Immunosuppression caused by avian leukemia virus J subgroup (ALV-J) infection includes atrophy or regeneration disorders of the lymphoid organs, decreased immune response, and termination of B lymphocyte maturation process and inhibition of T-lymphocyte development. The regulatory mechanism of the related resistance genes and protein expression is not clear. While searching for a molecular marker for the immune response to ALV-J infection, we detected differentially expressed proteins (DEPs) of spleens from chicken infected by ALV-J at 15th day and 30th day by the data-independent acquisition technique. Approximately 220 DEPs from the spleens of chickens infected by ALV-J were detected. To find a relatively stable biomarker molecule, we summarized the DEPs at two timepoints and selected activating signal cointegrator 1 complex subunit 3 (ASCC3), TBC1 domain family member 2 (TBC1D2), MHC class II beta chain 1 (BLB2), ensconsin (MAP7), complement component 1 Q subcomponent B chain (C1QB), and Follistatin-like 1 (FSTL1) from both comparisons for protein interaction network analysis. ASCC3, BLB2, C1QB, and FSTL1 were potential biomarkers for the complex infection mechanism of ALV-J and the dynamic immune mechanism of the body.
Keywords: ALV-J; ASCC3; BLB2; C1QB; FSTL1; Proteomic.