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Lack of HCV infection in malignant cells refutes the hypothesis of a direct transforming action of the virus in the pathogenesis of HCV-associated B-cell NHLs.

机译:恶性细胞中缺乏HCV感染反驳了该病毒在HCV相关B细胞NHL发病机理中直接转化作用的假说。

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AIMS AND BACKGROUND: Preliminary evidence suggests that hepatitis C virus (HCV) might play a pathogenetic role in autoimmune-related, non-malignant B-cell lymphoproliferation, as well as in a subset of B-cell non-Hodgkin's lymphomas (NHLs). With regard to the mechanism(s) by which HCV might favor B-cell expansion and malignant transformation, most data support an indirect pathogenetic role of the virus as an exogenous trigger. A direct oncogenetic role of HCV by direct cell infection and deregulation has only been hypothesized on the basis of the lymphotropism of the virus. METHODS: In this study we investigated the possible HCV infection of NHL B cells by means of sensitive and quantitative polymerase chain reaction (PCR) on affinity-purified neoplastic cells, and by HCV-specific immunohistochemistry and in situ hybridization. RESULTS: HCV infection of neoplastic B cells was documented in only three cases, namely the low-grade B-cell NHLs that arose in the course of mixed cryoglobulinemia syndrome (MC). HCV infection, below one viral genome per cell, was detectable only by PCR. All the remaining low-grade (one case) and high-grade B-cell NHLs (two cases) were HCV uninfected. Previous immunoglobulin gene analyses were consistent with an antigen-driven B-cell lymphoproliferation in the studied cases. CONCLUSIONS: Overall, our data are consistent with an indirect oncogenetic role of HCV in B-cell lymphomagenesis as an exogenous trigger. Infection of B cells by HCV appears possible in some NHL subsets, but the implications remain unknown.
机译:目的和背景:初步证据表明,丙型肝炎病毒(HCV)可能在自身免疫相关的非恶性B细胞淋巴瘤增殖以及部分B细胞非霍奇金淋巴瘤(NHL)中发挥致病作用。关于HCV可能促进B细胞扩增和恶性转化的机制,大多数数据支持病毒作为外源性触发因素的间接致病作用。 HCV通过直接细胞感染和失调而直接致癌的作用只是基于病毒的淋巴细胞趋向性进行了假设。方法:在这项研究中,我们通过亲和纯化的赘生性细胞上的敏感和定量聚合酶链反应(PCR)以及HCV特异性免疫组织化学和原位杂交研究了NHL B细胞可能的HCV感染。结果:仅三例记录了肿瘤性B细胞的HCV感染,即在混合性冷球蛋白血症综合征(MC)过程中出现的低度B细胞NHL。 HCV感染(每个细胞一个病毒基因组以下)只能通过PCR检测到。其余所有低级(1例)和高级B细胞NHL(2例)均未感染HCV。在研究病例中,先前的免疫球蛋白基因分析与抗原驱动的B细胞淋巴增殖一致。结论:总体而言,我们的数据与HCV在B细胞淋巴瘤发生中作为外源性触发因素的间接致癌作用一致。在某些NHL亚型中,HCV感染B细胞似乎是可能的,但其影响仍然未知。

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