 healthy-control donors (GSE194315), with corroboration assessed in 25 additional baseline AS patients (GSE277117). Results: Within classical monocytes, the continuous signature covaried with panel-excluded TNF-α/NF-κB signaling (ρ = 0.571; q = 0.000729), inflammatory response (ρ = 0.447; q = 0.0108), and eight of 10 AP-1-related TF activities. Target-excluded TF activities covaried with CXCL8 (8/10) and IL1B (10/10). AP-1-gene/CXCL8 co-expression received partial corroboration in the additional AS cohort (JUN–CXCL8: ρ = 0.92). Among 16 genes prioritized from 473 shared candidates, CXCL8, IL2RB, STAT5B and TNF were stable. The locked 14-gene model achieved an area under the receiver-operating-characteristic curve of 0.770 (DeLong 95% confidence interval, 0.596–0.943), supporting partial rank transportability. Secondary analyses showed a lower CD56bright fraction among natural killer (NK) cells in AS (−2.699 percentage points; 95% confidence interval, −4.575 to −0.611; q = 0.0498) and reduced NK-cell JUN expression (log₂ fold change = −0.995; adjusted p = 0.0497). Conclusions: The PAE–AS signature identifies an AP-1/CXCL8-associated classical-monocyte inflammatory program, with partial cross-cohort corroboration and secondary NK alterations, providing candidates for exposure-informed mechanistic studies. Full article

Bisphenol A (BPA) is a widespread plasticizer widely used in the food industry worldwide. However, a consensus on the safe level of its daily intake does not currently exist, while there are numerous data pointing to a link between prenatal exposure to BPA and early neuropsychiatric disorders, such as autism spectrum disorder (ASD) and attention deficit hyperactivity disorder (ADHD). The global average human-equivalent dose of BPA is estimated at 30 ng/kg body weight/day. Thus, the research herein was conducted on newborn and juvenile rat offspring of both sexes delivered from rats treated with 30 ng/kg body weight/day orally from day 6 to 21 of pregnancy and for a further 21 days during lactation. Our data indicate that prenatal exposure to 30 ng/kg/day from gestation day 6 to delivery induced sexually dimorphic, region-specific alterations in the neonatal (PD1) rat brains, impacting inflammatory reactions, estrogen receptor signaling, and neural progenitor dynamics. Prenatally BPA-treated males exhibited a pro-inflammatory state characterized by an increased total number of ramified Iba1+ microglia cells in the hippocampus alongside upregulation of Aif1, Nfkb, Tnf, Il1b, and Hif1a. Conversely, prenatally BPA-treated females showed only an increased total number of hippocampal Iba1+ cells and displayed inflammatory resilience, lacking upregulation of these markers. Both sexes exhibited a pro-inflammatory state in the prefrontal cortex via upregulation of Nfkb, Tnf, Il1b, and Hif1a. While both sexes showed decreased Tgfb in the prefrontal cortex, they deployed distinct compensatory responses: males upregulated the neuroprotector Igf1 only in the hippocampus, whereas in females, it was upregulated in both the hippocampus and the prefrontal cortex. Estrogen receptor expression was also highly dimorphic. In the hippocampus, males displayed an imbalance via Esr1 upregulation and Esr2 downregulation, while females showed Esr2 downregulation alone. In the prefrontal cortex, these transcriptional profiles were the opposite. Finally, neural progenitor markers were altered. In the prefrontal cortex, BPA drove the upregulation of Sox2 and Pax6 in males but Sox9 in females; in the hippocampus, only Pax6 was upregulated, and only in males. The PAX6 protein level in the hippocampus was significantly increased in males but decreased in females. In juvenile offspring (PD21), behavioral patterns characterized by hyper-exploration, increased environmental investigation, and heightened emotional reactivity during social exposure were more pronounced in female offspring. These baseline neonatal disparities followed by behavioral changes underscore the necessity of sex-specific approaches when evaluating early-life neurodevelopment and subsequent adult behavioral and biological vulnerabilities. Full article

This study examined Toll-like receptors (TLRs)/chemokine receptors (CCRs) gene expression levels in HIV-infected individuals at different stages of HIV infection. It has been demonstrated that in the advanced stages of HIV infection, aggravated by Mycobacterium tuberculosis (M. tuberculosis) infection, there was a significant increase in TLR2, TLR4, TLR7, and TLR9 expression levels (181-, 8.4-, 15-, and 3.4-fold, respectively), compared to the early stages of the disease, which also correlated with an increase in viral load. The advanced stages of HIV infection were also characterized by an increased CCR5 expression level (8.08-fold, p < 0.0001) on patients’ mononuclear cells, which was not observed in the early stages of the disease. A positive correlation was found between the enhanced levels of TLR2/TLR4 and CCR5 expression, which facilitates the entry of HIV-1 into the cell (r = 0.03564, p = 0.0423 for TLR2/TLR4; r = 0.3793, p = 0.0269 for CCR5). The advanced stages of HIV infection were characterized by a sharp increase in the expression levels of CXCR4 and CCR8 co-receptors which also play an important role in the entry of HIV-1 into the host cell (more than 537-fold, p = 0.0006, and 5000-fold, p = 0.004, respectively). At the advanced stages of HIV infection, a positive correlation was found between increased production of TLR and CCR and elevated expression of IL-12 and IL-18. These factors contribute to virus persistence and chronic immune activation observed in patients with opportunistic infections. Thus, the obtained data indicate that HIV-1 in the advanced stages of infection induces an increased TLRs; CCRs expression, which, together with enhanced viral production, leads to chronic inflammation and can contribute to tissue damage and exacerbate the disease’s progression. Full article

