根據(jù)一份研究報(bào)告,，一種新發(fā)現(xiàn)的化合物可能對(duì)生殖器皰疹的潛伏和再激活具有關(guān)鍵作用,。Philip Krause及其同事在專門搜索了單純皰疹病毒2型（HSV-2）遺傳結(jié)構(gòu)中的小分子RNA之后，發(fā)現(xiàn)了一段稱為“miR-I”的RNA序列,。單純皰疹病毒會(huì)導(dǎo)致生殖器皰疹。這組科學(xué)家發(fā)現(xiàn)，盡管這種皰疹病毒在兩次暴發(fā)之間處于休眠狀態(tài),，它的基因組幾乎不會(huì)產(chǎn)生什么,，除了潛伏相關(guān)轉(zhuǎn)錄體（LAT）。LAT含有小段RNA,，似乎只有一個(gè)功能——阻止這種病毒在神經(jīng)細(xì)胞中復(fù)制的“毒力因子”的表達(dá),。
一旦這組科學(xué)家知道了miR-I的基因序列，他們就能夠在被皰疹病毒感染的豚鼠的神經(jīng)元和被感染的人類的尸檢樣本中發(fā)現(xiàn)高水平表達(dá)的這種小分子RNA,。由于miR-I位于和HSV2的已知毒力因子相對(duì)的病毒DNA鏈上,，這組作者提出了一個(gè)假說并用實(shí)驗(yàn)進(jìn)行了驗(yàn)證，即miR-I可能通過起到一種分子開關(guān)的作用,，影響這種皰疹病原體在宿主體內(nèi)繁殖的能力,，從而調(diào)控周圍神經(jīng)系統(tǒng)的病毒感染的結(jié)果。相關(guān)論文發(fā)表在美國(guó)《國(guó)家科學(xué)院院刊》（PNAS）上,。（生物谷Bioon.com）
生物谷推薦原始出處：
PNAS,，doi: 10.1073/pnas.0801845105，Shuang Tang,，Philip R. Krause
An acutely and latently expressed herpes simplex virus 2 viral microRNA inhibits expression of ICP34.5, a viral neurovirulence factor
Shuang Tang*, Andrea S. Bertke*, Amita Patel*, Kening Wang†, Jeffrey I. Cohen†, and Philip R. Krause*,‡
+Author Affiliations
*Division of Viral Products, Office of Vaccines Research and Review, Center for Biologics Evaluation and Research, Food and Drug Administration, Bethesda, MD 20892; and
†Medical Virology Section, Laboratory of Clinical Infectious Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892
Edited by Thomas E. Shenk, Princeton University, Princeton, NJ, and approved June 3, 2008 (received for review March 6, 2008)
Abstract
Latency-associated transcript (LAT) sequences regulate herpes simplex virus (HSV) latency and reactivation from sensory neurons. We found a HSV-2 LAT-related microRNA (miRNA) designated miR-I in transfected and infected cells in vitro and in acutely and latently infected ganglia of guinea pigs in vivo. miR-I is also expressed in human sacral dorsal root ganglia latently infected with HSV-2. miR-I is expressed under the LAT promoter in vivo in infected sensory ganglia. We also predicted and identified a HSV-1 LAT exon-2 viral miRNA in a location similar to miR-I, implying a conserved mechanism in these closely related viruses. In transfected and infected cells, miR-I reduces expression of ICP34.5, a key viral neurovirulence factor. We hypothesize that miR-I may modulate the outcome of viral infection in the peripheral nervous system by functioning as a molecular switch for ICP34.5 expression.
