Athas G B, Starkey C R, Levy L S
Department of Microbiology and Immunology, SL-38, Tulane University School of Medicine, New Orleans, Louisiana 70112.
Crit Rev Oncog. 1994;5(2-3):169-99. doi: 10.1615/critrevoncog.v5.i2-3.40.
The slowly transforming, leukemogenic retroviruses of humans and other mammals induce malignant disease after prolonged latency but lack an oncogene to which their malignant potential can be attributed directly. The leukemogenic activity of these retroviruses can be attributed to at least three factors, including (1) transcriptional regulatory sequences in the long terminal repeat: (2) the insertional mutagenesis of cellular protooncogenes, thus activating their malignant potential; and (3) the actions of structural and regulatory proteins encoded by viral genes. The goal of this review is to summarize recent findings regarding the roles of these factors in retroviral leukemogenesis. The focus of the review is on the slowly transforming, leukemogenic retroviruses of mammals, including humans and experimental animals.
人类和其他哺乳动物的慢转化致白血病逆转录病毒在长时间潜伏期后诱发恶性疾病，但缺乏可直接归因其恶性潜能的癌基因。这些逆转录病毒的致白血病活性可归因于至少三个因素，包括：（1）长末端重复序列中的转录调控序列；（2）细胞原癌基因的插入诱变，从而激活其恶性潜能；以及（3）病毒基因编码的结构和调控蛋白的作用。本综述的目的是总结关于这些因素在逆转录病毒白血病发生中作用的最新发现。综述的重点是哺乳动物，包括人类和实验动物的慢转化致白血病逆转录病毒。
