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.
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基于TMT的蛋白质组学分析揭示整合素参与网状内皮增生病毒和禽白血病病毒J亚群的协同感染
DOI：
10.1186/s12917-022-03207-6
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发表时间：
2022-04-04
影响因子：
2.6
通讯作者：
Cheng Z
中科院分区：
文献类型：
--
作者：
Cui X;Zhang X;Xue J;Yao Y;Zhou D;Cheng Z
禽白血病病毒J亚群(ALV-J)和网状内皮组织增生症病毒(REV)的混合感染增加了病毒的相互复制，通过加速肿瘤的进展和扩大肿瘤谱而导致更严重的致病效应。然而，ALV-J和REV协同复制的分子机制尚不清楚。在这里，我们进行了这项研究，以比较在ALV-J和/或REV感染CEF细胞在最佳协同感染时间的差异蛋白质组基于TMT的定量蛋白质组。通过比较两种病毒共感染和单独感染ALV-J和REV，我们共鉴定出719个蛋白(上调292个，下调427个)和蛋白(35个上调，29个下调)。GO注释和KEGG通路分析表明，差异表达的蛋白质在蛋白质水平上参与了ALV-J和REV的协同作用中的病毒与载体的相互作用、生物黏附和免疫应答途径。在差异表达的蛋白质中，在合并感染组中有大量整合素被抑制或增加。进一步通过定量逆转录聚合酶链式反应和免疫印迹方法鉴定了8个整合素，包括α1、α3、α5、α6、α8、α9、α11和β3。这些结果证明整合素可能是REV和ALV-J协同感染机制中的关键调节因子，这将为从蛋白水平上更深入地了解REV和ALV-J协同感染的发病机制提供更多的信息。网上版载有补充材料，可在10.1186/s12917-022-03207-6查阅。
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. 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. 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. The online version contains supplementary material available at 10.1186/s12917-022-03207-6.
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影响因子：
14.9
作者：
Kanehisa M;Furumichi M;Sato Y;Ishiguro-Watanabe M;Tanabe M
通讯作者：
Tanabe M
影响因子：
14.9
作者：
Ma J;Chen T;Wu S;Yang C;Bai M;Shu K;Li K;Zhang G;Jin Z;He F;Hermjakob H;Zhu Y
通讯作者：
Zhu Y
影响因子：
11.4
作者：
De Arcangelis, A;Georges-Labouesse, E
通讯作者：
Georges-Labouesse, E
影响因子：
3.3
作者：
Deeg, Cornelia A.;Degroote, Roxane L.;Hauck, Stefanie M.
通讯作者：
Hauck, Stefanie M.
影响因子：
5.9
作者：
Gaglia MM;Munger K
通讯作者：
Munger K