Microbiol Spectr. 2026 Oct 19:e0203826. doi: 10.1128/spectrum.02038-26. Online ahead of print.

ABSTRACT

Streptococcus suis is an important swine pathogen and an emerging zoonotic threat, with serotype 9 (SS9) increasingly recognized as an important pathogenic serotype. Biofilm formation contributes to the persistence, antimicrobial tolerance, and pathogenicity of S. suis, yet effective strategies for controlling biofilm-associated infections caused by SS9 remain limited. In this study, we evaluated the antibacterial and antibiofilm activities of zinc oxide nanoparticles (ZnO-NPs) against SS9 and investigated whether their effects were associated with oxidative stress, biofilm formation, and alterations in virulence-associated genes. The minimum inhibitory concentration and minimum biofilm eradication concentration of ZnO-NPs against SS9 were both 49 μg/mL. ZnO-NPs exhibited potent antibacterial and antibiofilm activities, significantly inhibiting biofilm formation and reducing biofilm viability in a dose-dependent manner. Crystal violet staining demonstrated a marked reduction in biofilm biomass, while SEM analysis revealed substantial disruption of bacterial morphology and biofilm architecture following ZnO-NPs treatment. In addition, ZnO-NPs markedly increased intracellular reactive oxygen species levels, indicating the induction of oxidative stress in SS9. ZnO-NPs treatment also reduced the major extracellular matrix components of the biofilm, including extracellular proteins and extracellular DNA. Furthermore, RT-qPCR analysis showed that ZnO-NPs downregulated the expression of biofilm- and virulence-associated genes, including ef, fbps, gdh, and luxS. Collectively, these findings indicate that ZnO-NPs exert antibacterial and antibiofilm effects against SS9, accompanied by oxidative stress induction, disruption of biofilm architecture and extracellular matrix, and modulation of biofilm- and virulence-associated genes. ZnO-NPs may, therefore, represent a promising candidate for controlling SS9-associated infections.IMPORTANCEStreptococcus suis serotype 9 (SS9) is an important pathogen associated with disease in pigs and represents a potential zoonotic threat. The increasing prevalence of antimicrobial resistance highlights the need for alternative approaches to control SS9 infections. In this study, zinc oxide nanoparticles (ZnO-NPs) showed antibacterial and antibiofilm activity against SS9, including disruption of established biofilms. These findings provide evidence for further exploring ZnO-NPs as a non-antibiotic strategy for controlling SS9 infections and support future studies evaluating their safety and efficacy in animals.

PMID:42897438 | DOI:10.1128/spectrum.02038-26

Lancet Reg Health Eur. 2026 Aug 29;69:101848. doi: 10.1016/j.lanepe.2026.101848. eCollection 2026 Oct.

NO ABSTRACT

PMID:42892779 | PMC:PMC13675124 | DOI:10.1016/j.lanepe.2026.101848

IMetaOmics. 2026 Jul 2;3(3):e70116. doi: 10.1002/imo2.70116. eCollection 2026 Sep.

ABSTRACT

The high lethality of the Ebola virus (EBOV) underscores the critical need to understand its molecular lifecycle. Here, we systematically mapped EBOV-host interactions using affinity purification-mass spectrometry (AP-MS) and proximity labeling, generating a comprehensive protein-protein interaction (PPI) network, of which 1728 are high-confidence core PPIs involving nine EBOV proteins and 914 human interactors. Notably, we identified transmembrane 9 superfamily member 2 (TM9SF2) as a novel attachment factor that facilitates EBOV glycoprotein (GP)-mediated entry. Mechanistic studies demonstrated that the receptor-binding domain (RBD) of EBOV GP associates with the extracellular domain (ECD) of TM9SF2, enhancing cellular adhesion and viral attachment. Moreover, the anti-TM9SF2 antibodies effectively attenuated EBOV GP-mediated pseudovirus entry and infection in vitro. Additionally, Tm9sf2 ^{+/ -} knockout mice exhibited significantly reduced susceptibility to EBOV pseudoviruses. These findings provide critical insights into EBOV-host interactions and establish TM9SF2 as a promising therapeutic target for antiviral intervention.

PMID:42891291 | PMC:PMC13674394 | DOI:10.1002/imo2.70116

Front Cell Infect Microbiol. 2026 Sep 16;16:1922968. doi: 10.3389/fcimb.2026.1922968. eCollection 2026.

