ACSL1 Inhibits ALV-J Replication by IFN-I Signaling and PI3K/Akt Pathway

J subgroup avian leukosis virus (ALV-J) infection causes serious immunosuppression problems, leading to hematopoietic malignancy tumors in chicken. It has been demonstrated that interferon-stimulated genes (ISGs) could limit ALV-J replication; nevertheless, the underlying mechanisms remain obscure. Here, we demonstrate that Long-chain Acyl-CoA synthetase 1 (ACSL1) is an interferon (IFN)-stimulated gene that specifically restricts the replication of ALV-J due to the higher IFN-I production. More importantly, ACSL1 induces primary monocyte-derived macrophages (MDMs) to pro-inflammatory phenotypic states during ALV-J infection, and ACSL1 mediates apoptosis through the PI3K/Akt signaling pathway in ALV-J-infected primary monocyte-derived macrophages (MDMs). Overall, these results provide evidence that ACSL1 contributes to the antiviral response against ALV-J.

Automated summary

ACSL1, as an interferon-stimulated gene, plays a crucial role in restricting the replication of ALV-J and inducing apoptosis in primary monocyte-derived macrophages through the PI3K/Akt signaling pathway, leading to pro-inflammatory phenotypic changes. These results provide evidence that ACSL1 contributes to the antiviral response against ALV-J.