The gut microbiota, often referred to as the “forgotten organ”, plays an indispensable role in maintaining host physiological metabolism, immune function, and nutrient absorption. Moreover, the gut microbiome serves as a critical biological barrier against viral infections and is increasingly recognized as a potential target to augment antiviral therapies. Recent studies have revealed that microbial ligands and metabolites derived from the gut microbiota are pivotal in modulating respiratory immune responses, providing compelling evidence of the complex interaction network between microorganisms and the host, particularly the signaling pathways linking the gut to distal organs such as the lungs. This review examines the communication and regulatory mechanisms between the gut microbiota and pulmonary mucosal surfaces during influenza virus infection, emphasizing how gut microbial communities and probiotics influence host immune responses, promote the production of immune-related molecules, and enhance antiviral defenses. The aim is to provide comprehensive insights into the gut–lung axis and its implications for respiratory health.

The African swine fever virus (ASFV), particularly the genotypes I and II strains that have spread beyond Africa, continues to threaten global swine production and food security. Currently, African swine fever (ASF) control strategies rely heavily on biosecurity measures underpinned with molecular diagnostics. To address the need for genotyping, the present study developed a tetra‐primer amplification refractory mutation system PCR (ARMS‐PCR) assay capable of discriminating genotypes I and II ASFVs, as well as their mixed infections. The assay utilizes a multiplex of four primers: two outer universal primers and two allele‐specific inner primers targeting a conserved single nucleotide polymorphism (SNP, G1656A) of the B646L gene, specific to genotypes I and II ASFVs. The tetra‐primer ARMS‐PCR assay demonstrated a detection limit of 100 copies per reaction, which is comparable to that of the WOAH‐recommended PCR method, and no cross‐reactivity was observed with eight other porcine viruses. Furthermore, clinical validation confirmed that the assay demonstrated a 97.22% coincidence rate (35/36) with the standard WOAH‐recommended PCR method. In summary, the tetra‐primer ARMS‐PCR assay provides a practical, specific, and cost‐effective tool for ASF epidemiological surveillance, well‐suited for resource‐limited regions and those with cocirculation of genotypes I and II ASFVs.

Pulmonary arterial hypertension (PAH), a major subtype of pulmonary hypertension (PH), is a significant human pulmonary disease whose pathogenic mechanisms remain incompletely understood. Conventional animal models for PAH induction often fail to fully replicate the entire disease progression, making it difficult to trace the initial causes, key pathogenic events, and early disease mechanisms. We propose an evidence-based hypothesis that Broiler Ascites Syndrome (BAS) exhibits high similarity to human pulmonary arterial hypertension in terms of pathogenic triggers and molecular pathology, suggesting its potential as a spontaneous animal model for PAH research. This review systematically summarizes the pathogenic mechanisms and disease-inducing factors of BAS, analyzing its pathobiological commonalities with PAH. We demonstrate shared features in pulmonary vascular remodeling mechanisms, including cellular dysfunction, tissue fibrosis, and immune dysregulation. Furthermore, consistent reactive mechanisms are observed across different types of PAH-related studies and corresponding poultry research. This collective evidence supports the feasibility of utilizing BAS as a spontaneous animal model for PAH investigation. By comparing the pathogenic mechanisms of BAS and PAH, this work provides novel insights for developing animal models in PAH research. If validated, this model could address limitations of existing models regarding hypoxia tolerance, and right heart remodeling.

