Absence of Merkel cell polyomavirus in monocytic leukemias.

Absence of Merkel cell polyomavirus in monocytic leukemias.
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单核细胞白血病中不存在默克尔细胞多瘤病毒。

DOI:
10.1159/000347174
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发表时间:
2013
期刊:
影响因子:
2.4
通讯作者:
Masanori Daibata.
Masanori Daibata.
中科院分区:
医学4区
文献类型:
--
作者:
Yumiko Hashida;Masayuki Imajoh;Ayuko Taniguchi;Mikio Kamioka;Masanori Daibata.

文献摘要

相似文献

在全球范围内,估计约15%的人类恶性肿瘤是由病毒感染引起的[1]。这些肿瘤的特征是在最初感染和随后的恶性肿瘤之间有很长的潜伏期,大多数感染的个体实际上从未发展成恶性疾病。多种类型的白血病和淋巴瘤与先前的病毒感染有关,包括EB病毒、人类疱疹病毒8(也称为卡波西肉瘤相关疱疹病毒)和人类T淋巴细胞病毒。2008年,在皮肤神经内分泌癌默克尔细胞癌(MCC)中发现了一种新的人类肿瘤病毒,命名为“默克尔细胞多瘤病毒”(MCPyV)[2]。MCPyV与非洲绿色猴源嗜淋巴多瘤病毒具有密切的系统发育关系,并且可以感染人淋巴样细胞。由于在某些淋巴组织增生性疾病病例中证实了MCPyV DNA的存在[3,4],因此寻找MCPyV在发病机制中起作用的血液肿瘤已成为一个重要问题[5]。在淋巴组织增生性疾病患者中,慢性淋巴细胞白血病(CLL)(西方世界成人最常见的白血病)患者的MCPyV DNA检出率较高[4]。尽管大多数CLL肿瘤对MCPyV不呈阳性并且病毒载量较低,但MCPyV可能导致显著比例的CLL病例[6,7,8,9,10]。我们的报告是来自东方世界的第一份显示在少数日本CLL病例中存在MCPyV的报告[8]。
Globally, it is estimated that about 15% of all human malignancies are caused by viral infection [1]. These tumors characteristically have a long latent period between initial infection and subsequent malignancy, and most infected individuals never actually develop malignant disease. Multiple types of leukemia and lymphoma have been associated with preceding viral infection, including Epstein-Barr virus, human herpesvirus 8 (also called Kaposi sarcoma-associated herpesvirus) and human T-lymphotropic virus. These viruses establish their latency in lymphocytes and cause lymphoproliferative disorders.In 2008, a new human tumor virus designated ‘Merkel cell polyomavirus'(MCPyV) was identified in Merkel cell carcinoma (MCC), a neuroendocrine carcinoma of the skin [2]. MCPyV has a close phylogenetic relationship to the African green monkey-derived lymphotropic polyomavirus and can infect human lymphoid cells. Since the presence of MCPyV DNA was demonstrated in some cases of lymphoproliferative disorders [3, 4], the search for hematologic neoplasias in which MCPyV plays a role in the etiopathogenesis has become an important issue [5]. Among patients with lymphoproliferative disorders, patients with chronic lymphocytic leukemia (CLL), the most common leukemia of adults in the Western world, have higher MCPyV DNA detection rates [4]. Although most CLL tumors are not positive for MCPyV and the viral load is low, MCPyV may contribute to a significant proportion of CLL cases [6, 7, 8, 9, 10]. Our report is the first from the Eastern world to show the presence of MCPyV in a small number of Japanese CLL cases [8].