Korber B, Okayama A, Donnelly R, Tachibana N, Essex M
Department of Cancer Biology, Harvard School of Public Health, Boston, Massachusetts 02115.
J Virol. 1991 Oct;65(10):5471-6. doi: 10.1128/JVI.65.10.5471-5476.1991.
Human T-cell leukemia virus type I (HTLV-I) is the etiologic agent of adult T-cell leukemia, and the clonally derived leukemic cells all contain proviral genomes. Polymerase chain reaction with a variety of primers which span the HTLV-I genome was used to determine that a significant fraction of patients (at least 32%) carry deleted viral genomes in their leukemic cells. The pX region of the HTLV-I genome encoding the regulatory genes tax and rex was preferentially retained. The fact that the tax coding region was retained provides supporting evidence that the tax protein contributes to leukemogenesis in vivo. The reasonably high fraction of patients with adult T-cell leukemia carrying deleted genomes in their tumor cells suggests that the deletions have a role in leukemogenesis.
人类嗜T淋巴细胞病毒I型（HTLV-I）是成人T细胞白血病的病原体，克隆衍生的白血病细胞均含有前病毒基因组。使用跨越HTLV-I基因组的多种引物进行聚合酶链反应，以确定相当一部分患者（至少32%）的白血病细胞中携带缺失的病毒基因组。HTLV-I基因组中编码调节基因tax和rex的pX区域被优先保留。tax编码区域被保留这一事实为tax蛋白在体内白血病发生中起作用提供了支持证据。相当高比例的成人T细胞白血病患者肿瘤细胞中携带缺失基因组，这表明这些缺失在白血病发生中起作用。
