High-frequency and activation of CD4CD25 T cells maintain persistent immunotolerance induced by congenital ALV-J infection.

Congenital avian leukosis virus subgroup J (ALV-J) infection can induce persistent immunotolerance in chicken, however, the underlying mechanism remains unclear. Here, we demonstrate that congenital ALV-J infection induces the production of high-frequency and activated CD4CD25 Tregs that maintain persistent immunotolerance. A model of congenital infection by ALV-J was established in fertilized eggs, and hatched chicks showed persistent immunotolerance characterized by persistent viremia, immune organ dysplasia, severe imbalance of the ratio of CD4/CD8 T cells in blood and immune organs, and significant decrease in CD3 T cells and Bu-1 B cells in the spleen.

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

Immune tolerance induced by avian leukosis virus subgroup J (ALV-J) is a prerequisite for tumorigenesis. Although we had reported that B cell anergy induced by ALV-J was the main reason for immune tolerance, the molecular mechanism still remains unclear. Here, we found SU protein of ALV-J interacted with tyrosine kinase Lyn (a key protein in BCR signaling pathway) by confocal laser scanning microscopy and co-immunoprecipitation test, which suggested that Lyn might play an important role in B cell anergy induced by ALV-J.

Interplay between CTHRC1 and the SU protein of avian leukosis virus subgroup J (ALV-J) facilitates viral replication.

The lifecycle of avian leukosis virus subgroup J (ALV-J), a typical tumorigenic retrovirus, is highly dependent upon host cellular proteins. However, there have been few studies directed at uncovering the host proteins responsible for ALV-J replication, which could provide insights into new strategies for ALV-J prevention and control. Here, we used proteomics to identify the association of differential levels of collagen triple helix-repeat-containing 1 (CTHRC1) and with viral replication.

Clonal anergy of CD117chB6 B cell progenitors induced by avian leukosis virus subgroup J is associated with immunological tolerance.

Background: The pathogenesis of immunological tolerance caused by avian leukosis virus subgroup J (ALV-J), an oncogenic retrovirus, is largely unknown.

Results: In this study, the development, differentiation, and immunological capability of B cells and their progenitors infected with ALV-J were studied both morphologically and functionally by using a model of ALV-J congenital infection. Compared with posthatch infection, congenital infection of ALV-J resulted in severe immunological tolerance, which was identified as the absence of detectable specific antivirus antibodies.