ABSTRACT

BACKGROUND/OBJECTIVES: Novel influenza A viruses (NIAV) infection is a zoonotic acute respiratory disease. The H5N1 and H7N9 subtypes cause high mortality, posing major public health threats. This study aimed to establish rapid, field-deployable subtype-specific nucleic acid detection assays for H5 and H7 by integrating reverse-transcription enzymatic recombinase amplification (RT-ERA) with CRISPR/Cas12a. Two separate reactions are required per sample.

METHODS: Conserved hemagglutinin (H) sequences were retrieved from the NCBI database, and primers, probes, and crRNAs were designed using Primer Premier 5 and Primer-BLAST. The sensitivity of RT-ERA alone was compared with that of the ERA-CRISPR/Cas12a using serially diluted virus strain nucleic acid. The specificity was verified against other respiratory pathogens with similar clinical manifestations.

RESULTS: The optimal primers were F1R2 for H5 and F2R3 for H7. The limit of detection (LOD) of RT-ERA alone was 2.63×10³ copies/µL for H5 and 1.86×10³ copies/µL for H7; the ERA-CRISPR/Cas12a assay improved the LOD to 2.63×10¹ copies/µL for H5 and 1.86 copies/µL for H7, representing 100-fold and 1000-fold enhancements in sensitivity, respectively. Specificity testing showed that the assay exclusively detected H5N1 and H7N9 with no cross-reactivity to other tested pathogens.

CONCLUSION: The ERA-CRISPR/Cas12a method exhibits enhanced sensitivity for H5 and H7 subtypes detection, along with high specificity, rapidity, and minimal equipment requirements. It offers a promising screening tool for NIAV infections.

PMID:42818682 | PMC:PMC13623710 | DOI:10.3389/fcimb.2026.1922968

J Biol Chem. 2026 Sep 29:113612. doi: 10.1016/j.jbc.2026.113612. Online ahead of print.

ABSTRACT

Programmed death-ligand 1 (PD-L1) undergoes continuous endocytosis and post-endocytic sorting that determine its recycling to the plasma membrane, lysosomal degradation, and exosomal secretion. Although PD-L1 internalization depends on RAB5-mediated endocytosis, whether canonical autophagy contributes to the subsequent sorting of internalized PD-L1 remains unclear. Here, we show that canonical autophagy is dispensable for the post-endocytic fate of cell-surface PD-L1. Genetic disruption of core autophagy components, including LC3B, ATG4B, ATG5, and ATG7, did not impair delivery of internalized PD-L1 to early endosomes, multivesicular bodies (MVBs), late endosomes, or extracellular vesicles. Pharmacologic inhibition of autophagosome-lysosome fusion increased PD-L1 accumulation in RAB5- and CD63-positive compartments, but this effect persisted in cells lacking LC3B, ATG5, or ATG7, further indicating that canonical autophagy is not required for PD-L1 endosomal sorting or exosomal secretion. Instead, we identify CAPZ, a CAPZα-CAPZβ heterodimer best known for actin filament capping, as a regulator of PD-L1 post-endocytic sorting. Loss of CAPZ reduced PD-L1 delivery to CD63-positive MVBs and incorporation into exosomes while increasing its accumulation in RAB11-positive recycling endosomes, resulting in elevated cell-surface PD-L1. Functionally, CAPZ-deficient tumor cells were less sensitive to peripheral blood mononuclear cell-mediated killing, consistent with increased surface PD-L1 and enhanced immune-evasive capacity. Together, these findings indicate that CAPZ-dependent endosomal maturation controls the balance between PD-L1 recycling and MVB/exosomal sorting independently of canonical autophagy, thereby influencing PD-L1 surface abundance and tumor immune evasion.

PMID:42810685 | DOI:10.1016/j.jbc.2026.113612

Front Microbiol. 2026 Sep 8;17:1935172. doi: 10.3389/fmicb.2026.1935172. eCollection 2026.

ABSTRACT

INTRODUCTION: Goose adenovirus type 4 (GoAdV-4) is an emerging pathogen that causes inclusion body hepatitis and hepatic necrosis in goslings, with mortality rates reaching up to 80% in severe outbreaks. Since its first identification in China in 2022, GoAdV-4 has spread rapidly across major goose-producing provinces, posing a serious threat to the domestic goose industry. However, no sensitive and specific quantitative assay has been available for the rapid diagnosis and viral load monitoring of GoAdV-4.

