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當(dāng)前位置:首頁  >  技術(shù)文章  >  新研究:腸病毒D68 VP3靶向干擾素調(diào)節(jié)因子7抑制I型干擾素應(yīng)答

新研究:腸病毒D68 VP3靶向干擾素調(diào)節(jié)因子7抑制I型干擾素應(yīng)答

更新時間:2024-12-29  |  點擊率:68

20236月,中國天津大學(xué)生命科學(xué)學(xué)院;天津市生物大分子結(jié)構(gòu)功能與應(yīng)用重點實驗室研究所;天津大學(xué)環(huán)境科學(xué)與工程學(xué)院(School of Life Sciences, Tianjin University, Tianjin, China;Institute of Tianjin Key Laboratory of Function and Application of Biological Macromolecular Structures, Tianjin, ChinaSchool of Environmental Science and Engineering, Tianjin University, Tianjin, China) Jun Kang老師研究團隊在《MICROBIOL SPECTR》上發(fā)表論文:

Enterovirus D68 VP3 Targets the Interferon Regulatory Factor 7 To Inhibit Type I Interferon Response"

 

“腸病毒D68 VP3靶向干擾素調(diào)節(jié)因子7抑制I型干擾素應(yīng)答"

 

Abstract

Enterovirus D68 (EV-D68) is a globally emerging pathogen causing severe respiratory illnesses mainly in children. The protease from EV-D68 could impair type I interferon (IFN-I) production. However, the role of the EV-D68 structural protein in antagonizing host antiviral responses remains largely unknown. We showed that the EV-D68 structural protein VP3 interacted with IFN regulatory factor 7 (IRF7), and this interaction suppressed the phosphorylation and nuclear translocation of IRF7 and then repressed the transcription of IFN. Furthermore, VP3 inhibited the TNF receptor associated factor 6 (TRAF6)-induced ubiquitination of IRF7 by competitive interaction with IRF7. IRF7Δ305-503 showed much weaker interaction ability to VP3, and VP3Δ41-50 performed weaker interaction ability with IRF7. The VP3 from enterovirus A71 (EV-A71) and coxsackievirus A16 (CV-A16) was also found to interact with the IRF7 protein. These results indicate that the enterovirus structural protein VP3 plays a pivotal role in subverting host innate immune responses and may be a potential target for antiviral drug research. IMPORTANCE EV-D68 is a globally emerging pathogen that causes severe respiratory illnesses. Here, we report that EV-D68 inhibits innate immune responses by targeting IRF7. Further investigations revealed that the structural protein VP3 inhibited the TRAF6-induced ubiquitination of IRF7 by competitive interaction with IRF7. These results indicate that the control of IRF7 by VP3 may be a mechanism by which EV-D68 represses IFN-I production.


摘要:

腸病毒D68 (EV-D68)是一種全球新發(fā)病原體,主要在兒童中引起嚴(yán)重呼吸道疾病。EV-D68的蛋白酶可以抑制I型干擾素(IFN-I)的產(chǎn)生。然而,EV-D68結(jié)構(gòu)蛋白在拮抗宿主抗病毒反應(yīng)中的作用在很大程度上仍然未知。研究人員發(fā)現(xiàn)EV-D68結(jié)構(gòu)蛋白VP3IFN調(diào)控因子7 (IRF7)相互作用,抑制IRF7的磷酸化和核易位,進而抑制IFN的轉(zhuǎn)錄。此外,VP3通過與IRF7的競爭性相互作用抑制TNF受體相關(guān)因子6 (TRAF6)誘導(dǎo)的IRF7泛素化。IRF7Δ305-503VP3的互作能力弱得多,VP3Δ41-50IRF7的互作能力弱得多。來自腸病毒A71 (EV-A71)和柯薩奇病毒A16 (CV-A16)VP3也被發(fā)現(xiàn)與IRF7蛋白相互作用。這些結(jié)果表明,腸道病毒結(jié)構(gòu)蛋白VP3在破壞宿主先天免疫應(yīng)答中起著關(guān)鍵作用,可能是抗病毒的藥物研究的潛在靶點。EV-D68是一種全球新發(fā)病原體,可引起嚴(yán)重呼吸道疾病。在這里,研究人員報道EV-D68通過靶向IRF7抑制先天免疫反應(yīng)。進一步研究發(fā)現(xiàn),結(jié)構(gòu)蛋白VP3通過與IRF7的競爭相互作用抑制traf6誘導(dǎo)的IRF7泛素化。這些結(jié)果表明VP3IRF7的控制可能是EV-D68抑制IFN-I產(chǎn)生的機制之一。

 

該論文中,對HEK293T、橫紋肌肉瘤(RD)HeLa細胞及其經(jīng)過脂質(zhì)體轉(zhuǎn)染細胞的體外培養(yǎng)是使用Ausbian特級胎牛血清完成的。


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