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当前位置: 首页 > 文章 > PI3K/Akt信号转导通路在ALV-J感染中作用的初步研究 中国农业科学 2011,44 (16) 3446-3453
Position: Home > Articles > The Function of PI3K/Akt Signal Pathway During ALV-J Infection in DF-1 Cells Scientia Agricultura Sinica 2011,44 (16) 3446-3453

PI3K/Akt信号转导通路在ALV-J感染中作用的初步研究

作  者：
冯少珍;李娇;吴晓婵;曹伟胜;廖明
单  位：
华南农业大学兽医学院/农业部动物疫病防控重点开放实验室
关键词：
J亚群禽白血病病毒;血管瘤;髓细胞瘤;感染早期;PI3K/Akt
摘  要：
【目的】探讨ALV-J在宿主细胞中复制与PI3K/Akt信号转导通路的关系。【方法】将血管瘤病变型ALV-J毒株HN06和骨髓瘤病变型ALV-J毒株NX0101分别感染DF-1细胞,通过Western blot、Real-time PCR、IFA和ELISA等方法,观察细胞Akt蛋白磷酸化水平、病毒RNA表达水平和病毒蛋白表达水平等指标。【结果】HN06株和NX0101株在体外细胞中复制水平有差异。HN06株的早期感染可引起Akt转导通路的活化,病毒引起的Akt磷酸化具有病毒滴度依赖性,而且能被PI3K特异性抑制剂LY294002所抑制,表明HN06株诱导的Akt活化是PI3K途径依赖的。LY294002可在病毒感染早期呈剂量依赖性地显著降低受染细胞中HN06 RNA水平、囊膜蛋白水平和细胞培养物上清中的病毒粒子含量。【结论】PI3K/Akt信号转导通路活化对HN06株在细胞感染早期具有重要的作用,该结果与已报道的有关细胞PI3K/Akt信号转导通路参与NX0101株的早期感染的结论一致。本研究为进一步阐明ALV-J入侵宿主细胞和复制的精确机制等研究奠定了基础。
译  名：
The Function of PI3K/Akt Signal Pathway During ALV-J Infection in DF-1 Cells
作  者：
FENG Shao-zhen,LI Jiao,WU Xiao-chan,CAO Wei-sheng,LIAO Ming(Key Laboratory of Animal Disease Control and Prevention,Ministry of Agriculture/College of Veterinary Medicine,South China Agricultural University,Guangzhou 510642)
关键词：
subgroup J avian leukosis virus;hemangioma;myelocytomas;virus early infection;PI3K/Akt signal pathway
摘  要：
【Objective】 Given the biological importance of the PI3K/Akt pathway in virus infection,this experiment investigated whether or not the subgroup J avian leukosis virus(ALV-J) strain HN06 infection in DF-1 cells is correlated with the activity of Akt.【Method】After inoculation of ALV-J strain HN06 which mainly induces hemangiomas and strain NX0101 which induces myelocytomas in DF-1 cells,respectively,the expression levels of Akt phosphration,viral RNA transcription and viral protein synthesis were analyzed.【Result】 Results showed that the replication rates in vivo of ALV-J strains HN06 and NX0101 were different.HN06 infection led to increased Akt phosphorylation at a very early stage which was virus titer-dependent.LY294002,a PI3K-specific inhibitor,could suppress HN06 induced Akt phosphorylation,indicating that Akt phosphorylation was PI3K-dependent.Moreover,in the presence of LY294002,viral RNA transcription level,viral envelope protein ENV expression and virons secreted in supernatants were suppressed significantly.The PI3K/Akt activation profile and function of HN06 were similar to that of NX0101 reported.【Conclusion】These data suggest that PI3K/Akt signaling pathway plays an important role in ex vivo ALV-J replication,although the precise mechanism remains under investigation.

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