Abstract
Avian leukosis virus subgroup J (ALV-J) infection can cause tumors and immunosuppression. Since the precise mechanism of the innate immune response induced by ALV-J is unknown, we investigated the antiviral innate immune responses induced by ALV-J in chicks and chickens that had developed tumors. Spleen levels of interleukin-6 (IL-6), IL-10, IL-1β, and interferon-β (IFN-β) were not significantly different between the infected chick groups and the control groups from 1 day post hatch to 7 days post hatch. However, IL-6, IL-1β, and IFN-β protein levels in the three clinical samples with hemangiomas were dramatically increased compared to the healthy samples. In addition, the anti-inflammatory cytokine IL-10 increased sharply in two of three clinical samples. We also found a more than 20-fold up-regulation of ISG12-1 mRNA at 1 day post infection (d.p.i.) and a twofold up-regulation of ZC3HAV1 mRNA at 4 d.p.i. However, there were no statistical differences in ISG12-1 and ZC3HAV1 mRNA expression levels in the tumorigenesis phase. ALV-J infection induced a significant increase of Toll-like receptor 7 (TLR-7) at 1 d.p.i. and dramatically increased the mRNA levels of melanoma differentiation-associated gene 5 (MDA5) in the tumorigenesis phase. Moreover, the protein levels of interferon regulatory factor 1 (IRF-1) and signal transducer and activator of transcription 1 (STAT1) were decreased in chickens with tumors. These results suggest that ALV-J was primarily recognized by chicken TLR7 and MDA5 at early and late in vivo infection stages, respectively. ALV-J strain SCAU-HN06 did not induce any significant antiviral innate immune response in 1 week old chicks. However, interferon-stimulated genes were not induced normally during the late phase of ALV-J infection due to a reduction of IRF1 and STAT1 expression.
Highlights
Avian leukosis virus (ALV) is a member of the α-retrovirus genus of retroviridae, causing neoplastic disease, immunosuppression, and reproduction problems in the poultry industry worldwide
We investigated the effects of Avian leukosis virus subgroup J (ALV-J) infection on the in vivo mRNA and protein expression of related immune-response genes and cytokines during the early and late phases of infection
To determine whether the SPF chickens were successfully infected, we measured gene expression levels of ALV-J-specific genes from chickens infected with the SCAU-HN06 virus strain
Summary
Avian leukosis virus (ALV) is a member of the α-retrovirus genus of retroviridae, causing neoplastic disease, immunosuppression, and reproduction problems in the poultry industry worldwide. Avian leukosis virus subgroup J can induce the formation of different types of tumors such as haemangiomas and myelocytomas and immunosuppression due to ALV-J infection increases susceptibility to other avian diseases (Abolnik and Wandrag, 2014). In the current study we analyzed the transcriptional level of selected immune-response genes we had previously identified from whole-transcriptome profiling of ALV-J-induced tumors in chicken spleen samples (Li et al, 2015). These genes included those with known anti-viral properties such as the single copy Mx gene, ISG12-1 as well as the toll-like receptor TLR-7 and other cytokine-related genes. Our findings extend our current understanding of the host-response mechanism to exogenous ALV infection
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