African horse sickness (AHS) is an arthropod-borne, severe equid disease caused by African horse sickness virus (AHSV). AHSV has high mortality and is endemic to sub-Saharan Africa. It has been classified into nine distinct serotypes (AHSV-1 to AHSV-9) based on VP2 immunogenicity. The AHS outbreak in Thailand in 2020, caused by AHSV-1, marked the first occurrence of this disease in Southeast Asia. It posed a substantial threat to the security of the equine industry in the nations across the region. To ensure the emergency reserve for AHS prevention and control, the AHSV strain imported to China from abroad over 60 years ago was characterized in this study. The strain was passaged in mice and then blind-passaged in Vero cells. The plaque purification method was then used to purify the strain and obtain its cell-adapted version, named AHSV/C. Neutralization tests confirmed that the virus belongs to AHSV-1. Whole-genome sequencing revealed that AHSV/C was highly homologous to AHSV-1 isolate 1180, with over 95% homology of major antigenic protein VP2, as compared to other AHSV-1 strains, including the prevalent strain in Thailand. In the mouse models, AHSV/C exhibited no clinical signs or histopathological lesions, suggesting low virulence and safety. This research for the first time characterized the in vitro growth characteristics and viral subtypes of the AHSV in China, determined its complete whole-genome sequence, and evaluated its safety using a mouse model. It provides crucial experimental materials and scientific foundations for the development of diagnostic methods and vaccines against AHSV-1.

African horse sickness (AHS) is a lethal vector-borne disease caused by African horse sickness virus (AHSV) and represents a major threat to equine health and the horse industry. In 2020, outbreaks of AHS caused by AHSV serotype 1 (AHSV-1) were reported in Thailand, increasing the risk of AHS introduction into China. Given the safety issues associated with currently available live attenuated AHS vaccines, the development of safer and more effective vaccination strategies is urgently needed. In this study, we constructed a recombinant fowlpox virus (rFPV) expressing the AHSV-1 VP2 protein as a candidate vaccine, designated rFPV-VP2. The recombinant virus was verified by PCR and Western blot analysis, which confirmed the successful expression of VP2. Preliminary immunization trials were conducted in both mice and horses, and immune responses were evaluated via an indirect enzyme-linked immunosorbent assay (iELISA) and immunofluorescence assay (IFA). The results revealed that VP2-specific antibodies were successfully induced in the serum of rFPV-VP2-immunized animals. Notably, serum from immunized horses showed specific reactivity with AHSV-1, confirming the induction of AHSV-1-specific immune responses. Therefore, these results demonstrate that rFPV-VP2 is a promising candidate vaccine for AHSV-1 and provide a scientific basis for the development of safer preventive strategies.

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.

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.