Persistent infection with influenza A virus: evolution of virus mutants.
Persistent infection with influenza A virus: evolution of virus mutants.
复制标题
甲型流感病毒持续感染：病毒突变体的进化。
DOI：
10.1016/0042-6822(84)90151-x
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发表时间：
1984
期刊：
影响因子：
3.7
通讯作者：
Youngner,JS
中科院分区：
文献类型：
--
作者：
Frielle,DW;Huang,DD;Youngner,JS
利用含有高比例缺陷干扰(DI)颗粒的病毒库，建立了H1N1亚型流感病毒WSN(HlN1)株对新生仓鼠肾(BHK)细胞的持续感染(持续性感染I)。用从第92代(388天)持续感染I中恢复的病毒在BHK细胞中建立第二次持续感染(持续感染II)。在持续感染I型(早期pi病毒)的前50代期间分离的病毒中发现了许多表型变化。这些包括斑块大小的减小，对温度敏感的突变体的出现，以及扩增的pi病毒凝集鸡红细胞的能力降低。引起血凝的能力下降与病毒神经氨酸酶活性增加20-30倍有关。持续感染63代后分离的病毒在卵子或一些细胞系中不能扩增。尽管当这些晚期pi病毒感染细胞时产生的传染性病毒很少，但细胞病理学经常发生，并观察到病毒蛋白质合成的异常模式。在感染亲本WSN病毒的细胞中，NP蛋白是合成的主要蛋白质，而M蛋白的合成相对于其合成显著减少。未检测到HA、NS1和NS2蛋白，但观察到一种病毒特异性蛋白，其迁移速度快于NS2。从持续感染中恢复的病毒II在混合感染中干扰了亲本WSN病毒的复制。这种混合感染的蛋白质合成模式与单独感染晚期pi病毒的细胞相似。无论是在维持持续感染、表达pi蛋白合成表型，还是在pi病毒介导的干扰中，DI颗粒似乎都没有发挥明显的作用。
A persistent infection (persistent infection I) of baby hamster kidney (BHK) cells with the WSN (HlN1) strain of influenza A virus was established using a virus stock which contained a high proportion of defective-interfering (DI) particles. Virus recovered from passage 92 (388 days) of persistent infection I was used to establish a second persistent infection (persistent infection II) in BHK cells. A number of phenotypic changes were identified in the virus isolated during the first 50 passages of persistent infection I (early pi virus). These included a decrease in the size of plaques, the appearance of temperature-sensitive mutants, and a decreased ability of amplified pi virus to agglutinate chicken erythrocytes. The decreased ability to cause hemagglutination was associated with a 20- to 30-fold increase in viral neuraminidase activity. Virus isolated after passage 63 of persistent infection I could not be amplified in eggs or in a number of cell lines. Although very little infectious virus was produced when cells were infected with these late pi viruses, cytopathology frequently occurred and an unusual pattern of viral protein synthesis was observed. The NP protein was the predominant protein synthesized, while the synthesis of M protein was drastically reduced relative to its synthesis in cells infected with parental WSN virus. The HA, NS1, and NS2 proteins were not detected; however, a virus-specific protein which migrates faster than NS2 was observed. Virus recovered from persistent infection II interfered with the replication of parental WSN virus in a mixed infection. The pattern of protein synthesis in such mixed infections resembled that in cells singly infected with late pi virus. DI particles did not appear to play a significant role either in the maintenance of the persistent infection, in the expression of the pi protein synthesis phenotype, or in the pi virus-mediated interference.