Hiscott J B, Defendi V
J Virol. 1979 May;30(2):590-9. doi: 10.1128/JVI.30.2.590-599.1979.
The kinetics of host cellular DNA stimulation by simian virus 40 (SV40) tsA58 infection was studied by flow microfluorometry and autoradiography in two types of productively infected monkey kidney cells (AGMK, secondary passage, and the TC-7 cell line). Prior to infection, the cell populations were maintained predominantly in G0-G1 hase of the cell cycle by low (0.25%) serum concentration. Infection of TC-7 or AGMK cells by wild-type SV40, viable deletion mutant dl890, or by SV40 tsA58 at 33 degrees C induced cells through S phase after which they were blocked with a 4N DNA content in the G2 phase. The infection of TC-7 cells by tsA58 at 41 degrees C, which was a nonpermissive temperature for viral DNA replication, induced a round of cell DNA synthesis in approximately 30% of the cell population. These cells proceeded through S phase but then re-entered the G1 resting state. In contrast, infection of AGMK cells by tsA58 at 41 degrees C induced DNA synthesis in approximately 50% of the cells, but this population remained blocked in the G2 phase. These results indicate that the mitogenic effect of the A gene product upon cellular DNA is more heat resistant than its regulating activity on viral DNA synthesis and that the extent of induction of cell DNA synthesis by the A gene product may be influenced by the host cell.
通过流式细胞荧光测定法和放射自显影技术,在两种类型的高效感染猴肾细胞(AGMK,传代培养,以及TC - 7细胞系)中研究了猿猴病毒40(SV40)tsA58感染对宿主细胞DNA刺激的动力学。在感染前,通过低(0.25%)血清浓度将细胞群体主要维持在细胞周期的G0 - G1期。野生型SV40、存活缺失突变体dl890或SV40 tsA58在33℃感染TC - 7或AGMK细胞后,诱导细胞进入S期,之后它们在G2期被阻滞在4N DNA含量水平。tsA58在41℃感染TC - 7细胞(这是病毒DNA复制的非允许温度),在大约30%的细胞群体中诱导了一轮细胞DNA合成。这些细胞进入S期,但随后重新进入G1静止状态。相比之下,tsA58在41℃感染AGMK细胞在大约50%的细胞中诱导了DNA合成,但这群细胞仍被阻滞在G2期。这些结果表明,A基因产物对细胞DNA的促有丝分裂作用比其对病毒DNA合成的调节活性更耐热,并且A基因产物诱导细胞DNA合成的程度可能受宿主细胞影响。