Rabinowitz S G, Huprikar J
J Infect Dis. 1979 Sep;140(3):305-15. doi: 10.1093/infdis/140.3.305.
Homologous autointerference mediated by defective-interfering (DI) particles was first described with the PR-8 strain of influenza virus. However, little is actually known about the influence of DI particles of influenza virus on the pathogenesis of pulmonary infection. The present studies were designed to determine (1) the requirements for successful autointerference in vivo with DI particle-enriched PR-8 influenza virus and (2) the effects of DI particle-enriched virus on the development and progression of otherwise lethal pulmonary infection in mice. PR-8 influenza virus passaged in chicken eggs, but not that passaged in Madin-Darby bovine kidney cells, and enriched in DI particles markedly attenuated pulmonary infection in seven-week-old Swiss and four-week-old C57B16/Cr mice but not in three- to four-week-old Swiss mice. In addition, replication of influenza virus, straining of viral antigen, and numbers of infiltrates in lungs of mice infected with DI particle-enriched influenza virus were reduced in comparison with values in mice infected with comparable amounts of wild-type influenza virus. The protection mediated by DI particle-enriched virus appeared to be related to augmented humoral immune responses in infected mice rather than to autointerference with replication of wild-type virus.
由缺陷干扰（DI）颗粒介导的同源自身干扰最初是在流感病毒的PR - 8株中被描述的。然而，关于流感病毒DI颗粒对肺部感染发病机制的影响实际上所知甚少。本研究旨在确定：（1）体内利用富含DI颗粒的PR - 8流感病毒成功进行自身干扰的条件；（2）富含DI颗粒的病毒对小鼠原本致命的肺部感染的发生和发展的影响。在鸡胚中传代的PR - 8流感病毒，而非在马-达二氏牛肾细胞中传代并富含DI颗粒的病毒，能显著减轻7周龄瑞士小鼠和4周龄C57B16/Cr小鼠的肺部感染，但对3至4周龄瑞士小鼠无效。此外，与感染等量野生型流感病毒的小鼠相比，感染富含DI颗粒流感病毒的小鼠肺部流感病毒的复制、病毒抗原的染色以及浸润细胞数量均减少。富含DI颗粒的病毒介导的保护作用似乎与受感染小鼠体液免疫反应增强有关，而非与对野生型病毒复制的自身干扰有关。
