Avian leukosis virus subgroup J induces B cell anergy mediated by Lyn inhibited BCR signal transduction

Avian Leucosis Virus-Host Interaction: The Involvement of Host Factors in Viral Replication

“…If chicken infected with ALV-J, the bursa of Fabricius were poorly developed and the bursa follicles cannot differentiate into cortex and medulla due to the blocking of the differentiation of CD117 + chB6 + B cell progenitors, causing development arrest of B cells and the inhibition of humoral immunity ( 52 ). Additionally, tyrosine kinase Lyn (a key protein in the BCR signaling pathway) involved B cell anergy by inhibiting BCR signal transduction ( 53 ). Briefly, ALV-J SU interacts with Lyn, induces phosphorylation of Lyn at amino acid residue 507, activates the negative regulatory effect of Lyn on the BCR signal transduction pathway, and then mediates B cell anergy ( 53 ).…”

“…Additionally, tyrosine kinase Lyn (a key protein in the BCR signaling pathway) involved B cell anergy by inhibiting BCR signal transduction ( 53 ). Briefly, ALV-J SU interacts with Lyn, induces phosphorylation of Lyn at amino acid residue 507, activates the negative regulatory effect of Lyn on the BCR signal transduction pathway, and then mediates B cell anergy ( 53 ). Regulatory T cells (Tregs) are a subset of mature T cells with negative immunomodulatory effects ( 54 ).…”

Transcriptome-wide N6-methyladenosine modification and microRNA jointly regulate the infection of avian leukosis virus subgroup J in vitro

“…Avian leukosis virus subgroup J ( ALV-J ) is widely circulated in China, mainly because of vaccine contamination and its vertical transmission characteristics ( Payne and Nair, 2012 ; Wang et al, 2018 ; Shittu et al, 2019 ). ALV-J infection leads to severe immunosuppression and various myeloid leukemia and hemangiomas in infected chickens, resulting in huge economic losses to the poultry industry ( Liu et al, 2016 ; He et al, 2020 ).…”