Isom H C
J Gen Virol. 1979 Feb;42(2):265-78. doi: 10.1099/0022-1317-42-2-265.
Human cytomegalovirus (HCMV) infection of low serum-arrested confluent whole human embryo (Flow 5000) cells markedly stimulated ornithine decarboxylase (ODC) activity. Increased ODC activity was apparent by 12 h post-infection. The capacity of HCMV to stimulate ODC was: (1) dependent upon multiplicity of infection; (2) eliminated when the virus was neutralized with specific antiserum; and (3) sensitive to ultraviolet irradiation. Virus-mediated induction, in contrast to high serum induction of ODC, was not subject to inhibition by polyamines added to the growth medium. Phosphonoacetic acid (PAA) which blocks HCMV replication by inhibiting the activity of HCMV-specific DNA polymerase and which does not prevent HCMV induced stimulation of cell DNA synthesis, reversibly inhibited HCMV-induced stimulation of ODC activity by 74%. Studies with PAA indicated that HCMV-induced stimulation of ODC activity is independent of cell DNA synthesis and that the mechanism regulating virus-induced stimulation may be related to the HCMV-specific DNA polymerase.
人巨细胞病毒(HCMV)感染处于低血清停滞状态的汇合全人胚胎(Flow 5000)细胞,可显著刺激鸟氨酸脱羧酶(ODC)的活性。感染后12小时,ODC活性明显增加。HCMV刺激ODC的能力表现为:(1)依赖于感染复数;(2)用特异性抗血清中和病毒后这种刺激作用消失;(3)对紫外线照射敏感。与高血清诱导ODC不同,病毒介导的诱导不受添加到生长培养基中的多胺抑制。膦甲酸(PAA)通过抑制HCMV特异性DNA聚合酶的活性来阻断HCMV复制,且不阻止HCMV诱导的细胞DNA合成,它能可逆性地抑制HCMV诱导的ODC活性达74%。用PAA进行的研究表明,HCMV诱导的ODC活性刺激与细胞DNA合成无关,且调节病毒诱导刺激的机制可能与HCMV特异性DNA聚合酶有关。