最近，英國科學(xué)家研究發(fā)現(xiàn),，一些病毒會利用微RNA（MicroRNA）抑制人體免疫反應(yīng)的機(jī)會,，來實(shí)施攻擊，導(dǎo)致感染甚至癌癥的發(fā)生,。這一發(fā)現(xiàn)使微RNA成為癌癥治療的一個新靶點(diǎn),，有助于找到防治癌癥的新療法。
微RNA多見于人體中不產(chǎn)生蛋白質(zhì)的基因組——即所謂的“垃圾DNA”中,，是一種極小的非編碼RNA,，通常會抑制基因的表達(dá),。據(jù)估計(jì)，人體內(nèi)有三分之一的基因會受到微RNA調(diào)控,。有科學(xué)家認(rèn)為,，微RNA會對人體先天免疫系統(tǒng)進(jìn)行調(diào)節(jié)，但一直沒能證實(shí)這種調(diào)節(jié)會產(chǎn)生什么樣的后果,，也無法認(rèn)定這會與病毒感染有關(guān),。
倫敦大學(xué)學(xué)院的研究人員在最新一期的《自然·細(xì)胞生物學(xué)》雜志上發(fā)表論文指出，微RNA會為保持其對基因表達(dá)的調(diào)控而抑制人體的免疫反應(yīng),，而一些病毒則會刺激微RNA的活動,，利用其抑制人體免疫反應(yīng)的機(jī)會來進(jìn)行感染。他們研究證實(shí),，卡波西皰疹病毒（KSHV,，可引發(fā)卡波西惡性腫瘤）即可成功做到這一點(diǎn)。在皰疹病毒感染的早期階段（感染后6小時）,，微RNA的抗病毒反應(yīng)不僅會增強(qiáng)病毒基因的表達(dá),，且會影響干擾素刺激基因的表達(dá)效果，大大促進(jìn)了病毒的復(fù)制,。
研究人員稱,，在人與病毒的對抗中，人體免疫系統(tǒng)會采取多種方式來防止或清除病毒感染,，而與此同時,，病毒也在不斷進(jìn)化，采取更加復(fù)雜的對應(yīng)策略來躲避免疫系統(tǒng)的防御,。很可能一些病毒,，包括會引發(fā)致癌疾病的病毒，利用微RNA把細(xì)胞變成了一個可隨時入住的“病毒旅館”,，它們駐扎其中,，對人體進(jìn)行感染。
倫敦大學(xué)學(xué)院癌癥研究所的主任克里斯·博肖夫教授表示,，新發(fā)現(xiàn)表明,，微RNA可成為一個未來的治療靶點(diǎn)，有助于科學(xué)家找到防治病毒引發(fā)致癌感染的新方法,。（生物谷Bioon.com）
生物谷推薦原文出處：
Nature Cell Biology doi:10.1038/ncb2054
miR-132 regulates antiviral innate immunity through suppression of the p300 transcriptional co-activator
Dimitrios Lagos1, Gabriel Pollara1, Stephen Henderson1, Fiona Gratrix1, Martin Fabani2, Richard S.B. Milne3, Frances Gotch4 & Chris Boshoff1
MicroRNAs are small, non-coding RNAs that negatively regulate gene expression1. It has been proposed that microRNAs could function in the regulation of innate immunity2, 3, but this has not been demonstrated for viral infection. Here we test this hypothesis using the human pathogenic virus Kaposi's sarcoma-associated herpesvirus (KSHV) and one of its putative natural cellular targets, primary lymphatic endothelial cells4 (LECs). We show that an early antiviral microRNA response (6 h post-infection) includes expression of microRNAs that enhance viral gene expression. In particular, the CREB-induced miR-132 microRNA is highly upregulated after infection and has a negative effect on the expression of interferon-stimulated genes, facilitating viral replication. We show a similar function for miR-132 during infection of monocytes with herpes simplex virus-1 (HSV-1) and human cytomegalovirus (HCMV). miR-132 regulates innate antiviral immunity by inhibiting expression of the p300 transcriptional co-activator. p300 is downregulated early after KSHV infection, and inhibition of miR-132 induction restores p300 expression. Furthermore, p300 regulates miR-132 levels, revealing a dynamic equilibrium between miR-132 and p300. By targeting p300, rather than a transcription factor or signalling protein, miR-132 has a broad role in the regulation of antiviral immunity.
