Poult Sci. 2026 May 1;105(8):107060. doi: 10.1016/j.psj.2026.107060. Online ahead of print.

ABSTRACT

This study aims to investigate the efficacy and mechanism of action of a benzoic acid combined with cinnamon essential oil complex (SLLEO) in preventing and controlling necrotic enteritis (NE) in broiler chickens caused by Clostridium perfringens infection. A total of 300 one-day-old 817 broiler chickens were randomly divided into five groups, with six replicates per group and ten birds per replicate. The control group (CON) and challenge group (CP) were fed a basal diet; the low, medium, and high-dose benzoic acid combined with cinnamon essential oil groups (SLLEO-L, SLLEO-M, SLLEO-H) were fed basal feed supplemented with 0.1%, 0.2%, and 0.3% benzoic acid combined with cinnamon essential oil, respectively. The animal experiment lasted 35 days. Results indicate that supplementing feed with benzoic acid combined with cinnamon essential oil (SLLEO) effectively mitigates the adverse effects of NE infection on broiler chickens. Compared to the Clostridium perfringens infection model, SLLEO significantly increased the average daily weight gain of infected chickens while reducing abnormally elevated liver and bursa of Fabricius indices (P < 0.05). SLLEO elevated total antioxidant capacity (T-AOC) and superoxide dismutase (SOD) activity in plasma, liver, and jejunal mucosa while decreasing malondialdehyde (MDA) content (P < 0.05). Significantly increased plasma immunoglobulin A (IgA) levels, markedly elevated the villus height-to-crypt depth ratio (VH/CD), and reduced intestinal lesion scores (P < 0.05). Additionally, SLLEO downregulated mRNA expression of the proinflammatory factor TNF-α in the jejunum while upregulating the expression of the anti-inflammatory factor IL-10 and tight junction proteins ZO-1, Occludin, Claudin-1, and mucin MUC-2 (P < 0.05).In summary, dietary supplementation with SLLEO effectively mitigated growth performance decline in broilers caused by Clostridium perfringens infection, improved antioxidant function, alleviated immune organ hypertrophy, regulated plasma immunoglobulin levels, restored intestinal morphology, downregulated pro-inflammatory factors while upregulating anti-inflammatory factors, and enhanced intestinal barrier function by increasing tight junction protein and mucin gene expression.

PMID:42114283 | DOI:10.1016/j.psj.2026.107060

Animals (Basel). 2026 Apr 21;16(8):1273. doi: 10.3390/ani16081273.

ABSTRACT

This study developed a dual-antigen enzyme-linked immunosorbent assay (ELISA) based on σB protein and genotype 5-specific σC protein of avian reovirus (ARV). First, σB and σC proteins were expressed and purified using recombinant technology. Through optimization of coating conditions, the optimal antigen combination was determined to be a mixture of the two proteins at a 1:3 molecular ratio (total concentration: 0.8 μg/mL). Key parameters of the indirect ELISA were optimized via checkerboard titration. Validation confirmed that the dual-antigen ELISA exhibited a sensitivity of 1:3200 against genotype 5 ARV-positive sera, with no cross-reactivity and a coefficient of variation of 2.9-8.6%, demonstrating excellent reproducibility. In application testing, the method specifically detected serum antibodies against genotype 5 ARV variant strains, achieving a 100% positive detection rate in experimental chickens within the first week post-challenge and effectively monitoring dynamic antibody changes in infected flocks. Furthermore, the detection rate for genotype 5-positive serum samples (100%) was significantly higher than that of a commercial kit (75%). This dual-antigen indirect ELISA overcomes the sensitivity limitations associated with conventional genotype 5 ARV detection methods and provides a reliable tool for epidemiological surveillance and infection monitoring.

PMID:42072039 | PMC:PMC13113393 | DOI:10.3390/ani16081273

Emerg Microbes Infect. 2026 May 4:2668752. doi: 10.1080/22221751.2026.2668752. Online ahead of print.

