中文摘要：

【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。

英文摘要：

[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 supematants 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.