Prevalence of human cytomegalovirus, polyomaviruses, and oncogenic viruses in glioblastoma among Japanese subjects.

Prevalence of human cytomegalovirus, polyomaviruses, and oncogenic viruses in glioblastoma among Japanese subjects.
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DOI:
10.1186/1750-9378-10-3
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发表时间:
2015
影响因子:
3.7
通讯作者:
Daibata M
Daibata M
中科院分区:
医学3区
文献类型:
--
作者:
Hashida Y;Taniguchi A;Yawata T;Hosokawa S;Murakami M;Hiroi M;Ueba T;Daibata M

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人类巨细胞病毒(HCMV)和多形性胶质母细胞瘤(GBM)之间的关联正在成为一个新概念。然而,关于 GBM 中 HCMV 流行率的地理变异性的信息仍然很少。此外,各种病毒(例如多瘤病毒和致癌病毒)在神经胶质瘤发生中的潜在作用仍不清楚。我们的目的是调查日本患者 GBM 中 HCMV 的患病率。此外,这是第一项评估 GBM 中四种新型人类多瘤病毒感染的研究。这项研究还提供了东方世界在 GBM 中检测人乳头瘤病毒 (HPV) 的首个数据。我们使用实时定量 PCR 测量了 39 名日本患者的 GBM 样本中各种病毒基因组的数量。测试的病毒包括HCMV、默克尔细胞多瘤病毒、人多瘤病毒(HPyV)6、HPyV7、HPyV9、Epstein-Barr病毒、人疱疹病毒8和HPV。我们的定量 PCR 分析检测到 8 个 HCMV DNA 拷贝,与从 104 个 HCMV 阴性细胞中提取的 DNA 混合。还通过巢式 PCR 评估了 HCMV 和 HPV 基因组的存在。还进行了免疫组织化学研究以检测 GBM 组织中的 HPV 衍生蛋白。除 HPV 外,其他病毒 DNA 均未检测到,39 例 GBM 中有 8 例 (21%) 存在 HPV。所有 HPV 阳性病例均携带高危型 HPV(HPV16 和 HPV18)。此外,在 GBM 肿瘤细胞中检测到 HPV 主要衣壳蛋白。与之前来自白种人患者的报告相比,我们没有获得支持 HCMV 和 GBM 之间关联的直接证据。然而,高危型 HPV 感染可能在部分患者的神经胶质瘤发生中发挥潜在的病因作用。这些发现应促进进一步的全球流行病学研究,旨在确定病毒相关 GBM 的致病性。
The association between human cytomegalovirus (HCMV) and glioblastoma multiforme (GBM) is becoming a new concept. However, information on the geographic variability of HCMV prevalence in GBM remains scarce. Moreover, the potential roles of various viruses, such as polyomaviruses and oncogenic viruses, in gliomagenesis remain unclear. Our aim was to investigate the prevalence of HCMV in GBM among Japanese patients. Furthermore, this was the first study that evaluated infection with four new human polyomaviruses in GBMs. This study also provided the first data on the detection of human papillomavirus (HPV) in GBM in the Eastern world. We measured the number of various viral genomes in GBM samples from 39 Japanese patients using real-time quantitative PCR. The tested viruses included HCMV, Merkel cell polyomavirus, human polyomavirus (HPyV) 6, HPyV7, HPyV9, Epstein–Barr virus, human herpesvirus 8, and HPV. Our quantitative PCR analysis led to the detection of eight copies of the HCMV DNA mixed with DNA extracted from 104 HCMV-negative cells. The presence of HCMV and HPV genomes was also assessed by nested PCR. Immunohistochemical study was also carried out to detect HPV-derived protein in GBM tissues. The viral DNAs were not detectable, with the exception of HPV, which was present in eight out of 39 (21%) GBMs. All HPV-positive cases harbored high-risk-type HPV (HPV16 and HPV18). Moreover, the HPV major capsid protein was detected in GBM tumor cells. In contrast with previous reports from Caucasian patients, we did not obtain direct evidence in support of the association between HCMV and GBM. However, high-risk-type HPV infection may play a potential etiological role in gliomagenesis in a subset of patients. These findings should prompt further worldwide epidemiological studies aimed at defining the pathogenicity of virus-associated GBM.
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