Ginsenoside Rh2, a protopanaxadiol-type saponin derived from Panax ginseng, exhibits a broad spectrum of biological activities; however, its specific mechanisms in asthma remain elusive. In this study, we systematically evaluated the therapeutic efficacy of Rh2 against asthma using both in vitro and in vivo models. A lipopolysaccharide (LPS)-induced in vitro cell model was established and treated with low, medium, and high doses of Rh2 (1, 5, and 10 μg/mL). Concurrently, an in vivo asthma model was constructed via ovalbumin (OVA) sensitization and administered with three doses of Rh2 (2.5, 5, and 10 mg/kg). The results demonstrated that Rh2 significantly suppressed pro-inflammatory cytokines (interleukin-4 [IL-4], interleukin-5 [IL-5], interleukin-13 [IL-13], interleukin-33 [IL-33], and tumor necrosis factor-α [TNF-α]) and upregulated anti-inflammatory factors (interferon-γ [IFN-γ] and interleukin-10 [IL-10]) in both experimental models. Furthermore, Rh2 inhibited the expression of key inflammatory pathway proteins, including suppression of tumorigenicity 2 (ST2), Toll-like receptor 4 (TLR4), myeloid differentiation primary response 88 (MyD88), nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), and c-Jun N-terminal kinase (JNK). Transcriptomic and metabolomic analyses revealed that Rh2 primarily modulates the TNF-α signaling pathway, cytokine–cytokine receptor interaction, pyrimidine metabolism, and glycine, serine, and threonine metabolism. Integrated analysis further identified significant correlations between differentially expressed genes (C-X-C motif chemokine ligand 2 [CXCL2], C-X-C motif chemokine ligand 17 [CXCL17], and leukemia inhibitory factor [LIF]) and differential metabolites (cytosine, L-histidine, and creatine). Collectively, these findings suggest that ginsenoside Rh2 ameliorates asthma by modulating cytokine interactions and amino acid metabolism. Full article

Immunodeficient and humanized mouse models have become essential tools for investigating human immunity, disease pathogenesis, and therapeutic evaluation. This review summarizes the stepwise evolution of these platforms, from nude and SCID mice to advanced NOD/SCID/Il2rg^null strains (NCG, NSG, or NOG), and highlights how progressive removal of murine immune barriers has improved human cell engraftment and experimental utility. Major humanized immune system (HIS) approaches, including Hu-PBMC/PBL, Hu-HSC, and Hu-BLT models, are compared with respect to engraftment kinetics, immune composition, graft-versus-host disease, and suitability for distinct research applications. Particular emphasis is placed on next-generation engineered strains that enhance specific human immune compartments, including cytokine-humanized models for myeloid, dendritic cell, natural killer cell, and neutrophil reconstitution; TSLP-based models that restore secondary lymphoid organogenesis and improve adaptive immune responses; and advanced HLA-humanized models. These advances have substantially expanded the value of humanized mice in studies of autoimmune disease, cancer immunotherapy, and vaccine evaluation. Nevertheless, no single model fully reproduces the complexity of the human immune system, and major limitations remain, including incomplete stromal humanization, restricted HLA diversity, and inter-model variability. Continued refinement will be critical for improving translational relevance and predictive power in vaccine and immunology research. Full article

Background/Objective: Insufficient research has examined the muscle damage and inflammatory effects of training performed in a fasted state with reduced (low) glycogen reserves. Methods: This study aimed to investigate the acute effects of exercise sessions performed under fasting (FST) and liquid nutrient-supplemented postprandial (PPD) conditions, as well as with full and reduced body glycogen stores, on muscle damage markers creatine kinase (CK) and lactate dehydrogenase (LDH), and the inflammatory marker interleukin-6 (IL-6). Eleven male amateur football players (mean age 19.91 ± 1.64 years) were included in the study. Participants performed a single 60 min aerobic endurance exercise session at 70% VO₂max under the liquid nutrient-supplemented PPD condition, and two 60 min sessions with a 60 min recovery interval under 10–12 h FST conditions. Data were analyzed using paired samples t-test, ANOVA, Wilcoxon, and Friedman tests, depending on parametric and nonparametric assumptions. Results: In pre-exercise (PRE-FE) measurements, no significant differences were observed between the FST and PPD conditions for GLU, CK, LDH, and IL-6 levels. In postexercise (POST-FE) measurements, GLU levels were significantly higher in the PPD condition than in the FST condition (p < 0.05), whereas LA, CK, LDH, and IL-6 levels did not differ significantly between the two conditions. In the FST condition, following the second exercise session performed with default reduced glycogen availability (POST-SE), CK levels significantly increased from 279.36 ± 16.7 U/L to 335.63 ± 20.3 U/L, LDH levels from 178.72 ± 38.1 U/L to 208.09 ± 50.7 U/L, and IL-6 levels from 2.60 ± 2.4 pg/mL to 8.69 ± 5.8 pg/mL (p < 0.05). In the PPD condition, no significant changes were observed in any of the parameters following a single exercise session (p > 0.05). Conclusions: The two-a-day training approach performed with default reduced glycogen availability may increase muscle damage and inflammatory responses. These findings are considered as an inference that low-glycogen training should not be implemented during the pre-competition period because of the risk of inducing muscle damage. Full article