African horse sickness (AHS), a noncontagious insect-borne disease affecting equids, is caused by the African horse sickness virus (AHSV) and is associated with extremely high morbidity and mortality. AHSV has nine distinct serotypes (AHSV-1 to AHSV-9). In a previous study, we characterized the genome and in vitro growth properties of AHSV/C, a cell-adapted derivative of an AHSV-1 strain imported into China 60 years ago, and verified its safety in mice. This study preliminarily explored the pathogenicity of AHSV/C in guinea pigs and horses (its natural host). Six groups of guinea pigs were inoculated with three doses of AHSV/C (10^7.5, 10^6.5, and 10^5.5 TCID₅₀ per animal) via both intraperitoneal and subcutaneous routes; two horses were subcutaneously inoculated with 10^5.5 TCID₅₀ of AHSV/C. All animals received a booster inoculation three weeks later. During the entire observation period, we mainly monitored clinical signs, body temperature, viremia, virus shedding and pathological changes (examined only in guinea pigs), and collected serum samples for neutralizing antibody detection. The results showed that no abnormal clinical signs, evident viremia, or virus shedding were observed in either species. Histopathological examinations revealed no evident lesions in guinea pigs. Neutralization tests showed that AHSV/C induced only low neutralizing antibody titers after primary inoculation, with a marked increase after booster administration. Collectively, this study preliminarily characterized the pathogenicity of AHSV/C in guinea pigs and horses, confirming that the strain showed no evident pathogenicity in test animals. These findings suggest that AHSV/C may be an attenuated strain. Further studies with larger sample sizes are required to validate these findings and explore their potential applications.

H6 subtype avian influenza viruses (AIVs) have a broader host range and circulate globally in wild birds, domestic ducks, geese, and terrestrial poultry all over the world. Their demonstrated capacity to adapt receptor-binding affinity for mammalian species constitutes a persistent concern for zoonotic transmission and public health. In this study, a novel triple-reassortant H6N8 AIV strain was isolated from a chicken farm in southern China and designated as A/chicken/Guangdong/JM642/2023 (H6N8). The complete genome of the virus was sequenced using Next-Generation Sequencing. Phylogenetic analysis indicated that the HA gene of the isolate clustered into the Group III/HN573-like, which encompasses H6 subtype viruses bearing various NA genes and belonging to the Eurasian gene pool. The NA gene showed the closest genetic relationship with viruses originating from North America. All six internal genes were derived from H9N2 AIVs. The virus possesses several key molecular determinants known to contribute to an expanded host range and increased virulence. Animal infection studies demonstrated that the virus was capable of infecting mice without prior adaptation. It replicated efficiently in the lungs and nasal turbinates, followed by systemic dissemination resulting in lethal outcomes. Inoculated chickens remained asymptomatic; however, the virus replicated efficiently in multiple organs, with high viral loads detected particularly in the lungs and kidneys. Viral shedding occurred via both the respiratory and digestive tracts, and horizontal transmission was observed among chickens. Notably, infected and contacted chickens developed high levels of antibodies from 8 days post-inoculation (DPI) to the end of observation period. This study enhances our understanding of the genetic and biological characteristics of the novel reassortant H6N8 AIVs and underscores their potential risk to public health.

Avian influenza, a disease caused by avian influenza virus (AIV), mainly infects birds but can also infect mammals, which poses a serious threat to public health. Therefore, thorough understanding of its pathogenic mechanism and the identification of antiviral targets are essential for the prevention, control, and treatment of AIV. The polymerase acidic protein (PA) is a core component of the viral RNA-dependent RNA polymerase complex and plays a central role in viral transcription through its cap-snatching activity during early infection. We employed a multi-omics approach combining transcriptome analysis with PA interaction proteomics to characterize host responses during AIV infection and explore the PA–host interaction network. Transcriptomics revealed a polarized host response marked by activated translation-related processes, mitochondrial energy metabolism, and innate immune signaling, alongside broad suppression of nuclear transcriptional regulation and cell cycle pathways. Immunoprecipitation–mass spectrometry identified host proteins associated with PA that were enriched in RNA metabolism, ribosome biogenesis, and protein homeostasis. Integrative analysis of transcriptomic and interactome data, along with protein–protein interaction network analysis, prioritized a subset of high-confidence PA-interacting host factors. Among these, ribosomal protein RPS27A was validated to interact with PA and to support viral replication during early infection in this study.