ABSTRACT

Recent clinical data on seasonal influenza mRNA vaccines have demonstrated suboptimal efficacy against the influenza B virus (IBV). We employed sequence optimization strategies that successfully enhanced the antigen expression of hemagglutinin (HA), and developed mRNA vaccine candidates targeting the WHOrecommended strains. When administered at a low dose (0.1 μg), both mono-and trivalent influenza A mRNA vaccines induced robust humoral immunity and conferred complete protection against homologous viral challenge in murine models, outperforming the quadrivalent inactivated vaccine (QIV, 2 μg). In contrast, IBV mRNA vaccines at an equivalent dose failed to elicit detectable antibodies and offered no protection, consistent with prior of suboptimal immunogenicity in human trials. These findings highlight strain-specific immunogenicity constraints inherent to conventional mRNA platforms. To overcome these limitations, we systematically compared three distinct RNA vaccine modalities: (1) nucleoside-modified mRNA, (2) self-amplifying RNA (saRNA), and (3) circular RNA (circRNA). Notably, a single 0.1 µg dose of trivalent saRNA vaccine elicited robust humoral immunity and provided complete protection against IBV challenge, whereas mRNA vaccination achieved only 14% survival. Importantly, long-term antibody monitoring over 20 weeks showed that saRNA at the low 0.1 μg dose maintained high antibody levels, with a markedly more durable response to IBV antigens than other platforms. Moreover, the trivalent mRNA vaccine exhibited a favorable safety profile, with no obvious abnormal body weight changes or serum biochemical abnormalities observed after immunization. Our findings advocate for strain-adaptive platform selection: conventional mRNA for generating rapid, high-magnitude responses against influenza A, and next-generation saRNA vaccine for enhanced dose efficiency, particularly against IBV.

PMID:42081324 | DOI:10.1080/22221751.2026.2668752

Vet Immunol Immunopathol. 2026 Apr 27;297:111121. doi: 10.1016/j.vetimm.2026.111121. Online ahead of print.

ABSTRACT

Streptococcus suis (S. suis, SS), a significant zoonotic pathogen, causes large-scale swine epidemics and substantial economic losses. Based on capsule antigen differences, at least 29 serotypes have been identified. Given that existing commercial vaccines target only serotypes 2 or a few others, and lack immunoprotection against serotype 9, this study designed and developed a bivalent inactivated candidate vaccine to cover serotypes 2 and 9, evaluation of the protective efficacy of weaning piglets. The vaccinated piglets were in normal condition without adverse reactions and deaths, indicating that the vaccine was very safe. Experimental vaccine induced significantly higher levels of specific antibodies than the commercial vaccine. Further pathogenicity tests confirmed that the vaccine exhibited 100% immunoprotection efficacy against both Streptococcus suis serotype 2 and serotype 9 strains, and significantly reduced mortality and clinical severity of disease following infection with these two bacterial strains. According to a search of the public literature, this study provides evidence that the bivalent vaccine demonstrates no less than the efficacy of existing commercial vaccines, while exhibiting high safety and superior immunoprotection efficacy, offering a reliable technical solution for the prevention and control of co-infection with Streptococcus suis type 2 and type 9.

PMID:42068777 | DOI:10.1016/j.vetimm.2026.111121

Front Vet Sci. 2026 Apr 7;13:1803248. doi: 10.3389/fvets.2026.1803248. eCollection 2026.

ABSTRACT

Newcastle disease (ND) is a highly contagious and economically important viral disease of poultry, caused by virulent strains of Orthoavulavirus javaense (OAVJ). In Slovenia, vaccination is mandatory in commercial poultry and selected avian species, whereas backyard and free-range flock remain largely unregulated. In January and February 2025, two unrelated backyard and free-range flock of laying hens experienced acute outbreaks with severe clinical signs, increased mortality and distinct gross necropsy findings (haemorrhages in the mucosa of the gastrointestinal tract, multifocal pale foci in the liver, atrophy to enlarged hyperaemic spleen, oophoritis and salpingitis). OAVJ was detected in cloacal, oropharyngeal, and brain samples from both outbreaks using real-time RT-qPCR. Analysis of complete fusion (F) gene revealed identical nucleotide sequences in both outbreaks, with the cleavage site motif, characteristic of velogenic strains (amino acid sequence 112RRQKR116 at the C-terminus of the F2 protein and F at residue 117, the N-terminus of the F1 protein). Further phylogenetic analysis of the F gene demonstrated that both viruses belong to class II, sub-genotype VII.1.1, showing 99.6-100% identity with strains recently detected in Poland. The hemagglutinin-neuraminidase (HN) glycoprotein comprised 571 amino acids, consistent with genotype VII viruses, with several amino acid substitutions previously associated with functional relevance. These results highlight that, despite the absence of ND in Slovenia for more than three decades, local poultry populations remain highly susceptible to the introduction of the virus, especially in backyard flocks where monitoring and disease control are difficult to implement. Although a virulent virus was confirmed in both outbreaks, no further spread to other poultry holdings was detected.

PMID:42022388 | PMC:PMC13095595 | DOI:10.3389/fvets.2026.1803248

J Virol. 2026 Apr 21:e0020726. doi: 10.1128/jvi.00207-26. Online ahead of print.

