Loughran T P, Abbott L, Gentile T C, Love J, Cunningham C, Friedman-Kien A, Huang Y Q, Poiesz B J
Veterans Administration Hospital and the Department of Medicine, State University of New York, Syracuse 13210, U.S.A.
Leuk Lymphoma. 1997 Jun;26(1-2):177-80. doi: 10.3109/10428199709109173.
The etiology of large granular lymphocyte (LGL) leukemia is uncertain. Recently, a Kaposi's sarcoma-associated herpes virus, denoted as human herpes virus 8 (HHV-8), has been identified. Some data suggest that HHV-8 and Epstein-Barr virus (EBV) may interact to induce malignant transformation. Infection with EBV has been implicated in the pathogenesis of some cases of LGL leukemia. Therefore, we performed PCR analyses for HHV-8 detection in samples from nineteen patients with LGL leukemia; three of these samples contained the EBV genome. We could not detect HHV-8 sequences in any of these patients. Therefore, HHV-8 infection is not involved in the pathogenesis of T-LGL leukemia.
大颗粒淋巴细胞(LGL)白血病的病因尚不确定。最近,一种卡波西肉瘤相关疱疹病毒,即人类疱疹病毒8型(HHV-8)已被鉴定出来。一些数据表明,HHV-8和爱泼斯坦-巴尔病毒(EBV)可能相互作用诱导恶性转化。EBV感染与一些LGL白血病病例的发病机制有关。因此,我们对19例LGL白血病患者的样本进行了HHV-8检测的PCR分析;其中三个样本含有EBV基因组。我们在这些患者中均未检测到HHV-8序列。因此,HHV-8感染不参与T-LGL白血病的发病机制。