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This study comprehensively explored the epidemiology, virulence, antibiotic resistance, and genomic features of ovine-derived across three provinces in Northwest China (Gansu, Ningxia, and Shaanxi). Lung tissue samples were collected postmortem from sheep with respiratory disease (nine per province), cultured under sterile conditions, and screened by morphological, Gram staining, PCR, and NGS methods. Nine strains were successfully isolated (isolation rate 33.33%) and identified as serotypes A1, A2, and A6, with Shaanxi exhibiting a significantly higher isolation rate of 66.67%. Genomic analysis revealed that each isolate each harbored over 100 virulence genes and displayed notable genetic diversity. In murine assays, intraperitoneal inoculation in mice caused severe breathing problems and death within 24 h; necropsy revealed lung congestion, splenic necrosis foci, and hepatic congestion. Antibiotic susceptibility testing showed sensitivity to ciprofloxacin, azithromycin, gentamicin, and levofloxacin, while resistance was observed for tiamulin and enrofloxacin. These findings indicate a high prevalence and strong pathogenicity of ovine in Shaanxi, underscore the presence of key resistance traits, and provide a genomic and pathogenic reference to guide region-specific surveillance, therapeutic decisions, and vaccine-oriented control in small ruminant herds. Importantly, these results highlight the need for region-specific monitoring and judicious antibiotic use, which are essential to forestall the spread of resistant strains and to ensure sustainable disease management strategies.

Parthanatos is distinct from caspase-dependent apoptosis in that it does not necessitate the activation of caspase cascades; Instead, it relies on the translocation of Apoptosis-inducing Factor (AIF) from the mitochondria to the nucleus, resulting in nuclear DNA fragmentation. Newcastle Disease Virus (NDV) is an oncolytic virus that selectively targets and kills tumor cells by inducing cell apoptosis. It has been reported that NDV triggers classic apoptosis through the mitochondrial pathway. In this study, we observed that NDV infection induced endoplasmic reticulum stress (ERS), which caused a rapid release of endogenous calcium ions (Ca 2+ ). This cascade of events resulted in mitochondrial depolarization, loss of mitochondrial membrane potential, and structural remodeling of the mitochondria. The overload of Ca 2+ also initiated an increase in mitochondrial membrane permeability, facilitating the transfer of AIF to the nucleus to induce apoptosis. Damaged mitochondria produced excessive reactive oxygen species (ROS), which further exacerbated mitochondrial damage and increased mitochondrial membrane permeability, thus promoting additional intracellular Ca 2+ accumulation and ultimately triggering an ROS burst. Collectively, these findings indicate that NDV infection promotes excessive calcium accumulation and ROS generation, leading to mitochondrial damage that releases more calcium and ROS, creating a feedback loop that exacerbates AIF-dependent parthanatos. This study not only provides a novel perspective on the oncolytic mechanism of NDV but also highlights new targets for antiviral research.

Porcine epidemic diarrhea virus (PEDV) is a porcine enteric coronavirus, which is one of the main causative agents of porcine epidemic diarrhea (PED), with 100% morbidity and 80–100% mortality in neonatal piglets. Since 2010, large-scale PED caused by highly pathogenic variants of PEDV has occurred successively in China and other countries in the world, posing a great threat to the global pig industry. It has been demonstrated in many investigations that the classic attenuated vaccine strain, PEDV CV777, is insufficient to fully protect against the PEDV variants. Moreover, the maternally derived antibodies elicited by inactivated vaccines also cannot completely protect piglets from infection. In addition, feedback feeding poses a risk of periodic PEDV recurrence in pig farms, making it challenging to successfully limit the spread of PEDV in China. This review focuses on the etiology, epidemiology, antigenicity, and control strategies of PEDV in China and provides information for the formulation of effective control measures.

