2015年10月26日 訊 /生物谷BIOON/ –近日，一項刊登在國際雜志the Journal of Virology上的研究論文中，來自內(nèi)布拉斯加林肯大學(University of Nebraska-Lincoln，UNL)的研究人員通過研究首次給出直接證據(jù)表明，感染藻類的病毒可以在某些哺乳動物機體中侵襲并且發(fā)生潛在復制。
圖片來源：medicalxpress.com
被稱為刺胞蟲綠藻病毒1（ATCV-1）的病原體被認為是在綠藻中長期寄生的一種綠藻病毒，2014年的一項研究發(fā)現(xiàn)在人類咽喉拭子中的ATCV-1會發(fā)生基因序列的重組。這項研究中研究者則將ATCV-1引入到巨噬細胞中，巨噬細胞在小鼠、人類及其他哺乳動物機體的免疫反應中扮演著關鍵的作用，利用熒光染料和組裝的三維成像技術(shù)對小鼠細胞中的病毒進行標記，研究者就會發(fā)現(xiàn)ATCV-1可以潛在成功地潛入細胞中去。
隨后研究者還發(fā)現(xiàn)，在小鼠細胞中引入ATCV-1后24小時病毒的水平會增加至原先的三倍，病毒水平的增加就表明，ATCV-1可以在巨噬細胞中進行復制，此前有研究發(fā)現(xiàn)，綠藻病毒屬的病毒僅會在有限的動物宿主體內(nèi)進行復制；研究者Dunigan表示，巨噬細胞通常會因病毒而進行多種特性改變，包括程序性的細胞死亡等，本文研究中研究者指出，我們想通過研究證實是否以及病毒以何種方式來潛入到哺乳動物的機體中。
目前研究者仍然并不清楚是否，基于細胞的病毒誘導產(chǎn)生的因子可以在整個動物機體中被誘導，而且是否這些誘導產(chǎn)生的因子會引發(fā)動物或者人類認知能力的損傷，Dunigan說道，目前我們?nèi)匀辉谔剿骷毎麑TCV-1的其它反應，同時調(diào)查這些反應是否會引發(fā)小鼠機體的系統(tǒng)性改變。（生物谷Bioon.com）
doi:10.1128/JVI.01254-15
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Response of mammalian macrophages to challenge with the Chlorovirus ATCV-1.
Petro TM1, Agarkova IV2, Zhou Y3, Yolken RH4, Van Etten JL2, Dunigan DD5.
It was recently reported that 44% of healthy humans in a study cohort had DNA sequences similar to Chlorovirus ATCV-1 (family Phycodnaviridae) in oropharyngeal samples and had decreases in visual processing and visual motor speed compared with individuals in whom no virus was detected. Moreover, mice inoculated orally with ATCV-1 developed immune responses to ATCV-1 proteins and had decreases in certain cognitive domains. Because heightened IL-6, nitric oxide (NO), and ERK MAP-kinase activation from macrophages are linked to cognitive impairments, we evaluated cellular responses and viral plaque forming units in murine RAW264.7 and primary macrophages after exposure to ATCV-1 in vitro for up to 72 h after virus challenge. Approximately 8% of the ATCV-1 inoculum was associated with macrophages after 1 h and increased 2-3 fold over 72 h. Immunoblots using rabbit anti-ATCV-1 detected a 55 kDa protein consistent with viral capsid protein from 1 to 72 h and an increasing de novo synthesis of a previously unidentified 17 kDa protein beginning at 24 h. Emergence of the 17 kDa protein did not occur and persistence of the 55 kDa protein declined over time when cells were exposed to heat-inactivated ATCV-1. Moreover, starting at 24 h, RAW264.7 cells exhibited cytopathic effects, Annexin V staining and cleaved-caspase 3. Activation of ERK MAP-kinases occurred in these cells by 30 min post challenge, which preceded expression of IL-6 and NO. Therefore ATCV-1 persistence in and induction of inflammatory factors by these macrophages may contribute to declines in cognitive abilities of mice and humans.