Psoriasis is a chronic skin disease manifesting scaly, indurated erythema and an enhanced interleukin (IL)-23/IL-17 immune axis. A high-salt diet (HSD) is known to promote several autoimmune or autoinflammatory diseases. We examined whether an HSD might exacerbate topical imiquimod (IMQ)-induced psoriasis-like dermatitis in mice. Balb/c female mice were fed a normal diet (ND, 0.2% NaCl) or an HSD (4.2% NaCl) for 3 weeks, and 25 mg IMQ was applied to shaved back skin for 5 consecutive days. Compared to ND, the HSD exacerbated IMQ-induced psoriasiform dermatitis with increased scale, skin thickness, and total scores, and histologically enhanced epidermal thickening, hyperkeratosis, and dermal inflammatory infiltrates, including Ly6G+ neutrophils and CD3+ T cells. HSD increased mRNA levels of Il17a, Il22, Tnfa, Il1b, Il23a, Il23r, Cxcl1, Ccl20, Krt16, and Ccnd1 in IMQ-induced dermatitis. HSD increased the immunostaining areas of whole and Ser 422-phosphorylated forms of serum- and glucocorticoid-inducible kinase 1 (SGK1) in epidermal keratinocytes and dermal-infiltrating cells in IMQ-induced dermatitis. Intraperitoneal SGK1 inhibitor EMD638683 reversed the above effects of HSD in exacerbating IMQ-induced dermatitis. Our present results indicate that HSD may exacerbate murine IMQ-induced psoriasis-like dermatitis at least partially through the activation of SGK1. Full article

Background/Objectives: Streptococcus suis is an important zoonotic pathogen responsible for severe infections in animals and humans, and the emergence of diverse strains has reduced the effectiveness of conventional antimicrobial therapies. Since there is no broadly protective vaccine, there is a need for new vaccination strategies that focus on conserved antigens from a variety of strains. This study aimed to design and evaluate a multi-epitope vaccine candidate against diverse S. suis strains using an integrated pangenome-guided reverse vaccinology approach. Methods: To design a multi-epitope vaccine (MEV) candidate against diverse S. suis, an integrated computational framework was employed, incorporating pangenome analysis, subtractive proteomics, reverse vaccinology, immunoinformatics, structural modeling, molecular docking, molecular dynamics simulation, immune simulation, and in silico cloning. The conserved core proteins were systematically screened for essential, non-homologous, antigenic, non-allergenic and non-toxic vaccine candidates for epitope prediction. Results: A total of 7421 gene families, including 1169 conserved core genes, were identified through pangenome analysis of 24 complete S. suis genomes. Three computationally prioritized candidate proteins were identified through sequential subtractive proteomics: sucrose phosphorylase, peptidoglycan hydrolase PcsB and an RND transporter-associated adaptor protein, annotated in the source database as an RND efflux transporter periplasmic adaptor subunit. We selected eight cytotoxic T-lymphocyte (CTL) epitopes, five helper T-lymphocyte (HTL) epitopes, and three linear B-cell epitopes with favorable predicted immunological properties to develop a 397-amino acid multi-epitope vaccine construct that contains the S. suis 50S ribosomal protein L7/L12 adjuvant with rationally designed peptide linkers. The vaccine construct exhibited favorable physicochemical properties, predicted structural stability, and high antigenicity scores. The predicted combined HLA population coverage of the selected CTL and HTL epitopes was 90.77% across the populations included in the analysis. Immune simulation predicted patterns consistent with humoral and cellular immune activation, including sustained IgG production, elevated IFN-γ and IL-2 secretion, efficient antigen clearance, and generation of immunological memory, whereas molecular docking and molecular dynamics simulations characterized the predicted interaction and conformational behavior of the MEV–TLR1/TLR2 complex. Codon optimization (CAI = 0.996) and in silico cloning into the pET-30a(+) expression vector supported the potential feasibility of recombinant expression in Escherichia coli. Conclusions: In this study, a rationally designed multi-epitope vaccine candidate against diverse S. suis strains was developed using an integrated pangenome-guided reverse vaccinology approach. Based on these computational analyses, the proposed vaccine candidate showed favorable predicted immunogenicity, predicted structural quality, predicted HLA population coverage, and expression feasibility, providing a foundation for future experimental validation and development of a vaccine against diverse S. suis. Full article