Quantification of human herpesvirus 6 in healthy volunteers and patients with lymphoproliferative disorders by PCR-ELISA

Ohyashiki, Junko H.; Abe, Kenji; Ojima, Tomoko; Wang, Ping; Zhou, Chang Fang; Suzuki, Akitaka; Ohyashiki, Kazuma; Yamamoto, Kohtaro

doi:10.1016/s0145-2126(99)00079-x

Cited by 22 publications

(18 citation statements)

References 16 publications

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“…Similar results were obtained by Di Luca et al (10). To our knowledge, the only report of precise HHV-6 quantitation in lymph nodes from lymphomas was by Ohyashiki et al (33), using a PCRenzyme-linked immunosorbent assay. The values that they observed for positive samples ranged between 6.4 copies per g of DNA for a B-cell lymphoma and 3,705 copies per g of DNA in the case of an immunoblastic lymphadenopathy.…”

Section: Discussionsupporting

confidence: 86%

Real-Time PCR for Quantification of Human Herpesvirus 6 DNA from Lymph Nodes and Saliva

Collot¹,

Petit²,

Bron

et al. 2002

J Clin Microbiol

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A real-time quantitative PCR assay has been developed to measure human herpesvirus 6 (HHV-6) DNA in biological specimens. The assay sensitivity was 10 copies of DNA per well, with a linear dynamic range of 10 to 10 7 copies of HHV-6 DNA. Intra-and interassay variations were, respectively, 0.88 and 0.8% for samples containing 10 2 DNA copies, 0.99 and 0.96% for samples containing 10 4 copies, and 0.76 and 0.9% for samples containing 10 6 copies. Among 34 saliva samples from healthy subjects, 26 were found to contain HHV-6 DNA (76.5%; median, 23,870 copies/ml), and following a single freeze-thaw cycle, 25 of the same samples were found to be positive for HHV-6 DNA, although at a statistically significantly lower concentration (median, 3,497 copies/ml). The assay enabled detection of HHV-6 DNA in lymph node biopsies from patients with Hodgkin's disease (

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Section: Discussionsupporting

confidence: 86%

Real-Time PCR for Quantification of Human Herpesvirus 6 DNA from Lymph Nodes and Saliva

Collot¹,

Petit²,

Bron

et al. 2002

J Clin Microbiol

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show abstract

“…Nevertheless, studies aimed to establish a link between HHV-6 infections and hematological malignancies showed discordant results. High viral load was found in patients with lymphoproliferative disorders [Ohyashiki et al, 1999] or in patients with B-cell malignancies [Hermouet et al, 2003] compared to patients with acute myeloblastic leukemia or healthy donors, but other studies demonstrated no link between HHV-6 and adult acute lymphoblastic leukemia [Barozzi et al, 1995].…”

Section: Introductionmentioning

confidence: 99%

Quantitation of human herpes virus 6 genome in children with acute lymphoblastic leukemia

Seror

Coquerel

Gautheret‐Dejean

et al. 2008

Journal of Medical Virology

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Acute lymphoblastic leukemia is the main type of leukemia in children. An infectious etiology has been suspected and the role of the Human herpesvirus-6 (HHV-6) has been suggested. Several studies have tried to establish a link between HHV-6 infections and hematological malignancies, with discordant results. The potential role of HHV-6 in the pathogenesis of pediatric acute lymphoblastic leukemia was investigated. HHV-6 genome copy number was measured by quantitative real-time PCR (RQ-PCR) in bone marrow or peripheral blood samples obtained from 36 children (median age = 4 years) with B acute lymphoblastic leukemia (n = 31) and T acute lymphoblastic leukemia (n = 5) at diagnosis and during complete remission. Positive samples were further characterized to define viral variant, A or B. A total of 24.7% of samples were positive for HHV-6 genome: 13.9% were leukemia samples and 34.1% were complete remission samples. Viral load was low with values lower at diagnosis (median viral copy number = 22.9) than at complete remission (median copy number = 60.1). Among the 17 patients with positive samples, 15 were typed as B-variant whereas 2 could not be typed. These results argue against a role of HHV6 infection in the development of pediatric acute lymphoblastic leukemia. They also suggest that HHV-6 may infect latently bone marrow progenitors but seems not able to infect leukemic cells, raising again the question of the mechanism of virus fusion and entry. This observation shows that a reactivation may be observed during complete remission supporting the possibility of virus reactivation in immunocompromised hosts.

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“…1,7,8 The role played by HHV-6, a virus with T lymphocyte tropism but reportedly found in tumor cells of several patients with B cell lymphoma, is still uncertain. 9,10 The potential involvement of HHVs in well-characterized hematological malignancies can be more precisely investigated using recently developed sensitive and quantitative methods, such as qPCR, 11,12 to relate virus loads to disease emergence and progression. In addition, the increase in comparative sequence information of genes from various species has allowed the development of a number of nucleic acidbased approaches to search for additional HHV homologues.…”

Section: Introductionmentioning

confidence: 99%

Qualitative and quantitative analysis of human herpesviruses in chronic and acute B cell lymphocytic leukemia and in multiple myeloma

et al. 2003

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Quantification of human herpesvirus 6 in healthy volunteers and patients with lymphoproliferative disorders by PCR-ELISA

Cited by 22 publications

References 16 publications

Real-Time PCR for Quantification of Human Herpesvirus 6 DNA from Lymph Nodes and Saliva

Real-Time PCR for Quantification of Human Herpesvirus 6 DNA from Lymph Nodes and Saliva

Quantitation of human herpes virus 6 genome in children with acute lymphoblastic leukemia

Qualitative and quantitative analysis of human herpesviruses in chronic and acute B cell lymphocytic leukemia and in multiple myeloma

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