Jingrui Liu

Influenza A viruses remain a persistent global health challenge due to their rapid antigenic evolution, zoonotic potential, and pandemic threat. Universal countermeasures targeting conserved viral components are urgently needed to enhance diagnostic, surveillance, and therapeutic capabilities. Here, we report the generation and characterization of a high-affinity monoclonal antibody (2D8 mAb) against the nucleoprotein (NP) of the H9N2 avian influenza virus, a subtype with increasing relevance to human infections. Importantly, 2D8 mAb exhibited robust cross-reactivity with a broad spectrum of influenza A viruses, including H1, H3, H5, H7, and H9 subtypes, while showing no cross-reactivity with unrelated viral pathogens. Epitope mapping identified its binding target as a highly conserved NP motif ³⁸RFYIQMCTEL⁴⁷, which is invariant across all major human influenza A lineages. Isotyping revealed 2D8 mAb to be of the IgG2b/κ subclass, with an exceptionally high titer (1:20,480,000) as determined by ELISA. Given the essential role of NP in viral replication and host adaptation, this antibody offers a powerful platform for next-generation diagnostic assays capable of detecting a wide range of human and zoonotic influenza A viruses using a single reagent. Moreover, it holds potential for guiding the design of universal antiviral strategies targeting structurally constrained regions of the influenza virus. Our findings provide a valuable resource for advancing pan-influenza A interventions, with direct implications for improving pandemic preparedness and strengthening global influenza surveillance in both clinical and public health settings.

Vaccination remains the primary strategy for controlling infectious diseases in farm animals. However, current conventional vaccines demonstrate clinical limitations including suboptimal immunogenicity and frequent booster requirements, which compromise disease management efficacy. This study presents an innovative vaccine platform combining yolk immunoglobulin (IgY) with inactivated antigens as co-immunization components. We developed two formulations targeting economically significant pathogens: avian Fowl Adenovirus Serotype 4 (FAdV-4) and Porcine Epidemic Diarrhea Virus (PEDV). For FAdV-4 vaccine evaluation in specific pathogen-free (SPF) chickens, the IgY-antigen complex demonstrated superior immunogenic properties compared to conventional inactivated vaccines. When administered as a single dose at 14 days of age, the experimental formulation elicited significantly stronger humoral responses as measured by both serum neutralization (SN₅₀) and ELISA. Notably, this vaccination strategy provided 100% protection against lethal FAdV-4 challenge from 0 h to 20 weeks post-vaccination, with complete absence of clinical disease manifestations. In PEDV assessment using mouse models, the IgY-antigen formulation induced significantly higher antibody titers than inactivated antigen alone at all post-immunization timepoints (p < 0.01). Comparative analysis revealed our dual-component platform enhanced both the intensity and rapidity of protective immune responses compared to traditional inactivated vaccines. These findings establish that the IgY-antigen co-immunization strategy represents a promising approach for developing new veterinary vaccines with improved protective efficacy. The platform’s ability to generate robust, rapid-onset immunity while maintaining single-dose effectiveness addresses critical limitations of current vaccine technologies.

In recent years, the prevalence and variation of goose adenoviruses, especially Goose Adenovirus Type 4 (GoAdV-4), have threatened waterfowl farming, while their genetic evolution and pathogenic mechanisms remain unelucidated. In May 2024, a novel GoAdV-4 strain (JA2485) was isolated from diseased Sanhua geese in Jian City, Jiangxi Province, China. It propagated in 11–13-day-old goose embryos, with a 50% embryo infectious dose (EID₅₀) of 10^2.2/0.1 mL. Whole-genome sequencing (GenBank Accession No. PQ152938) showed its genome is 43,030 base pairs long, containing 33 protein-coding regions and 2 fiber genes. Phylogenetic analysis revealed JA2485 is closely related to the Hungarian P29 strain and Chinese CH-FJZZ-202201 strain (nucleotide similarity: 94–96.8%), but clusters in a different branch from other avian adenoviruses. In pathogenicity tests on 1-day-old Sanhua geese, both subcutaneous injection and oral inoculation groups had 50% mortality. Infected geese showed weight loss, depression, reduced appetite, increased recumbency, and even paralysis in severe cases. Post mortem examination revealed hepatic rounded margins, yellowing, focal hemorrhages, and renal hemorrhagic lesions. Notably, viral loads were highest in the liver, duodenum, and cloacal swabs, suggesting fecal transmission. This study provides a key basis for clarifying GoAdV-4’s evolutionary characteristics and pathogenic mechanisms, and formulating targeted prevention strategies.

The chicken infectious anemia virus (CIAV) and fowl adenovirus serotype E8b (FAdV E8b) are pathogens that cause aplastic anemia and inclusion body hepatitis (IBH) in chickens, respectively. The co-infection of CIAV and FAdV E8b poses a significant threat to poultry health, potentially worsening clinical symptoms and increasing mortality rates. This study aimed to explore the combined pathogenic effects of FAdV E8b and CIAV co-infection on one-day-old specific pathogen-free (SPF) chickens. The results showed that co-infection led to significantly higher clinical scores and mortality rates compared to FAdV E8b infection alone. Additionally, there were different tissue distribution patterns for FAdV E8b between the single infection and co-infection groups, indicating potential changes in viral tropism. Biochemical analysis revealed elevated markers of liver and/or muscle damage in both the FAdV E8b infection group and the co-infection group, consistent with the viral infection process. These findings suggest that co-infection with FAdV E8b and CIAV can intensify clinical signs and mortality, and may potentially alter viral replication and tissue tropism in chickens. This study establishes a foundation for future investigations into the underlying mechanisms governing the interaction between CIAV and FAdV E8b during co-infection.