Kaposi’s Sarcoma-Associated Virus Governs Gene Expression Profiles Toward B Cell Transformation

Kaposi’s Sarcoma-Associated Virus Governs Gene Expression Profiles Toward B Cell Transformation
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DOI:
10.5772/23250
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发表时间:
2012-03
期刊:
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影响因子:
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通讯作者:
K. Ueda;E. Ito;M. Karayama;Eriko Ohsaki;K. Nakano;Shinya Watanabe
K. Ueda;E. Ito;M. Karayama;Eriko Ohsaki;K. Nakano;Shinya Watanabe
中科院分区:
其他
文献类型:
--
作者:
K. Ueda;E. Ito;M. Karayama;Eriko Ohsaki;K. Nakano;Shinya Watanabe

文献摘要

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Kaposi肉瘤相关疱疹病毒(KSHV),又称人类疱疹病毒-8(HHV-8),是通过代表性差异分析(RDA)在患者标本中发现的(Chang等人,1994)。RDA最初鉴定的片段是KS330Bam和KS631Bam,它们分别与编码塞米里疱疹病毒(HVS)衣壳蛋白VP23的开放阅读框(ORF)的一部分和EB病毒(EBV)相应的BDLF1 ORF编码的氨基酸序列以及被盖蛋白ORF75和EBV被盖蛋白BNRF1(P140)的序列相似。下面的全序列分析表明,KSHV属于疱疹病毒亚科,属于大疱疹病毒属,而不是淋巴分泌病毒,可能是一种新的致癌DNA病毒(Moore等人,1996年;Russo等人,1996年)。KSHV被认为至少通过使用整合素V作为受体在体外感染各种组织(Garrigue等人,2008年),并在B细胞中建立潜伏期(Chen和Lagunoff,2005年)。据报道,KSHV可以感染原代内皮细胞,并将其转化为梭形细胞,这是KSHV在内皮细胞中致癌活性的特征(Lagunoff等人,2002)。然而,由于EBV可以形成淋巴母细胞系(LCL),它在体外对原代外周血单核细胞(PBMC)(当然包括B细胞)尚未被发现有效。到目前为止,广泛的研究表明KSHV应该是Kaposi肉瘤(KS)、多中心Castleman病(MCD)和原发渗出性淋巴瘤(PEL)的病原体(Hengge等人,2002a;Hengge等人,2002b)。致癌病毒如何参与它们相关的癌症,这是一个相当大的问题。尤其是仅感染人类的病毒宿主范围有限,这使得这个问题变得更加无法回答。了解这个问题并解决它的一种方法是观察病毒相关肿瘤的基因表达谱。最近,我们分析了三种典型的淋巴细胞源肿瘤细胞系--原发渗出性淋巴瘤(PEL)细胞系,
Kaposi’s sarcoma-associated herpesvirus (KSHV), also called human herpesvirus-8 (HHV-8) was found in patients’ specimens as a causative agent of Kaposi’s sarcoma by representational difference analysis (RDA) (Chang et al., 1994). Initially identified fragments by RDA were KS330Bam and KS631Bam, which showed a sequence similarity to a portion of the open reading frame (ORF) 26 open reading frame encoding the capsid protein VP23 of herpesvirus saimiri (HVS) and the amino acid sequence encoded by the corresponding BDLF1 ORF of Epstein-Barr virus (EBV), and to the tegment protein, ORF75 and also the tegment protein of EBV, BNRF1 (p140), respectively. The following full sequence analysis revealed that KSHV was belonging to the -herpesvirus subfamily, the genus rhadinovirus rather than lymphocryptic virus and could be a new oncogenic DNA virus (Moore et al., 1996; Russo et al., 1996). KSHV is supposed to infect various kinds of tissue in vitro at least by using integrin V as a receptor (Garrigues et al., 2008) and establishes latency in B cells (Chen and Lagunoff, 2005). KSHV has been reported to infect a primary endothelial cell and can transform it into a spindle cell which is a characteristic feature of the oncogenic activity of KSHV in endothelial cells (Lagunoff et al., 2002) However, it has not been revealed effective in vitro infection to primary peripheral blood mononuclear cells (PBMC), which of course include B cell, as EBV can form lymphoblastoid cell lines (LCL). Extensive studies so far have revealed that KSHV should be an etiologic agent for Kaposi’s sarcoma (KS), multicentric Castleman’s disease (MCD), and primary effusion lymphoma (PEL) (Hengge et al., 2002a; Hengge et al., 2002b). It is quite a big question how oncogenic viruses are involved in their related cancers. Especially limited host ranges of viruses only infecting with humans make this question more unanswerable. One approach to get a hint about this question and solve it is to see gene expression profiles of viruses-associated tumors. Recently, we analyzed three types of typical lymphocyte-originated tumor cell lines-primary effusion lymphoma (PEL) cell lines,