METHODS: We developed a TaqMan-based real-time quantitative PCR (qPCR) assay targeting the hexon gene of GoAdV-4 and systematically validated its analytical sensitivity, specificity, and repeatability. The assay was then applied to 582 clinical samples of five specimen types (tissues, blood, goose embryos, and cloacal swabs), and its diagnostic performance was compared with conventional PCR.

RESULTS: The assay demonstrated a linear detection range of 6.4 × 10¹ to 6.4 × 10⁷ copies/μL (R ² = 0.9968) with an amplification efficiency of 97.5%, and a limit of detection (LOD) as low as 6.4 × 10¹ copies/μL. No cross-reactivity was observed with fowl adenovirus serotype 4, duck adenovirus type 3, egg drop syndrome virus, goose circovirus, goose astrovirus, goose parvovirus, or nuclease-free water. Intra-assay and inter-assay coefficients of variation ranged from 0.87% to 1.17% and 1.06% to 1.48%, respectively, indicating high reproducibility. The assay identified 55 GoAdV-4-positive samples (9.45%), compared with 48 positives (8.25%) detected by conventional PCR, with an overall concordance rate of 98.80% (positive concordance 87.27%, negative concordance 100%).

DISCUSSION: The TaqMan qPCR assay detected seven additional positive samples missed by conventional PCR, all confirmed as true positives by Sanger sequencing, demonstrating superior sensitivity. These results show that the established TaqMan qPCR assay is a rapid, sensitive, specific, and reproducible tool for GoAdV-4 detection, providing a valuable diagnostic instrument for the surveillance and control of this emerging waterfowl pathogen.

PMID:42774421 | PMC:PMC13593879 | DOI:10.3389/fmicb.2026.1935172

One Health. 2026 Aug 27;23:101556. doi: 10.1016/j.onehlt.2026.101556. eCollection 2026 Dec.

ABSTRACT

Management of free-roaming animal populations in human-dominated environments presents persistent ecological, ethical, and public-health challenges worldwide. Removal of animals from open populations is often assumed to reduce population size and associated risks. However, ecological theory suggests that removal may be followed by compensatory responses through immigration, increased survival, or enhanced reproduction among the remaining animals. This phenomenon, commonly referred to as the "vacuum effect", has been widely invoked in debates on the management of free-roaming dogs and other urban animals, but its empirical basis and the conditions under which it operates remain incompletely understood. Here, we review the conceptual foundations and available evidence for replacement dynamics in free-roaming dog populations, with particular attention to urban systems where food, shelter, and human tolerance support high dog densities. We show that although the "vacuum effect" is ecologically plausible, its empirical manifestations in free-roaming dog populations are limited. The outcome of removal of the free-roaming dogs from a particular area depends on several factors, including the spatial scale and continuity of removal, recruitment through reproduction and abandonment, environmental carrying capacity shaped by human-provided resources, and the strength of institutional regulation. We propose a conceptual framework in which removal does not inevitably lead to rapid replacement. Instead, outcomes vary according to the characteristics of the system and the way interventions are implemented. This interpretation helps to reconcile the opposing positions and highlights the need for integrated approaches combining population management, regulation of resources and recruitment, and disease prevention. Understanding the conditions that influence replacement is important for developing sustainable and humane approaches to free-roaming dog management and control of dog-mediated rabies.

PMID:42729580 | PMC:PMC13563226 | DOI:10.1016/j.onehlt.2026.101556

Front Cell Infect Microbiol. 2026 Aug 26;16:1896940. doi: 10.3389/fcimb.2026.1896940. eCollection 2026.

ABSTRACT

INTRODUCTION: Lawsonia intracellularis causes Porcine Proliferative Enteritis (PPE), leading to significant economic losses, yet obtaining isolates for vaccine development remains challenging.

METHODS: In this study, a novel L. intracellularis strain, designated LIGD01, was isolated from the ileum of a pig with acute hemorrhagic enteritis in Guangdong, China. The strain was stably passaged in McCoy cells for 40 generations.

