Bukrinsky Michael
The George Washington University School of Medicine and Health Sciences, 2300 Eye St NW, Washington, DC 20037 USA.
Cell Biosci. 2017 Feb 20;7:12. doi: 10.1186/s13578-017-0139-5. eCollection 2017.
Accumulating evidence implicates Zika virus (ZIKV) in pathogenesis of microcephaly in newborns and Guillain-Barré syndrome in adults. However, it remains unclear which viral proteins are responsible for these effects and what are the underlying mechanisms of their pathogenic activity. A recent paper by Drs. Zhao and Gallo, and their colleagues at University of Maryland in Baltimore used fission yeast for genome-wide analysis of ZIKV proteins. They demonstrated cytopathogenic activity for seven ZIKV proteins, anaC, C, prM, M, E, NS2B and NS4A. This activity was shown to be dependent on oxidative stress, and for NS4A they demonstrated involvement of the TOR stress-response pathway. Taken together, the findings presented in this paper provide the basis for further mechanistic studies that potentially can identify therapeutic means to treat neuro and immune complications of ZIKV infection.
越来越多的证据表明，寨卡病毒（ZIKV）与新生儿小头畸形以及成人吉兰 - 巴雷综合征的发病机制有关。然而，尚不清楚哪些病毒蛋白导致了这些影响，以及它们致病活性的潜在机制是什么。巴尔的摩马里兰大学的赵博士、加洛博士及其同事最近发表的一篇论文利用裂殖酵母对寨卡病毒蛋白进行了全基因组分析。他们证明了七种寨卡病毒蛋白（anaC、C、prM、M、E、NS2B和NS4A）具有细胞致病活性。这种活性被证明依赖于氧化应激，对于NS4A，他们证明其与TOR应激反应途径有关。综上所述，本文提出的研究结果为进一步的机制研究提供了基础，这些研究可能会确定治疗寨卡病毒感染所致神经和免疫并发症的治疗方法。
