Interaction of human herpesvirus 6 with human CD34 positive cells

Isomura, Hiroki; Yoshida, Minoru; Namba, Hikaru; Yamada, Masao

doi:10.1002/jmv.10415

Cited by 21 publications

(15 citation statements)

References 32 publications

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“…Studies of human CMV, a ␤-herpesvirus that is 67% homologous to HHV-6 at the protein level (Dominguez et al, 1999), as well as murine CMV have demonstrated an inhibition of the G 1 /S phase transition in several distinct cell systems (Wiebusch and Hagemeier, 1999;Kosugi et al, 2000;Flemington, 2001;Castillo and Kowalik, 2002). HHV-6 has been demonstrated to be able to infect and arrest human bone marrow progenitor cells in vitro (Luppi et al, 1999;Isomura et al, 2003) and in vivo (Wilborn et al, 1994;Rosenfeld et al, 1995;Secchiero et al, 1995) and to suppress proliferative responses to antigens and mitogens (Burd and Carrigan, 1993;Horvat et al, 1993;Carrigan and Knox, 1995). Our studies now extend the importance of viral-mediated cell cycle arrest to relevant neural precursor cells and show that this arrest is coupled with alterations in their differentiation potential.…”

Section: Discussionmentioning

confidence: 99%

Infection with an Endemic Human Herpesvirus Disrupts Critical Glial Precursor Cell Properties

Dietrich¹,

Blumberg²,

Roshal³

et al. 2004

J. Neurosci.

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Human herpesvirus 6 (HHV-6), a common resident virus of the human CNS, has been implicated in both acute and chronic inflammatory-demyelinating diseases. Although HHV-6 persists within the human CNS and has been described to infect mature oligodendrocytes, nothing is known about the susceptibility of glial precursors, the ancestors of myelin-producing oligodendrocytes, to viral infection.We show that HHV-6 infects human glial precursor cells in vitro. Active infection was demonstrated by both electron microscopy and expression of viral gene transcripts and proteins, with subsequent formation of cell syncytia. Infection leads to alterations in cell morphology and impairment of cell replication but not increased cell death. Infected cells showed decreased proliferation as measured by bromodeoxyuridine uptake, which was confirmed by blunting of the cell growth rate of infected cells compared with uninfected controls over time. The detailed analysis using novel, fluorescent-labeled HHV-6A or HHV-6B reagents demonstrated strong G 1 /S phase inhibition in infected precursor cells. Cell cycle arrest in HHV-6-infected cells was associated with a profound decrease in the expression of the glial progenitor cell marker A2B5 and a corresponding increase in the oligodendrocyte differentiation marker GalC.These data demonstrate for the first time that infection of primary human glial precursor cells with a neurologically relevant human herpesvirus causes profound alterations of critical precursor cell properties. In light of recent observations that repair of CNS demyelination is dependent on the generation of mature oligodendrocytes from the glial precursor cell pool, these findings may have broad implications for both the ineffective repair seen in demyelinating diseases and the disruption of normal glial maturation.

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Section: Discussionmentioning

confidence: 99%

Infection with an Endemic Human Herpesvirus Disrupts Critical Glial Precursor Cell Properties

Dietrich¹,

Blumberg²,

Roshal³

et al. 2004

J. Neurosci.

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“…HHV-6 has been suspected of causing vascular endothelial damage in BMT recipients, a process that may lead to thrombotic microangiopathy, which is a major complication of BMT (273,389). Lastly, HHV-6 infection has been associated with bone marrow suppression (52,113), an observation that is supported by in vitro data on the suppressive effects of HHV-6 on proliferation of stromal cells of granulocyte/macrophage, erythroid, or megakaryocyte lineages (48,(187)(188)(189)212). A recent retrospective study by Boutolleau et al (42) in 78 stem cell transplant recipients found a correlation between HHV-6 viral load in PBMCs and delayed neutrophil engraftment, severe graft-versus-host disease, and classical HHV-6 manifestations, such as fever and rash.…”