ABSTRACT

Porcine deltacoronavirus (PDCoV) has been prevalent worldwide for over a decade, causing considerable economic damage to the pig industry and posing a potential threat to public biosecurity. In this study, we found that one of the interferon-stimulated genes (ISGs), swine guanylate-binding proteins 1 (sGBP1), was induced by PDCoV. In the experiments we describe below, we demonstrate that sGBP1 is an antiviral gene inhibiting PDCoV infection by utilizing the sGBP1 stable expression cell line and sGBP1 knockout cell line. Both the large GTPase domain and the α-helical domain are responsible for sGBP1 anti-PDCoV replication. Notably, sGBP1 directly interacts with the scaffold protein NSP8 of the PDCoV replication and transcription complex (RTC). Moreover, the large GTPase domain of sGBP1 interacts with the NTD domain of NSP8, which disrupts the interaction between NSP8 and NSP12 in RTC. In addition, sGBP1 is able to bind with the RNA of PDCoV and inhibits RTC from binding with virus RNA. Here, our research uncovers a new mechanism through which sGBP1 inhibits PDCoV replication. This finding not only deepens our comprehension of the antiviral roles of ISG molecules but also offers a promising target for the prevention of PDCoV infections.IMPORTANCEPDCoV is an enteric coronavirus that has garnered significant global attention due to its current prevalence in causing diarrhea and even mortality in pigs, as well as its broad host range encompassing poultry, rodents, ruminants, and even humans. Understanding the mechanism by which host factors inhibit viral replication is critical for developing effective antiviral strategies. Here, we found that PDCoV induced swine guanylate-binding proteins 1 (sGBP1) to inhibit viral replication. Our study first reveals that sGBP1 impairs the replication and transcription complex (RTC) formation through two ways: (i) competes with the RNA-dependent RNA polymerase (RdRp) NSP12 to bind with NSP8; (ii) sGBP1 binds with PDCoV RNA to inhibit the RNA binding of RTC. Our results uncover a previously unknown antiviral mechanism of GBP1, offering a promising target for the prevention of viral infections.

PMID:42012181 | DOI:10.1128/jvi.00207-26

IDCases. 2026 Mar 25;44:e02555. doi: 10.1016/j.idcr.2026.e02555. eCollection 2026.

ABSTRACT

BACKGROUND: Immunocompromised patients presenting with encephalitis can present a diagnostic conundrum as infection can be caused by a broad range of pathogens, many of which are not detected by standard of care testing pathways. Untargeted metagenomics has proven utility in the diagnosis of such infections, particularly for immunocompromised patients.

METHODS: An immunosuppressed adolescent presented with idiopathic progressive muscle weakness resulting in respiratory failure, 16 years after haematopoeitic stem cell transplant for familial haemophagocytic lymphohistiocytosis type 5. Clinical and radiological findings suggested a diagnosis of isolated central nervous system haemophagocytic lymphohistiocytosis, however the patient demonstrated no improvement on immunosuppressive therapy. Untargeted metagenomics was performed on brain biopsy tissue.

RESULTS: Clinical metagenomics detected avian paramyxovirus 1 (APMV-1) in the brain tissue 12 days after biopsy, confirmed by targeted PCR and immunohistochemistry. The metagenomics results guided treatment; immunosuppression was stopped and medication with potential activity against RNA viruses started. The patient died 8 months after symptom onset.

CONCLUSIONS: We describe the third published case of fatal encephalitis caused by APMV-1, detectable only in brain parenchyma and only by clinical metagenomics, demonstrating the utility of brain biopsy and metagenomics when investigating encephalitis in immunocompromised patients. Case series review suggests profoundly immunocompromised patients are at risk of severe infection caused by AMPV-1.

PMID:41953529 | PMC:PMC13054261 | DOI:10.1016/j.idcr.2026.e02555

Poult Sci. 2026 Mar 27;105(7):106873. doi: 10.1016/j.psj.2026.106873. Online ahead of print.

