水稻白叶病毒的NS3蛋白补充了HIV-1 Tat的RNA干扰抑制功能。
The NS3 protein of rice hoja blanca virus complements the RNAi suppressor function of HIV-1 Tat.
作者信息
Schnettler Esther, de Vries Walter, Hemmes Hans, Haasnoot Joost, Kormelink Richard, Goldbach Rob, Berkhout Ben
机构信息
Laboratory of Virology, Wageningen University, Binnenhaven 11, 6709 PD Wageningen, The Netherlands.
出版信息
EMBO Rep. 2009 Mar;10(3):258-63. doi: 10.1038/embor.2009.6. Epub 2009 Feb 13.
Abstract
The question of whether RNA interference (RNAi) acts as an antiviral mechanism in mammalian cells remains controversial. The antiviral interferon (IFN) response cannot easily be distinguished from a possible antiviral RNAi pathway owing to the involvement of double-stranded RNA (dsRNA) as a common inducer molecule. The non-structural protein 3 (NS3) protein of rice hoja blanca virus (RHBV) is an RNA silencing suppressor (RSS) that exclusively binds to small dsRNA molecules. Here, we show that this plant viral RSS lacks IFN antagonistic activity, yet it is able to substitute the RSS function of the Tat protein of human immunodeficiency virus type 1. An NS3 mutant that is deficient in RNA binding and its associated RSS activity is inactive in this complementation assay. This cross-kingdom suppression of RNAi in mammalian cells by a plant viral RSS indicates the significance of the antiviral RNAi response in mammalian cells and the usefulness of well-defined RSS proteins.
摘要
RNA干扰（RNAi）在哺乳动物细胞中是否作为一种抗病毒机制仍存在争议。由于双链RNA（dsRNA）作为常见的诱导分子参与其中，抗病毒干扰素（IFN）反应难以与可能的抗病毒RNAi途径区分开来。水稻白叶病毒（RHBV）的非结构蛋白3（NS3）是一种RNA沉默抑制因子（RSS），它专门与小dsRNA分子结合。在这里，我们表明这种植物病毒RSS缺乏IFN拮抗活性，但它能够替代人类免疫缺陷病毒1型Tat蛋白的RSS功能。在这种互补试验中，缺乏RNA结合及其相关RSS活性的NS3突变体没有活性。这种植物病毒RSS对哺乳动物细胞中RNAi的跨界抑制表明了抗病毒RNAi反应在哺乳动物细胞中的重要性以及明确的RSS蛋白的有用性。
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