| Project/Area Number |
11671002
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Hematology
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| Research Institution | Kochi Medical School |
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Principal Investigator |
DAIBATA Masanori Faculty of Medicine, Kochi Medical School, Assistant Professor, 医学部・附属病院, 講師 (50263976)
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| Co-Investigator(Kenkyū-buntansha) |
TAGUCHI Takahiro Faculty of Medicine, Kochi Medical School, Instructor, 医学部, 助手 (80127943)
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| Project Period (FY) |
1999 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥3,100,000 (Direct Cost: ¥3,100,000)
Fiscal Year 2001: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 2000: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1999: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Keywords | Epstein-Barr virus / human herpesvirus 6 / human herpesvirus 7 / human herpesvirus 8 / hematological malignancies / virus reactivation / vertical transmission / Epstein-Barrウイルス / ヒトへルペスウイルス8 |
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| Research Abstract |
1. Over the past 15 years three new human hepesviruses (HHV-6, HHV-7 and HHV-8) have been recognized and implicated as eliological agents of several human diseases. HHV-6 has been cited as a possible cause or as a modulating element of certain human lymphoproliferative disorders. We found two cases of lymphoma and ALL carrying chromosomally integrated HHV-6 genomes. To assess the possibility of chromosomal transmission of HHV-6 DNA, we looked for the viral genome in their families. In both cases, the HHV-6 genomes were detected in their offspring at the identical sites of viral integration of the patients. We propose a novel latent form for HHV-6, in which integrated HHV-6 genome can be chromosomally inherited.
2.(1) Despite the genomic homology, and serological cross-reactivity between HHV-6 and HHV-7, evidence for the association of HHV-7 with lymphoproliferative disorders has been scarce. We searched for the HHV-7 genome in patients with lymphocytic leukemia. Sixty-one patients were enrolled : 33 adult ALL ; 15 childhood ALL ; and 13 CLL. HHV-7 genome was not found in any of our samples, suggesting that HHV-7 is unlikely to play a pathogenetic role in lymphocytic leukemia.
(2) We evaluated the presence of four human herpesviruses (EBV, HHV-6, HHV-7 and HHV-8) in the specimens from 14 patients with primary ocular MALT lymphoma. EBV DNA were detected in 4 samples by PCR, and 4 cases were positive for HHV-6DNA. Neither HHV-7 nor HHV-8DNA could by detected. These findings suggested the possible involvement of EBV and HHV-6 in the pathogenesis of a subset of low-grade primary ocular lymphomas.
(3) HHV-6 genome was detected in the brain lesions of progressive multifocal leukoencephalopathy (PML) developing in a lymphoma patient. HHV-6 is known to be reactivated during immunosuppression and can cause several fatal complications. We propose an association of HHV-6 with the pathogenesis of PML in immunocompromised hosts.
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