Peste des petits ruminants (PPR), caused by the peste des petits ruminants virus (PPRV), is a highly contagious disease affecting ruminants. While goats and sheep are well-known hosts, PPRV has also spread to wild ruminants, and it remains unclear which ruminant species can be infected. SLAM (Signaling lymphocytic activation molecule) acts as the primary receptor for PPRV, playing a crucial role in the viral infection process. Identifying which ruminant SLAMs can mediate PPRV infection is essential for understanding the potential hosts of PPRV, which is vital for effective eradication efforts. In this study, we first extracted 77 ruminant species’ SLAM sequences from ruminant genome database. Based on these sequences, we predicted the structures of ruminant SLAMs. The analysis revealed that SLAM conformation is similar across ruminant species, and the potential PPRV H protein binding domain residues were conserved among SLAMs of these 77 species. Phylogenetic analysis of SLAM grouped ruminants into six families. We then selected representative SLAMs from each ruminant family to assess their role in PPRV infection. Our findings demonstrated that ruminant SLAMs efficiently mediated PPRV infection, with enhanced viral amplification observed in cells expressing SLAM from java mouse deer ( Tragulidae ) and goat ( Bovidae ), compared to cells expressing SLAM from white tailed deer ( Cervidae ) and giraffe ( Giraffidae ). These results underscore the need to consider a broader range of potential host populations beyond goat and sheep in efforts to prevent and eradicate PPRV.

Deoxyribonucleic acid (DNA) damage response (DDR) is the fundamental cellular response for maintaining genomic integrity and suppressing tumorigenesis. The activation of ataxia telangiectasia-mutated (ATM) kinase is central to DNA double-strand break (DSB) for maintaining host-genome integrity in mammalian cells. Oncolytic Newcastle disease virus (NDV) can selectively replicate in tumor cells; however, its influence on the genome integrity of tumor cells is not well-elucidated. Here, we found that membrane fusion and NDV infection triggered DSBs in tumor cells. The late replication and membrane fusion of NDV mechanistically activated the ATM-mediated DSB pathway via the ATM-Chk2 axis, as evidenced by the hallmarks of DSBs, i.e., auto-phosphorylated ATM and phosphorylated H2AX and Chk2. Immunofluorescence data showed that multifaceted ATM-controlled phosphorylation markedly induced the formation of pan-nuclear punctum foci in response to NDV infection and F-HN co-expression. Specific drug-inhibitory experiments on ATM kinase activity further suggested that ATM-mediated DSBs facilitated NDV replication and membrane fusion. We confirmed that the Mre11-RAD50-NBS1 (MRN) complex sensed the DSB signal activation triggered by NDV infection and membrane fusion. The pharmacological inhibition of MRN activity also significantly inhibited intracellular and extracellular NDV replication and syncytia formation. Collectively, these data identified for the first time a direct link between the membrane fusion induced by virus infection and DDR pathways, thereby providing new insights into the efficient replication of oncolytic NDV in tumor cells.

Newcastle disease virus (NDV) is a contagious agent of Newcastle disease in avian species and seriously affects the poultry industry. The cleavage site of the viral F protein (Fcs) is a key determinant of membrane fusion and viral virulence. In this study, we investigated the precise effect of variable amino acid sequences of the Fcs on fusogenic activity. Based on viral pathogenicity, the Fcs sequences of natural isolates (n = 1572) are classified into eight types of virulent Fcs (VFcs) with the motif \"G/R/K-R-Q/R/K-R/K-R↓F\" and ten types of the avirulent Fcs (AFcs) with the motif \"G/R/E-R/K/Q-Q-G/E-R↓L\". The VFcs is only found in the Class II cluster of viral classification and not in Class I. The AFcs exists in both Class I and II isolates. The VFc and AFc types present an evolutionary relationship with temporal distribution and host species. Using a fusion assay in vitro, VFcs-1 \"RRQKR↓F\" and VFcs-2 \"RRQRR↓F\" show the highest efficiency in triggering membrane fusion. The neutral residue Q at the P3 position of the VFcs plays an enhancing role compared to effect of the basic residues R and K. A single residue K at P3 or P5 is less efficient of the fusogenic activity in the VFcs with all basic residues. Moreover, the cleavage efficiencies of F0 proteins with different types of Fcs motifs do not appear to affect membrane fusion. Our findings offer insight into the effect of amino acid variation of the Fcs on the fusion triggered by NDV.

