Lamivudine Inhibits the Replication of ALV-J Associated Acutely Transforming Virus and its Helper Virus and Tumor Growth In vitro and In vivo

Lamivudine Inhibits the Replication of ALV-J Associated Acutely Transforming Virus and its Helper Virus and Tumor Growth In vitro and In vivo
复制标题

拉米夫定在体外和体内抑制ALV-J相关急性转化病毒及其辅助病毒的复制和肿瘤生长

DOI:
10.3389/fmicb.2075.01306
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发表时间:
2015-12-01
影响因子:
5.2
通讯作者:
Cui, Zhizhong
Cui, Zhizhong
中科院分区:
生物学2区
文献类型:
--
作者:
Wang, Yixin;Xu, Shuzhen;Cui, Zhizhong

文献摘要

被引文献

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为研究拉米夫定对J亚群禽白血病病毒(ALV-J)的抗病毒作用及其对急性转化型禽白血病病毒(ALV-J)引起的纤维肉瘤生长的抑制作用,采用鸡胚成纤维细胞培养法和1日龄雏鸡接种急性转化型禽白血病病毒(SDAU 1005)的方法,研究拉米夫定对ALV-J的抗病毒作用。该原种是从鸡场的急性纤维肉瘤现场病例中制备的,含有携带v-fps癌基因的复制缺陷型病毒Fu-J及其辅助病毒ALV-J株SDAU 1005。三种不同的细胞培养试验结果表明,拉米夫定对SDAU 1005和Fu-J病毒的复制具有显著的抑制作用。此外,在1-4 μ g/ml的浓度范围内,该作用是剂量依赖性的。在雏鸡实验中,拉米夫定可降低SDAU 1005和Fu-J在接种鸡血浆中的病毒载量,延缓急性肉瘤的发生,降低早期鸡的死亡率。该模型可用于直接评估拉米夫定对此类肿瘤的抑制作用,并了解复制缺陷病毒及其辅助病毒之间的关系,同时也评估肿瘤过程。
To study the antiviral effects of lamivudine on avian leukosis virus subgroup J (ALV-J) and its inhibitory effect on the growth of fibrosarcomas caused by acute transforming avian leukosis virus, a series of experiments were performed in chicken embryo fibroblast cultures and 1-day-old chickens inoculated with an acutely transforming viral stock Fu-J (SDAU1005). This stock was prepared from an acutely fibrosarcoma of field cases in chicken farms and contained both the replication-defective virus Fu-J carrying v-fps oncogene and its helper virus ALV-J strain SDAU1005. The results from three different assays in cell cultures demonstrated the significant inhibitory effect of lamivudine on the replication of both SDAU1005 and Fu-J viruses. Furthermore, the effect was dose dependent in the concentration range of 1-4 mu g/ml. In chicken experiments, lamivudine could decrease the viral loads of SDAU1005 and Fu-J in the plasma of inoculated chickens, delay the appearance of acute sarcomas, and decrease chicken mortality in the early stage. This model may be used to directly evaluate the inhibitory effects of lamivudine on such tumors and to understand the relationship between the replication-defective virus and its helper virus while also assessing tumor processes.