Among herpesviruses, γ-herpesviruses are supposed to have typical oncogenic activities. Two human γ-herpesviruses, Epstein-Barr virus (EBV) and Kaposi's sarcoma-associated herpesvirus (KSHV), are putative etiologic agents for Burkitt lymphoma, nasopharyngeal carcinoma, and some cases of gastric cancers, and Kaposi's sarcoma, multicentric Castleman's disease, and primary effusion lymphoma (PEL) especially in AIDS setting for the latter case, respectively. Since such two viruses mentioned above are highly species specific, it has been quite difficult to prove their oncogenic activities in animal models. Nevertheless, the viral oncogenesis is epidemiologically and/or in vitro experimentally evident. This time, we investigated gene expression profiles of KSHV-oriented lymphoma cell lines, EBV-oriented lymphoma cell lines, and T-cell leukemia cell lines. Both KSHV and EBV cause a B-cell-originated lymphoma, but the gene expression profiles were typically classified. Furthermore, KSHV could govern gene expression profiles, although PELs are usually coinfected with KSHV and EBV. 1. Introduction Several viruses could induce cancers in human beings. For examples, some papilloma viruses (PVs) should be etiologic agents for cervical cancers [1], hepatitis B virus (HBV) [2] and hepatitis C virus (HCV) [3] for hepatocellular carcinomas, human T-lymphotropic virus 1 (HTLV-1) for adult T-cell leukemia (ATL) [4], Epstein-Barr virus (EBV) for Burkitt lymphomas, nasopharyngeal carcinomas (NPCs), and some of gastric carcinomas [5, 6], and Kaposi’s sarcoma-associated virus (KSHV) for Kaposi’s sarcoma [7], primary effusion lymphomas (PELs), and multicentric Castleman’s disease [8–13]. Recently, a newly identified polyomavirus, Merkel cell polyomavirus, is nominated as an etiologic agent for Merkel cell carcinoma [14]. These viruses have too narrow host ranges to meet Koch’s principles, and, therefore, there are a lot of augments about it. Nevertheless, causation between the viral infection and the related cancer formation could be evident epidemiologically and in vitro experimentally. Chronic inflammation caused by these viruses should be important factors, but it is not forgettable to keep in our minds that such inflammation itself is primarily caused by the viral infection [17]. Except for HCV and HTLV-1, these oncogenic viruses are usually DNA viruses and establish persistent or latent infection [18, 19]. Of course, HCV also establishes persistent infection in the infected hepatocytes [3]. Parts of some viral genomes in case of DNA viruses are integrated into host
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