Section: Clinical Manifestations Of Hhv-6 Infectionmentioning

confidence: 97%

Update on Human Herpesvirus 6 Biology, Clinical Features, and Therapy

2005

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Human herpesvirus 6 (HHV-6) is a betaherpesvirus that is closely related to human cytomegalovirus. It was discovered in 1986, and HHV-6 literature has expanded considerably in the past 10 years. We here present an up-to-date and complete overview of the recent developments concerning HHV-6 biological features, clinical associations, and therapeutic approaches. HHV-6 gene expression regulation and gene products have been systematically characterized, and the multiple interactions between HHV-6 and the host immune system have been explored. Moreover, the discovery of the cellular receptor for HHV-6, CD46, has shed a new light on HHV-6 cell tropism. Furthermore, the in vitro interactions between HHV-6 and other viruses, particularly human immunodeficiency virus, and their relevance for the in vivo situation are discussed, as well as the transactivating capacities of several HHV-6 proteins. The insight into the clinical spectrum of HHV-6 is still evolving and, apart from being recognized as a major pathogen in transplant recipients (as exemplified by the rising number of prospective clinical studies), its role in central nervous system disease has become increasingly apparent. Finally, we present an overview of therapeutic options for HHV-6 therapy (including modes of action and resistance mechanisms)

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“…After re-suspension, cells were counted. Semi-solid cultures of granulocyte/monocyte colony-forming units (CFU-GM), erythroid burst-forming units (BFU-E), and megakaryocyte CFUs (CFU-Meg) were established according to the published literature [20].…”

Section: Methodsmentioning

confidence: 99%

Reconstruction of Hematopoietic Inductive Microenvironment after Transplantation of VCAM-1-Modified Human Umbilical Cord Blood Stromal Cells

Liu

Chen

et al. 2012

PLoS ONE

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The hematopoietic inductive microenvironment (HIM) is where hematopoietic stem/progenitor cells grow and develop. Hematopoietic stromal cells were the key components of the HIM. In our previous study, we had successfully cultured and isolated human cord blood–derived stromal cells (HUCBSCs) and demonstrated that they could secret hemopoietic growth factors such as GM-CSF, TPO, and SCF. However, it is still controversial whether HUCBSCs can be used for reconstruction of HIM. In this study, we first established a co-culture system of HUCBSCs and cord blood CD34 + cells and then determined that using HUCBSCs as the adherent layer had significantly more newly formed colonies of each hematopoietic lineage than the control group, indicating that HUCBSCs had the ability to promote the proliferation of hematopoietic stem cells/progenitor cells. Furthermore, the number of colonies was significantly higher in vascular cell adhesion molecule-1 (VCAM-1)-modified HUCBSCs, suggesting that the ability of HUCBSCs in promoting the proliferation of hematopoietic stem cells/progenitor cells was further enhanced after having been modified with VCAM-1. Next, HUCBSCs were infused into a radiation-damaged animal model, in which the recovery of hematopoiesis was observed. The results demonstrate that the transplanted HUCBSCs were “homed in” to bone marrow and played roles in promoting the recovery of irradiation-induced hematopoietic damage and repairing HIM. Compared with the control group, the HUCBSC group had significantly superior effectiveness in terms of the recovery time for hemogram and myelogram, CFU-F, CFU-GM, BFU-E, and CFU-Meg. Such differences were even more significant in VCAM-1-modified HUCBSCs group. We suggest that HUCBSCs are able to restore the functions of HIM and promote the recovery of radiation-induced hematopoietic damage. VCAM-1 plays an important role in supporting the repair of HIM damage.

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Interaction of human herpesvirus 6 with human CD34 positive cells

Cited by 21 publications

References 32 publications

Infection with an Endemic Human Herpesvirus Disrupts Critical Glial Precursor Cell Properties

Infection with an Endemic Human Herpesvirus Disrupts Critical Glial Precursor Cell Properties

Update on Human Herpesvirus 6 Biology, Clinical Features, and Therapy

Reconstruction of Hematopoietic Inductive Microenvironment after Transplantation of VCAM-1-Modified Human Umbilical Cord Blood Stromal Cells

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