Bluetongue virus belongs to the Reoviridae family, which causes morbidity in ruminants. Herein, we report the full-length genome sequence of a recombinant BTV strain of serotype 1 (YNDH/103/2013) isolated from sentinel cattle in Yunnan Province, China, in 2013. To identify and understand the characteristics of YNDH/103/2013, we screened closely related viruses using Simplot 3.5.1 software and conducted verification via phylogenetic analysis using MEGA 11.0.13 software. Phylogenetic analysis and segment examination showed that the YNDH/103/2013 strain likely originated from multiple recombination events involving prevalent strains such as Y863, NRT37/ABT/HSR, and YTS-4 in China and India. The genome of BTV-1/YNDH/103/2013 derives from at least three reassortments with these strains, showing recombination breakpoints mainly in segments 4, 6, 8, and 9. This study improves our understanding of the origin and spread of BTV-1 in China.

Manganese superoxide dismutase (MnSOD) and catalase (CAT) could eliminate reactive oxygen species (ROS) and maintain the reduction-oxidation balance in cells. This study aimed to investigate their functions in turbot (Scophthalmus maximus) response to the Vibro anguillarum challenge. SmMnSOD, the full-length liver cDNA of MnSOD from S. maximus , was cloned by fast amplification of cDNA ends (RACE). Sequencing of nucleotides indicated that the SmMnSOD cDNA was 1267 base pairs with a 684-base-pair open reading frame, encoding a 228 amino acid protein with 28 amino acid residues. The SmMnSOD sequence contains MnSOD signatures (DVWEHAYY) and probable N-glycosylation sites (NVT, NHT, and NLS). The deduced sequence of SmMnSOD revealed sequence homology between 85.3% and 92.9% with those of other species. A phylogenetic study found that SmMnSOD clustered with other fish MnSOD, indicating that SmMnSOD was a member of the MnSOD family. The SmMnSOD transcript was discovered by qRT-PCR in the gill, stomach, head-kidney, muscle, liver, intestine, and heart of S. maximus , with the highest expression in the liver. Upon intervention by V. anguillarum , the liver and head kidney transcript levels of SmMnSOD were up-regulated at 12 and 48 h, whereas the temporal expression profiles of the CAT transcript increased at 6 and 24 h. As the pathogenic bacterial stress processing was prolonged to 72 h, the liver and head kidney transcript levels of SmMnSOD and CAT decreased gradually. Thus, SmMnSOD was triggered and may be related to S. maximus ’ immunological responses against V. anguillarum .

Bluetongue virus (BTV) infects various ruminant species, posing significant threats to animal health and causing substantial economic losses to the livestock industry. Ovine type II alveolar epithelial cells (OAECIIs) play crucial roles in maintaining pulmonary structural integrity and modulating immune responses. Their dysfunction is closely associated with lung disease pathogenesis, making them important therapeutic targets. However, OAECIIs’ immunoregulatory functions and early response mechanisms during BTV infection remain unclear. To address this, we analyzed transcriptomic changes in OAECIIs following BTV-1 infection. RNA-seq revealed 1047 and 852 differentially expressed genes (DEGs) at 8 and 12 h post-infection (hpi), respectively, compared to uninfected controls. Bioinformatics analysis showed significant upregulation of nucleic acid-sensing receptors, interferon-stimulating factors, inflammatory mediators, and cytokines during early infection, mediated primarily through type I interferon signaling, TNF signaling, and cytosolic DNA-sensing pathways. We identified MAD5, ZNFX1, cGAS, OAS, PKR and ZBP1 as key pattern recognition receptors in OAECIIs during BTV infection. The IFN-β, MX1/2, RSAD2 and PLSCR1 pathways mediated antiviral responses, while IL-15, CXCL10, CCL2 triggered inflammatory responses, collectively causing structural alterations through AQP1/9 and tight junction protein modulation. These findings provide critical insights into early antiviral mechanisms and cellular structural changes in OAECIIs during BTV infection, establishing a foundation for understanding pneumonia pathogenesis and developing targeted BTV therapies.

To analyze the full nucleotide sequence of a null allele of major histocompatibility complex class I chain-related gene (MICA). A sequence-based typing method was used to determine the nucleotide sequence of the MICA gene. Potential alleles were identified with a computer program. The identified allele has possessed a sequence similar to that of MICA*027 except for a C→T substitution at position 184 in codon 62 (CAG→TAG) of exon 2. As a stop codon, this may result in a truncated protein. A null allele of MICA gene has been identified. The sequence has been submitted to the Genbank nucleotide sequence database (submission No. HWS10011131), which was officially named as MICA*063N by the WHO Nomenclature Committee in October 2010.