Dual mechanisms of pestiviral superinfection exclusion at entry and RNA replication
Dual mechanisms of pestiviral superinfection exclusion at entry and RNA replication
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DOI：
10.1128/jvi.79.6.3231-3242.2005
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发表时间：
2005-03-01
影响因子：
5.4
通讯作者：
Rice, CM
中科院分区：
文献类型：
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作者：
Lee, YM;Tscherne, DM;Rice, CM
对于许多病毒，原发性感染已被证明可以防止同源的第二种病毒的重复感染。在这项研究中，我们研究了牛病毒性腹泻病毒（BVDV），一种正义RNA瘟病毒的重叠感染排除。BVDV急性感染的细胞受到同源BVDV的双重感染保护，但不受异源水泡性口炎病毒的双重感染保护。在30至60分钟内建立了重复感染排除，但在持续感染细胞传代后丢失。重复感染BVDV未能将可翻译的基因组递送至急性感染细胞中，表明病毒进入受阻。从原代感染BVDV中删除结构蛋白E2消除了这种排除。通过RNA转染对进入阻断进行验证，揭示了复制水平上的第二个阻断，但不是翻译。这种排除不需要结构蛋白表达，并且与原代BVDV RNA复制水平呈负相关。这些发现表明瘟病毒重叠感染排除的双重机制，一个在病毒进入水平，需要病毒糖蛋白E2和第二个在病毒RNA复制水平。
For many viruses, primary infection has been shown to prevent superinfection by a homologous second virus. In this study, we investigated superinfection exclusion of bovine viral diarrhea virus (BVDV), a positive-sense RNA pestivirus. Cells acutely infected with BVDV were protected from superinfection by homologous BVDV but not with heterologous vesicular stomatitis virus. Superinfection exclusion was established within 30 to 60 min but was lost upon passaging of persistently infected cells. Superinfecting BVDV failed to deliver a translatable genome into acutely infected cells, indicating a block in viral entry. Deletion of structural protein E2 from primary infecting BVDV abolished this exclusion. Bypassing the entry block by RNA transfection revealed a second block at the level of replication but not translation. This exclusion did not require structural protein expression and was inversely correlated with the level of primary BVDV RNA replication. These findings suggest dual mechanisms of pestivirus superinfection exclusion, one at the level of viral entry that requires viral glycoprotein E2 and a second at the level of viral RNA replication.