Screening of immune biomarkers in different breeds of chickens infected with J subgroup of avian leukemia virus by proteomic

Ye, Fei; Wang, Yan; He, Qijian; Wang, Zhaoshuo; Ma, Enyue; Zhu, Shiliang; Yu, Heling; Yin, Huadong; Zhao, Xiaoling; Li, Diyan; Xu, Hengyong; Li, Hua; Zhu, Qing

doi:10.1080/21505594.2020.1809323

Cited by 3 publications

(1 citation statement)

References 49 publications

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“…Notably, avian leukosis virus subgroup J (ALV-J) belongs to the genus Alpharetrovirus and family Retroviridae . The virus has been reported to spread in all species of chicken and is known to induce myelocytomas, hemangioma and fibrosarcoma [ 6 – 8 ]. On the other hand, reticuloendotheliosis virus (REV) belongs to the genus Gammaretrovirus and the family Retroviridae.…”

Section: Introductionmentioning

confidence: 99%

TMT-based proteomic analysis reveals integrins involved in the synergistic infection of reticuloendotheliosis virus and avian leukosis virus subgroup J

et al. 2022

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Background Co-infection with the avian leukosis virus subgroup J (ALV-J) and the reticuloendotheliosis virus (REV) increases mutual viral replication, causing a more serious pathogenic effect by accelerating the progression of neoplasia and extending the tumor spectrum. However, the molecular mechanism underlying the synergistic replication of ALV-J and REV remains unclear. Results Here, we performed this study to compare the differentially expressed proteins among CEF cells infected with ALV-J, REV or both at the optimal synergistic infection time using TMT-based quantitative proteomics. We identified a total of 719 (292 upregulated and 427 downregulated) and 64 (35 upregulated and 29 downregulated) proteins by comparing co-infecting both viruses with monoinfecting ALV-J and REV, respectively. GO annotation and KEGG pathway analysis showed the differentially expressed proteins participated in virus-vector interaction, biological adhesion and immune response pathways in the synergistic actions of ALV-J and REV at the protein levels. Among the differentially expressed proteins, a large number of integrins were inhibited or increased in the co-infection group. Further, eight integrins, including ITGα1, ITGα3, ITGα5, ITGα6, ITGα8, ITGα9, ITGα11 and ITGβ3, were validated in CEF cells by qRT-PCR or western blot. Conclusions These findings proved that integrins may be key regulators in the mechanism of synergistic infection of REV and ALV-J, which will provide more insight into the pathogenesis of synergism of REV and ALV-J at protein level.

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Section: Introductionmentioning

confidence: 99%

TMT-based proteomic analysis reveals integrins involved in the synergistic infection of reticuloendotheliosis virus and avian leukosis virus subgroup J

et al. 2022

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Proteomic profiling of purified avian leukosis virus subgroup J particles

Chen

Yan

Gao

et al. 2023

Veterinary Microbiology

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Chicken telomerase reverse transcriptase promotes the tumorigenicity of avian leukosis virus subgroup J by regulating the Wnt/β-catenin signaling pathway

Xiang

Liang

et al. 2022

Vet Res

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This research aimed to analyze the regulatory effect of chicken telomerase reverse transcriptase (chTERT) on the Wnt/β-catenin signaling pathway and its effect on the tumorigenicity of avian leukosis virus subgroup J (ALV-J) through in vivo experiments. The chTERT eukaryotic expression plasmid and its recombinant lentivirus particles were constructed for in vivo transfection of chTERT to analyze the effect of chTERT continuously overexpressed in chickens on the tumorigenicity of ALV-J. During 156 days of the artificial ALV-J tumor-inducing process, 7 solid tumors developed in 3 chickens in the chTERT-overexpression group (n = 26*2) and no tumors developed in the control group (n = 26*2). Another 18 tumors induced by ALV-J were confirmed and collected from breeding poultry farms. And we confirmed that chTERT was significantly highly expressed in ALV-J tumors. The ELISA data suggested that the protein levels of β-catenin and c-Myc in the chicken plasma of the chTERT-overexpressing group with ALV-J infected were consistently and significantly higher than those of the control group. Compared with that of the tumor-adjacent tissues, the activity of the Wnt/β-catenin signaling pathway and expression of the c-Myc was significantly increased in ALV-J tumors. And the percentage of apoptosis in ALV-J tumors significantly lower than that in tumor-adjacent tissues. Immunohistochemistry, Western blot and RT-qPCR suggested that the replication level of ALV-J in tumors was significantly higher than that in tumor-adjacent tissues. This study suggests that chTERT plays a critical role in the tumorigenicity of ALV-J by enhancing the Wnt/β-catenin signaling pathway, which will contribute to further elucidating the tumor-inducing mechanism of ALV-J.

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Screening of immune biomarkers in different breeds of chickens infected with J subgroup of avian leukemia virus by proteomic

Cited by 3 publications

References 49 publications

TMT-based proteomic analysis reveals integrins involved in the synergistic infection of reticuloendotheliosis virus and avian leukosis virus subgroup J

TMT-based proteomic analysis reveals integrins involved in the synergistic infection of reticuloendotheliosis virus and avian leukosis virus subgroup J

Proteomic profiling of purified avian leukosis virus subgroup J particles

Chicken telomerase reverse transcriptase promotes the tumorigenicity of avian leukosis virus subgroup J by regulating the Wnt/β-catenin signaling pathway

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