To identify the major splicing variant of the sheep irf7 gene that suppresses bluetongue virus （BTV） replication，the sheep irf7 gene was cloned using specific primers，cDNA，reverse-transcribed from total RNA extracted from BTV-infected immortalized sheep pulmonary artery endothelial （SPAE） cells，served as the template.The cloned sheep irf7 gene was then overexpressed in SPAE cells.Real-time fluorescence quantitative RT-PCR，western blotting，and immunofluorescence assays were employed to detect the transcriptional and translational levels of host genes and protein，as well as viral protein.Additionally，the proportion of SPAE cells co-localized with the non-structural protein NS3 and lentivirus GFP，along with the number of viral genome copies，were quantified.The results showed that the short splicing variant of the sheep irf7 gene，designated irf7b，has a full-length sequence of 1 206 bp and encodes a total of 401 amino acids.In BTV-infected SPAE cells overexpressing the irf7b splicing variant，the transcriptional levels of the sheep irf7 and β-interferon （ifn-β） genes were significantly upregulated （P<0.01），with log₂（FC） values of 1.62 and 1.14，respectively.The expression level of the sheep IRF7 protein increased significantly by 1.19-fold （P<0.01），whereas the expression level of the viral non-structural protein NS3 decreased significantly by 14.20% （P<0.05）.The proportion of SPAE cells co-localized with NS3 and GFP was reduced by 11.44% （P<0.05）； concurrently，the number of viral genome copies was decreased by 18.05% （P<0.05）.These results indicate that the short splicing variant irf7b of the sheep irf7 gene plays a crucial role in suppressing BTV replication.