RESULTS: Phylogenetic analysis of the 16S rRNA gene confirmed its identity, and indirect immunofluorescence assay (IIFA) and scanning electron microscopy (SEM) demonstrated characteristic intracellular colonization and curved rod-shaped morphology. LIGD01 induced intermittent fecal shedding starting at 3 days post-infection (dpi), with seroconversion in all challenged pigs by 21 dpi. Necropsy revealed distinct ileal hyperplasia. Histopathology showed villous blunting, epithelial exfoliation, and inflammatory infiltration. Crucially, infection significantly reduced Average Daily Gain (ADG) (252.21 ± 17.07 g/day vs. 300.98 ± 19.39 g/day in controls, p < 0.05) and suppressed the activities of key digestive enzymes (trypsin, lipase, amylase) in the pancreas and intestine. Furthermore, Lawsonia intracellular infection characterized by a reduction in beneficial genera (Lactobacillus, Christensenellaceae) and an increase in opportunistic pathogens (Streptococcus, Enterococcus), concomitant with upregulated pro-inflammatory cytokines (TNF-α, IFN-γ, IL-1α).

DISCUSSION: This study not only provides a new candidate strain for vaccine development but also elucidates the physiological and microbial mechanisms underlying growth retardation in PPE.

PMID:42718558 | PMC:PMC13553240 | DOI:10.3389/fcimb.2026.1896940

Food Waterborne Parasitol. 2026 Aug 26;44:e00356. doi: 10.1016/j.fawpar.2026.e00356. eCollection 2026 Sep.

ABSTRACT

Parasitic helminths can modulate host inflammatory responses, but whether this regulation involves remodeling of the intestinal neurochemical environment remains unclear. Here, we investigated whether Trichinella spiralis infection alters intestinal neurotransmitter-related metabolism during lipopolysaccharide (LPS)-induced systemic inflammation. In this study, we established an LPS-induced inflammatory model and a T. spiralis-infection with LPS challenge model. At 14 days after infection, mice were challenged with LPS, and inflammatory responses and duodenal neurotransmitter-related metabolites were assessed. T. spiralis infection reduced serum TNF-α and IL-1β levels and alleviated LPS-induced lung pathology. Targeted LC-MS/MS profiling revealed treatment-specific neurochemical signatures in duodenal tissues. Under basal conditions, T. spiralis infection increased histamine levels and reduced norepinephrine, 5-hydroxyindoleacetic acid, and xanthurenic acid. During LPS challenge, prior T. spiralis infection was associated with increased dopamine, epinephrine, levodopa, 5-hydroxytryptophan, histamine, and tyramine compared with LPS challenge alone. These changes suggest that T. spiralis infection remodels tyrosine-, histidine-, and tryptophan-related neurochemical pathways in the intestine. Receiver operating characteristic analysis further identified several metabolites that discriminated LPS-challenged mice from T. spiralis-infected, LPS-challenged mice, although these candidate signatures require validation in larger independent cohorts. Together, our findings indicate that intestinal neurochemical remodeling may represent a previously underappreciated component of helminth-associated anti-inflammatory regulation.

PMID:42713351 | PMC:PMC13551873 | DOI:10.1016/j.fawpar.2026.e00356

Antioxidants (Basel). 2026 Aug 15;15(8):1019. doi: 10.3390/antiox15081019.

ABSTRACT

Superoxide dismutase 2 (SOD2), a key mitochondrial antioxidant enzyme, is essential for maintaining cellular redox homeostasis by scavenging superoxide radicals. While viruses often induce oxidative stress, the specific role of SOD2 in antiviral defense remains unclear. Here, we report that vaccinia virus (VACV) infection triggers mitochondrial and cellular reactive oxygen species (ROS) and selectively upregulates SOD2, but not SOD1. Genetic knockout of SOD2 exacerbated mitochondrial ROS (mtROS) accumulation and significantly enhanced VACV replication and spread, resulting in larger viral plaques. Conversely, SOD2 overexpression constrained plaque formation and suppressed viral dissemination. Mechanistically, the antiviral function of SOD2 does not strictly rely on its enzymatic activity or mitochondrial targeting, as neither the deacetylation-mimicking mutant nor the mutant lacking the mitochondrial localization signal peptide appreciably impaired its antiviral potency. Furthermore, in a rabbit model, local overexpression of human SOD2 attenuated the poxvirus lesion formation. Our findings unveil an important yet easily overlooked role of SOD2 in antiviral defense and posit it as a promising candidate for the development of host-directed therapeutics against poxviruses.

PMID:42650283 | PMC:PMC13509771 | DOI:10.3390/antiox15081019