African swine fever (ASF) is a highly pathogenic swine
infectious disease that affects domestic pigs and wild boar, which is caused by the African swine fever virus (ASFV). ASF has caused huge economic losses to the pig industry and seriously threatens global food security and livestock health. To date, there is no safe and effective commercial
vaccine against ASF. Unveiling the underlying mechanisms of ASFV-host interplay is critical for developing effective
vaccines and drugs against ASFV. In the present study,
RNA-sequencing, RT-qPCR and Western blotting analysis revealed that the transcriptional and
protein levels of the host factor FoxJ1 were significantly down-regulated in primary porcine alveolar macrophages (PAMs) infected by ASFV. RT-qPCR analysis showed that overexpression of FoxJ1 upregulated the transcription of
type I interferon and
interferon stimulating genes (ISGs) induced by
poly(dA:dT). FoxJ1 revealed a function to positively regulate innate immune response, therefore, suppressing the replication of ASFV. In addition, Western blotting analysis indicated that FoxJ1 degraded ASFV MGF505-2R and E165R
proteins through autophagy pathway. Meanwhile, RT-qPCR and Western blotting analysis showed that ASFV S273R inhibited the expression of FoxJ1. Altogether, we determined that FoxJ1 plays an
antiviral role against ASFV replication, and ASFV
protein impairs FoxJ1-mediated
antiviral effect by degradation of FoxJ1. Our findings provide new insights into the
antiviral function of FoxJ1, which might help design
antiviral drugs or
vaccines against ASFV
infection.