Vesicular stomatitis virus (VSV) therapy of tumors
Vesicular stomatitis virus (VSV) therapy of tumors
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DOI：
10.1080/15216540050212169
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发表时间：
2000-08-01
期刊：
影响因子：
4.6
通讯作者：
Barber, GN
中科院分区：
文献类型：
--
作者：
Balachandran, S;Barber, GN
水泡性口炎病毒（VSV）是一种非致病性负链RNA病毒，其复制对干扰素（IFN）的抗病毒作用极为敏感。我们在这里证明，VSV选择性地诱导细胞溶解的许多转化的人细胞系在体外，所有的形态特征的凋亡细胞死亡。重要的是，VSV还可以在体内有效抑制p53缺失的C6胶质母细胞瘤肿瘤的生长，而不会在正常组织中感染和复制。我们以前的研究结果表明，原代细胞含有双链RNA激活的蛋白激酶PKR和一个功能性的IFN系统是不允许VSV复制，这些结果表明，在许多恶性肿瘤中，IFN信号可能是有缺陷的，因此VSV可能是有用的新的治疗策略，针对肿瘤性疾病。
Vesicular stomatitis virus (VSV) is an essentially nonpathogenic negative-stranded RNA virus, the replication of which is extremely sensitive to the antiviral effects of interferon (IFN). We demonstrate here that VSV selectively induces the cytolysis of numerous transformed human cell lines in vitro, with all the morphological characteristics of apoptotic cell death. Importantly, VSV can also potently inhibit the growth of p53-null C6 glioblastoma tumors in vivo without infecting and replicating in normal tissue. With our previous findings demonstrating that primary cells containing the double-stranded RNA-activated protein kinase PKR and a functional IFN system are not permissive to VSV replication, these results suggest that signaling by IFN may be defective in many malignancies, Thus VSV might be useful in novel therapeutic strategies for targeting neoplastic disease.