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Attempts to Detect Homologous Autointerference In vivo with Influenza Virus and Vesicular Stomatitis Virus

机译:尝试检测体内流感病毒和水泡性口腔炎病毒的同源自动干扰

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Von Magnus particles of influenza virus and defective interfering T particles of vesicular stomatitis virus were unable to provide significant protection of mice from disease or death when inoculated intranasally or intracerebrally along with moderate or high doses of homologous infectious challenge virus. However, yields of infectious virus from the affected organs were reduced as compared to controls inoculated with infectious virus alone. Serial intracerebral passage of vesicular stomatitis virus in mouse brain at high doses failed to produce T particles detectable by in vitro autointerference assays on BHK21 cells, whether or not T particles were introduced along with B virions at the first passage. When very low challenge doses of infectious B virions were inoculated intracerebrally along with high doses of homologous defective particles, there was significant prolongation of life, although most mice died eventually of slowly progressing disease. Also, the virus yields in the brains of these mice were significantly reduced, and virus was no longer detectable in the brains of “protected” mice surviving for 10 days or more. Our results suggest that although homologous autointerference does occur in vivo, it is a more complex phenomenon than in vitro cell culture experiments might indicate.
机译:流感病毒的Von Magnus颗粒和水泡性口腔炎病毒的缺陷性T干扰颗粒与中等剂量或高剂量的同源感染性攻击病毒一起鼻内或脑内接种后,无法为小鼠提供有效的保护,使其免受疾病或死亡的伤害。但是,与单独接种感染性病毒的对照相比,来自受影响器官的感染性病毒的产量降低了。大剂量水泡性口炎病毒在小鼠脑中的连续脑内传代未能通过BHK 21 细胞的体外自动干扰法检测到可检测到的T颗粒,无论是否首先将T颗粒与B病毒颗粒一起引入通道。当在脑内接种极低剂量的感染性B病毒颗粒以及高剂量的同源缺陷颗粒时,寿命会显着延长,尽管大多数小鼠最终死于缓慢进展的疾病。此外,这些小鼠大脑中的病毒产量显着降低,并且在存活10天或更长时间的“受保护”小鼠的大脑中不再检测到病毒。我们的结果表明,尽管同源自我干扰确实在体内发生,但它是比体外细胞培养实验所表明的更为复杂的现象。

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