Lee J C, Chao Y C
Graduate Institute of Life Sciences, National Defence Medical Center, Taipei, Taiwan, Republic of China.
J Gen Virol. 1998 Sep;79 ( Pt 9):2293-300. doi: 10.1099/0022-1317-79-9-2293.
Superinfection of Spodoptera frugiperda insect cells that are persistently infected with Heliothis zea 1 (Hz-1) virus induces general cellular apoptosis and subsequently results in homologous virus interference. Since apoptosis correlates closely with both a significant decrease in yield of virus progeny and expansion of virus infection among cells, further experiments were designed to verify the direct association of apoptosis with homologous interference. It was found that superinfection-induced apoptosis can be efficiently blocked by the stable transfection of p35 into cells before or after the establishment of persistent virus infection. However, persistently infected cells are still strongly resistant to the challenge of Hz-1 virus, indicating that the induction of apoptosis is not essential for the resulting homologous Hz-1 virus interference. Replication and transcription of viral genomes are greatly retarded upon Hz-1 virus superinfection of persistently infected cells, whether stably transfected with p35 or not, suggesting that upon superinfection, the decreasing yield of virus progeny in these persistently infected cells is caused by a blockage early after virus infection.
被玉米夜蛾1型（Hz-1）病毒持续感染的草地贪夜蛾昆虫细胞发生的二次感染会诱导细胞普遍凋亡，随后导致同源病毒干扰。由于凋亡与病毒子代产量的显著降低以及病毒在细胞间感染的扩展密切相关，因此设计了进一步的实验来验证凋亡与同源干扰之间的直接关联。研究发现，在持续病毒感染建立之前或之后，通过将p35稳定转染到细胞中，可以有效阻断二次感染诱导的凋亡。然而，持续感染的细胞对Hz-1病毒的攻击仍具有很强的抗性，这表明凋亡的诱导对于产生的同源Hz-1病毒干扰并非必不可少。无论是否稳定转染p35，在持续感染的细胞被Hz-1病毒二次感染后，病毒基因组的复制和转录都会受到极大阻碍，这表明在二次感染时，这些持续感染细胞中病毒子代产量的降低是由病毒感染后早期的阻断所致。
