Failure to detect human T-lymphotropic virus type-I proviral DNA in cell lines and tissues from patients with cutaneous T-cell lymphoma.
Failure to detect human T-lymphotropic virus type-I proviral DNA in cell lines and tissues from patients with cutaneous T-cell lymphoma.
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未能在皮肤 T 细胞淋巴瘤患者的细胞系和组织中检测到人类 T 淋巴细胞病毒 I 型前病毒 DNA。
DOI：
10.1111/1523-1747.ep12363017
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发表时间：
1996
期刊：
影响因子：
--
通讯作者：
Lessin,SR
中科院分区：
文献类型：
--
作者：
Li,G;Vowels,BR;Benoit,BM;Rook,AH;Lessin,SR
先前的分子研究调查了皮肤T细胞淋巴瘤（CTCL）患者的细胞系和组织样本中HTLV-I前病毒DNA的存在，报告了0- 92%的检出率。尽管缺乏HTLV-I感染与CTCL相关的流行病学数据，但分子数据仍引起人们对HTLV-I在CTCL发病机制中确切作用的猜测。为了确定CTCL患者中HTLV-I前病毒DNA的检出率，我们分析了从7名CTCL患者的外周血和22名不同疾病阶段患者的43份组织样本中建立的EB病毒转化细胞系。用HTLV-Itaxgene区域内的引物对基因组DNA进行聚合酶链反应扩增。通过Southern印迹分析用巢式寡核苷酸探针探测扩增产物。在样品中未检测到HTLV-I前病毒序列（0/50）。使用HTLV-I/IIpolprimers，没有检测到HTLV-Ipolgene序列。在一名患者的组织中，检测到HTLV-IIpolandtax基因序列;然而，通过基因组DNA的Southern印迹分析未检测到HTLV-II前病毒整合。我们的数据表明：（i）HTLV-I似乎不是CTCL的主要病因;（ii）在少数CTCL患者中可以检测到HTLV-II polandtax基因序列，但这并不一定意味着病因作用。
Previous molecular studies investigating the presence of HTLV-I proviral DNA in cell lines and tissue samples of patients with cutaneous T-cell lymphoma (CTCL) have reported a detection rate ranging from 0-92%. Despite the lack of epidemiologic data linking HTLV-I infection with CTCL, the molecular data still invite speculation regarding the precise role of HTLV-I in the pathogenesis of CTCL. To determine the detection rate of HTLV-I proviral DNA among CTCL patients referred to our medical center, we analyzed Epstein–Barr virus–transformed cell lines established from peripheral blood of seven CTCL patients and 43 tissue samples from 22 patients with different stages of disease. Genomic DNA was polymerase chain reaction-amplified with primers within the HTLV-Itaxgene region. Amplification products were probed with nested oligonucleotide probes by Southern blot analysis. No HTLV-I proviral sequences were detected in the samples (0/50). Using HTLV-I/IIpolprimers, no HTLV-Ipolgene sequences were detected. In tissues from one patient, HTLV-IIpolandtaxgene sequences were detected; however, HTLV-II proviral integration was not detected by Southern blot analysis of the genomic DNA. Our data suggest: (i) HTLV-I does not appear to be a primary etiologic agent in CTCL; and (ii) HTLV-IIpolandtaxgene sequences can be detected in a minority of CTCL patients, but this does not necessarily imply an etiologic role.