Newcastle disease virus (NDV), as an avian pathogen, can infect a broad spectrum of cell lines in vitro. However, noncarcinoma cell lines possessing nonsusceptibility to NDV are rare. Here, we isolated primary mouse embryonic fibroblasts (MEFs), which are nonsusceptible to NDV. MEF-derived cells were generated by passaging the cells over fifty times to achieve spontaneous immortalization. Two of the resulting cell lines were named SLM-21 and MEF50. Karyotype analysis revealed that SLM-21 has a near-tetraploid karyotype and that MEF50 shows a near-tetraploid and near-hexaploid chimeric karyotype. NDV exerted a significant cytopathic effect on MEF50, and substantial viral replication was observed. In contrast, NDV did not have a significant effect on SLM-21, indicating that SLM-21 was a nonsusceptible cell line to NDV, while MEF50 was a susceptible cell line. The NDV authentic sialic acid (SA) receptors SA 2,3-Gal and SA 2,6-Gal were expressed in SLM-21. Transcriptomic analysis revealed that the non-susceptibility of SLM-21 may be related to its broadly activated antiviral pathways and fine-tuned regulation of the cell cycle and DNA damage. This study provides a basic cell platform for exploring viral susceptibility and pathogenesis as well as host–virus interactions during NDV infection.

Molting is induced in commercial laying hens to rejuvenate the reproductive system and increase egg production. However, this process causes stress and reduces bird health and performance. The experiment was conducted to study the effect of multi probiotics and vitamin additives on induced molting in 240 ISA Brown hens. Hens were randomly divided into four groups receiving probiotic and vitamin additives (I-IV) during different period of molting. During the whole molting process, the laying performance indexes such as egg laying rate, egg quality, ovary weight and oviduct lengths were measured, and the spleen index, serum immunoglobulin, immune response of NDV and AIV vaccine were monitored. Molted hens resumed 50% egg production in just 37 days, with 1.62% mortality. Egg quality such as egg weight, yolk color, Haugh unit, eggshell strength and protein height were significantly improved. After the second production peak, the reproductive organs and immune organs returned to normal, and the immune antibody titer of NDV vaccine increased significantly. Molting with probiotic and vitamin additives improve the laying performance and egg quality, reduce mortality, significantly improve immune function and vaccine titer, and help to enhance disease resistance and maintain production performance of aged laying hens.

Background/Objectives: In an era of increasing bacterial resistance, Enterococcus, as a reservoir of antibiotic resistance genes, poses a serious threat to public health. Methods: This study conducted antibiotic susceptibility tests, whole-genome sequencing, and bioinformatics analysis on 89 Enterococcus isolates from chickens, pigs, cattle, and sheep in Ningxia Autonomous Region. Results: The resistance rates of Enterococcus to clindamycin, cefoxitin, sulfamethoxazole, and tamoxifen were all above 95%, and 96.6% (86/89) of the isolates were multi-antibiotic resistant. There were significant differences in resistance phenotypes among different species, with Enterococcus from pigs showing significantly higher resistance than those from other animals. optrA was commonly found in Enterococcus from pigs, accounting for 61.5% (8/13). ST480, ST16, ST116, and ST300 were the main MLST types, and ST16 was one of the important pathogenic Enterococcus types. Conclusions: The study revealed the occurrence of inter-species transmission events of Enterococcus. In conclusion, this study comprehensively described the resistance spectrum, sequence characteristics, and transmission features of resistance genes in Enterococcus isolated from farm animals, and emphasized the possibility of the spread of resistance genes carried by Enterococcus from farm animals to humans.

The fusion (F) and haemagglutinin-neuraminidase (HN) proteins of Newcastle disease virus (NDV) are viral entry proteins and are recognized as the major virulence determinants. Previously, a lentogenic NDV virus (CE16) was derived from a mesogenic strain (CI10) through sequential passages in chick embryos. Whole-genome sequence analysis revealed that the two homologous strains shared the same F protein but differed in HN with two amino acid (aa) substitutions (A215G and T430A). To elucidate the molecular reasons for virulence attenuation, two original plasmids (HN-CI10 and HN-CE16) and two single-point mutants (G215A and A430T) reverse-mutated from HN-CE16 were constructed to analyse the known biological functions of HN. The results showed that the A430T substitution significantly weakened the haemadsorption (HAd) activity, increased the neuraminidase (NA) activity, improved the fusion-promoting activity, and enhanced the cleavage-promoting activity of HN-CE16. However, G215A failed to induce obvious functional changes. Therefore, the aa residue HN430 may play a key role in determining virulence. To test this hypothesis, further studies on A430T were conducted through reverse genetics using an infectious cDNA clone. At the viral level, the A430T-mutated virus showed dramatic promotion of viral plaque formation, propagation, and pathogenicity in vitro and in vivo. This study demonstrates a new virulence site associated with HN protein functions, viral propagation, and pathogenicity. All these findings could lay a foundation for illuminating the molecular mechanism of NDV virulence.