ABSTRACT

Interleukin-17A (IL-17A) is a key pro-inflammatory cytokine that plays a crucial and complex role in immune regulation, infection, and inflammation under both physiological and pathological conditions, demonstrating significant potential in these fields. However, research on its interaction with the avian respiratory system and its potential application as a mucosal immune adjuvant is limited. To investigate its functional relevance, a comparison was first performed of the genetic and structural features of chicken IL-17A (chIL-17A) with those of its mammalian homologs. Recombinant chIL-17A was subsequently produced via a prokaryotic expression system and evaluated through in vitro assays using chicken embryo fibroblasts (CEFs) and peripheral blood mononuclear cells (PBMCs), as well as in vivo experiments in specific-pathogen-free (SPF) chickens. In the in vivo study, 3-week-old SPF White Leghorn chickens (mixed sex) were nebulized with a single or double dose (20 μg/kg per dose, n = 12 per group) of chIL-17A. The results demonstrated that chIL-17A treatment markedly upregulated the transcription of proinflammatory cytokines (e.g., IL-1β, IL-6, and TNF-α), type I interferons, and multiple interferon-stimulated genes in a dose-and time-dependent manner. Notably, a second administration further enhanced its stimulatory effect on these immune mediators. In vivo, nebulized chIL-17A significantly induced pulmonary proinflammatory responses, particularly on day 5 post-treatment, with IL-1β and IL-6 mRNA levels increasing by 67.35-fold (P < 0.001) and 130.19-fold (P < 0.001), respectively, in lung tissues. Modulation of IFN responses was most pronounced in the lower trachea and lung tissues, with minimal effects in the upper tracheal region. These findings unequivocally demonstrate the potent immunomodulatory capacity of chIL-17A and underscore its potential as a mucosal immune enhancer in poultry.

PMID:41933529 | PMC:PMC13087765 | DOI:10.1016/j.psj.2026.106873

Front Microbiol. 2026 Mar 11;17:1744587. doi: 10.3389/fmicb.2026.1744587. eCollection 2026.

ABSTRACT

INTRODUCTION: Hepatitis E virus (HEV) is a globally prevalent zoonotic pathogen posing major public health risks. Swine, a major meat source, carry HEV strains genetically similar to those in humans, highlighting the risk of zoonotic foodborne transmission. This study aimed to investigate the evolutionary history of HEV through phylogenetic and recombination analyses, further provide key reference bases for public health management, improve food safety standards, and offer support for developing effective strategies to prevent foodborne hepatitis E infections.

METHODS: We analyzed 348 full-length genomes of HEV isolated from humans and pigs in Asia over the past three decades. Phylogenetic analysis was conducted using the neighbor-joining method in MEGA11. Recombination analysis was performed with seven methods in RDP4, and sequence similarity was visualized using Simplot.

RESULTS: HEV-4 predominated in Asia, especially China, whereas HEV-3 was regionally endemic. Through genomic analysis, we identified 34 potential natural recombination events, predominantly occurring in the RNA-dependent RNA polymerase (RdRp) region; 14 events occurred between swine and human strains, supporting the hypothesis of cross-species transmission. Moreover, 20 recombination events occurred in China and mainly involved HEV-4 strains, suggesting that HEV has distinct evolutionary dynamics. The detection of five inter-genotypic recombination events may highlight ongoing genetic exchange within HEV populations in Asia, and the biological significance of these events remains to be determined.

DISCUSSION: These findings highlight the importance of tracking the evolutionary dynamics of HEV through genomic surveillance, and further underscore the necessity of conducting ongoing HEV surveillance and research to inform prevention strategies.

PMID:41889644 | PMC:PMC13013505 | DOI:10.3389/fmicb.2026.1744587

Front Microbiol. 2026 Feb 17;17:1708036. doi: 10.3389/fmicb.2026.1708036. eCollection 2026.

ABSTRACT

The detrimental effects of microplastics on environmental and biological health have been extensively documented, encompassing various aspects such as growth inhibition, metabolic disorders, and organ damage. However, current research predominantly focuses on model organisms, with limited studies investigating their effects on broiler chickens. Therefore, this study aims to examine the impact of microplastics exposure on the gut microbiota and antioxidant function in broiler chickens. The results indicated that microplastics significantly affect serum biochemical and antioxidant parameters, evidenced by marked increases in AST, ALT, and MDA levels, alongside decreases in SOD and GSH-Px levels. Microbiome analysis revealed a significant decrease in the alpha diversity of the gut microbiota, accompanied by significant alterations in microbial structure. Additionally, metastats analysis demonstrated a significant increase in the relative abundances of one phylum and 12 genera during microplastics exposure, contrasted with a significant decrease in the relative abundances of three phyla and 108 genera. Importantly, microplastics exposure also led to changes in gut microbial function, affecting energy metabolism, coenzyme transport and metabolism, and amino acid metabolism, etc. In summary, our study demonstrates that microplastics can adversely affect the health of broiler chickens by reducing their antioxidant capacity, and causing gut microbial dysbiosis. In light of the increasing pollution from microplastics, this study provides crucial information for assessing the risks posed by microplastics to livestock production. Furthermore, future research should prioritize monitoring the migration of microplastics within the food chain and examining their long-term effects on biological behavior and ecological functions.

PMID:41783496 | PMC:PMC12953438 | DOI:10.3389/fmicb.2026.1708036