Interaction of p10/p27 with macrophage migration inhibitory factor promotes avian leukosis virus subgroup J infection

Avian leukosis virus subgroup J (ALV-J), an oncogenic retrovirus, induces myelocytoma and various other tumors in broilers and layers. Many recent studies have shown that ALV-J can hijack host molecules to facilitate infection. However, the molecular mechanisms of this process are not clear. Here, we aimed to elucidate the molecular mechanisms contributing to ALV-J infection. ALV-J hijacked MIF via p10 and p27 to facilitate ALV-J infection. ALV-J persistently activated MIF expression in DF-1 cells, and MIF significantly facilitated ALV-J internalization and replication, which demonstrated by MIF overexpression and knockdown experiments and treatment with the MIF antagonist ISO-1. Furthermore, we found that the two subunit proteins of Gag, p10 and p27, interacted with MIF in the cytoplasm, respectively. These results suggested that the p10 and p27 subunit in Gag protein recruited MIF to promote ALV-J infection, providing insights into the roles of the p10/p27 and the host factor MIF in ALV-J infection. The finding may facilitate the development of new strategies for controlling ALV-J or retrovirus infections.

Automated summary

In this study, the molecular mechanisms contributing to Avian leukosis virus subgroup J (ALV-J) infection were elucidated. It was found that ALV-J hijacked MIF through its p10 and p27 subunit proteins to facilitate infection. MIF overexpression and knockdown experiments as well as treatment with the MIF antagonist ISO-1 confirmed that MIF significantly promoted ALV-J internalization and replication. Additionally, the interaction between the subunit proteins p10 and p27 of Gag and MIF in the cytoplasm was observed. These findings provide insights into the roles of p10/p27 and the host factor MIF in ALV-J infection.