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

Front Immunol. 2021 Oct 29:12:774323. doi: 10.3389/fimmu.2021.774323. eCollection 2021.

Abstract

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.

Keywords: ACSL1; ALV-J; IFN-Ⅰ; PI3K/Akt; apoptosis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis
  • Avian Leukosis / metabolism*
  • Avian Leukosis / virology*
  • Avian Leukosis Virus / physiology*
  • Biomarkers
  • Chickens
  • Coenzyme A Ligases / genetics
  • Coenzyme A Ligases / metabolism*
  • Disease Susceptibility
  • Gene Expression Regulation
  • Host-Pathogen Interactions / genetics
  • Interferon Type I / metabolism*
  • Models, Biological
  • Phosphatidylinositol 3-Kinases / metabolism*
  • Promoter Regions, Genetic
  • Proto-Oncogene Proteins c-akt / metabolism*
  • Virus Replication*

Substances

  • Biomarkers
  • Interferon Type I
  • Proto-Oncogene Proteins c-akt
  • Coenzyme A Ligases