PMAIP1 promotes J subgroup avian leukosis virus replication by regulating mitochondrial function

Area of Science:

• Veterinary Virology
• Molecular Biology
• Immunology

Background:

• Avian leukosis virus Subgroup J (ALV-J) causes significant economic losses in poultry due to neoplastic diseases and immunosuppression.
• Phorbol-12-myristate-13-acetate-induced protein 1 (PMAIP1) is a proapoptotic protein involved in cancer cell apoptosis.
• The role of PMAIP1 in ALV-J infection and pathogenicity is currently unknown.

Purpose of the Study:

• To investigate the impact of the PMAIP1 gene on ALV-J replication and its regulatory mechanisms.
• To explore the relationship between PMAIP1 expression and ALV-J infection in vivo and in vitro.
• To elucidate the role of PMAIP1 in modulating mitochondrial function during ALV-J infection.

Main Methods:

• Quantitative real-time PCR (qRT-PCR) to assess PMAIP1 expression in infected chickens and cells.
• Manipulation of PMAIP1 expression in chicken fibroblast DF-1 cells.
• Immunofluorescence assay (IFA) and western blotting (WB) to evaluate viral infection and protein expression.
• Assessment of mitochondrial function in relation to PMAIP1 and ALV-J.

Main Results:

• ALV-J infection led to differential expression of PMAIP1 in various chicken organs (down-regulation in spleen, lung, kidney; up-regulation in bursa, liver).
• PMAIP1 expression was significantly up-regulated in ALV-J infected DF-1 cells over time.
• Over-expression of PMAIP1 enhanced ALV-J replication, interferon, and proinflammatory factor expression.
• PMAIP1 interference resulted in opposite effects, indicating its crucial role.

Conclusions:

• The PMAIP1 gene facilitates ALV-J replication by modulating mitochondrial function.
• PMAIP1 plays a significant role in the pathogenicity of ALV-J infection.
• Understanding PMAIP1's role provides insights for developing strategies to enhance avian leukosis disease resistance.