Chen I S, Temin H M
J Virol. 1982 Jan;41(1):183-91. doi: 10.1128/JVI.41.1.183-191.1982.
The relationship of two early events in the establishment of infection by avian retroviruses, the inhibition of viral DNA synthesis in stationary avian cells and the secondary infection which occurs after infection of replicating cells, was investigated. When neutralizing antibody to spleen necrosis virus was used to prevent secondary infection, the amount of unintegrated linear spleen necrosis virus DNA detected was much lower in infected stationary cells than in infected replicating cells. The amount of unintegrated linear spleen necrosis virus DNA in stationary cells was less than one copy per cell even at high multiplicities of infection. Viral DNA synthesis resumed after stimulation of the cells to replicate. The time of this viral DNA synthesis was closely correlated with renewed cellular DNA synthesis. In addition, blocking secondary infection of replicating cells prevented the rate of virus production from reaching the high levels usually associated with a normal productive infection by SNV. Virus production increased if secondary infection was allowed. However, this rise in virus production was not proportional to the amounts of viral DNA integrated after secondary infection.
研究了禽逆转录病毒建立感染过程中两个早期事件之间的关系，即静止禽细胞中病毒DNA合成的抑制以及复制细胞感染后发生的二次感染。当使用抗脾坏死病毒的中和抗体来预防二次感染时，在感染的静止细胞中检测到的未整合线性脾坏死病毒DNA的量比感染的复制细胞中的要低得多。即使在高感染复数下，静止细胞中未整合线性脾坏死病毒DNA的量也少于每个细胞一个拷贝。在刺激细胞进行复制后，病毒DNA合成恢复。这种病毒DNA合成的时间与细胞DNA合成的重新开始密切相关。此外，阻断复制细胞的二次感染可防止病毒产生速率达到通常与脾坏死病毒正常生产性感染相关的高水平。如果允许二次感染，病毒产量会增加。然而，这种病毒产量的增加与二次感染后整合的病毒DNA量不成比例。
