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副黏病毒在不合成病毒蛋白的情况下激活β干扰素启动子。

Activation of the beta interferon promoter by paramyxoviruses in the absence of virus protein synthesis.

机构信息

School of Biology, Centre for Biomolecular Sciences, BMS Building, North Haugh, University of St Andrews, St Andrews, Fife KY16 9ST, UK.

Division of Basic Medical Sciences, St George's, University of London, London SW17 0RE, UK.

出版信息

J Gen Virol. 2012 Feb;93(Pt 2):299-307. doi: 10.1099/vir.0.037531-0. Epub 2011 Nov 2.

Abstract

Conflicting reports exist regarding the requirement for virus replication in interferon (IFN) induction by paramyxoviruses. Our previous work has demonstrated that pathogen-associated molecular patterns capable of activating the IFN-induction cascade are not normally generated during virus replication, but are associated instead with the presence of defective interfering (DI) viruses. We demonstrate here that DIs of paramyxoviruses, including parainfluenza virus 5, mumps virus and Sendai virus, can activate the IFN-induction cascade and the IFN-β promoter in the absence of virus protein synthesis. As virus protein synthesis is an absolute requirement for paramyxovirus genome replication, our results indicate that these DI viruses do not require replication to activate the IFN-induction cascade.

摘要

关于副黏液病毒诱导干扰素(IFN)产生是否需要病毒复制,目前存在相互矛盾的报道。我们之前的工作表明,能够激活 IFN 诱导级联反应的病原体相关分子模式通常不会在病毒复制过程中产生,而是与缺陷干扰(DI)病毒的存在有关。我们在这里证明,包括副流感病毒 5、腮腺炎病毒和仙台病毒在内的副黏液病毒的 DI 可以在没有病毒蛋白合成的情况下激活 IFN 诱导级联反应和 IFN-β 启动子。由于病毒蛋白合成是副黏液病毒基因组复制的绝对要求,我们的结果表明这些 DI 病毒不需要复制即可激活 IFN 诱导级联反应。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/062a/3352343/0670b23b133e/037531-f1.jpg

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