• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Journal of Virology >Inhibition of host cell protein synthesis by UV-inactivated poliovirus.
【24h】

Inhibition of host cell protein synthesis by UV-inactivated poliovirus.

机译：UV灭活脊髓灰质炎病毒抑制宿主细胞蛋白合成。

获取原文
       
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

The ability of poliovirus that was irradiated with UV light at energies up to 2,160 ergs/mm2 to subsequently inhibit host cell protein synthesis was measured. The inactivation of the host cell shutoff function followed one-hit kinetics. Increasing irradiation did not affect the rate of inhibition until the multiplicity of infection after irradiation was reduced to approximately 1 PFU/cell. At higher functional multiplicities, the rate was unchanged, but an increasing lag before the onset of inhibition was observed with increasing irradiation. The energy levels required to inactivate virus-induced inhibition of host cell protein synthesis suggest that damage to virus RNA rather than to virus capsid proteins is responsible for the loss of function. When the inactivation of host cell shutoff was compared with the inactivation of other viral functions by UV irradiation, it correlated exactly with the loss of infectivity but not with other viral functions measured. Guanidine treatment, which prevents detectable viral RNA and protein synthesis, completely inhibited host cell shutoff by low multiplicities of unirradiated virus infection but not higher multiplicities. When a high multiplicity of virus was first reduced to a low titer by irradiation, host cell shutoff was still evident in the presence of guanidine. The results demonstrate that the complete inhibition of host cell protein synthesis can be accomplished by one infectious viral genome per cell.
机译：测量用UV光照射的脊髓灰质炎病毒的能力，其能量高达2,160 ergs / mm 2，以随后抑制宿主细胞蛋白合成。宿主细胞关闭功能的失活遵循一击动力学。越来越多的辐射不会影响抑制率，直到照射后的多重感染降至约1pfu /细胞。在较高的功能多样性下，速率不变，但随着辐射的增加，观察到抑制开始前的滞后。失活病毒诱导的宿主细胞蛋白合成所需的能量水平表明病毒RNA的损伤而不是病毒衣壳蛋白质负责丧失功能。当宿主细胞闭塞的灭活与UV照射的其他病毒功能的失活进行比较时，它与感染性的损失完全相同，但没有测量其他病毒功能。胍治疗，可防止可检测的病毒RNA和蛋白质合成，通过低多个未辐射的病毒感染而完全抑制宿主细胞关闭，但不具有更高的多重性。当首先通过辐射将高分性的病毒减少到低滴度时，在胍存在下宿主细胞截止仍然是显而易见的。结果表明，宿主细胞蛋白合成的完全抑制可以通过每个细胞的一种传染性病毒基因组完成。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号