AI Article Synopsis
- Avian leukosis virus subgroup J (ALV-J) is an oncogenic retrovirus that causes tumors in chickens.
- Recent research has revealed that ALV-J uses host molecules like MIF to enhance its infection process, although the exact molecular mechanisms are not fully understood.
- The study shows that proteins p10 and p27 from ALV-J's Gag protein interact with MIF, promoting ALV-J infection by aiding its internalization and replication, which could lead to new methods for controlling such viruses.
Article Abstract
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.
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| http://dx.doi.org/10.1016/j.vetmic.2022.109389 | DOI Listing |
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