Human Herpesvirus-6 (HHV-6) Infection in Allogeneic Bone Marrow Transplant Recipients: Evidence of a Marrow-Suppressive Role for HHV-6 In Vivo

Sixteen adults were studied for the first 100 days after allogeneic bone marrow transplant to assess the pathogenic role of human herpesvirus-6 (HHV-6) infection in patients with unexplained febrile illnesses. HHV-6 was directly isolated from the blood of 6 patients. Analysis of the clinical courses...

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Veröffentlicht in:The Journal of infectious diseases 1993-03, Vol.167 (3), p.735-739
Hauptverfasser: Drobyski, William R., Dunne, W. Michael, Burd, Eileen M., Knox, Konstance K., Ash, Robert C., Horowitz, Mary M., Flomenberg, Neal, Carrigan, Donald R.
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container_issue 3
container_start_page 735
container_title The Journal of infectious diseases
container_volume 167
creator Drobyski, William R.
Dunne, W. Michael
Burd, Eileen M.
Knox, Konstance K.
Ash, Robert C.
Horowitz, Mary M.
Flomenberg, Neal
Carrigan, Donald R.
description Sixteen adults were studied for the first 100 days after allogeneic bone marrow transplant to assess the pathogenic role of human herpesvirus-6 (HHV-6) infection in patients with unexplained febrile illnesses. HHV-6 was directly isolated from the blood of 6 patients. Analysis of the clinical courses of these 16 patients revealed otherwise unexplained posttransplant marrow suppression in 5 patients. Idiopathic marrow suppression occurred more frequently in patients with concurrent HHV-6 viremia (4/6) than in those from whom HHV-6 was not isolated from peripheral blood (1/10, P < .05). An etiologic role for the virus was also supported by isolation of HHV-6 from the bone marrow of all 4 patients at the time of marrow suppression and by in vitro colony-forming unit (cfu) assays that demonstrated that HHV-6 could inhibit cfu-granulocytemacrophage and burst-forming unit-erythroid growth from human bone marrow. By restriction enzyme mapping, all clinical isolates were type B, suggesting that bone marrow transplant recipients may be preferentially infected with and reactivate this HHV-6 subtype. This study implicates HHV-6 as a novel cause of bone marrow suppression in marrow transplant recipients.
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An etiologic role for the virus was also supported by isolation of HHV-6 from the bone marrow of all 4 patients at the time of marrow suppression and by in vitro colony-forming unit (cfu) assays that demonstrated that HHV-6 could inhibit cfu-granulocytemacrophage and burst-forming unit-erythroid growth from human bone marrow. By restriction enzyme mapping, all clinical isolates were type B, suggesting that bone marrow transplant recipients may be preferentially infected with and reactivate this HHV-6 subtype. 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Michael</creatorcontrib><creatorcontrib>Burd, Eileen M.</creatorcontrib><creatorcontrib>Knox, Konstance K.</creatorcontrib><creatorcontrib>Ash, Robert C.</creatorcontrib><creatorcontrib>Horowitz, Mary M.</creatorcontrib><creatorcontrib>Flomenberg, Neal</creatorcontrib><creatorcontrib>Carrigan, Donald R.</creatorcontrib><title>Human Herpesvirus-6 (HHV-6) Infection in Allogeneic Bone Marrow Transplant Recipients: Evidence of a Marrow-Suppressive Role for HHV-6 In Vivo</title><title>The Journal of infectious diseases</title><addtitle>J Infect Dis</addtitle><description>Sixteen adults were studied for the first 100 days after allogeneic bone marrow transplant to assess the pathogenic role of human herpesvirus-6 (HHV-6) infection in patients with unexplained febrile illnesses. HHV-6 was directly isolated from the blood of 6 patients. Analysis of the clinical courses of these 16 patients revealed otherwise unexplained posttransplant marrow suppression in 5 patients. Idiopathic marrow suppression occurred more frequently in patients with concurrent HHV-6 viremia (4/6) than in those from whom HHV-6 was not isolated from peripheral blood (1/10, P &lt; .05). An etiologic role for the virus was also supported by isolation of HHV-6 from the bone marrow of all 4 patients at the time of marrow suppression and by in vitro colony-forming unit (cfu) assays that demonstrated that HHV-6 could inhibit cfu-granulocytemacrophage and burst-forming unit-erythroid growth from human bone marrow. By restriction enzyme mapping, all clinical isolates were type B, suggesting that bone marrow transplant recipients may be preferentially infected with and reactivate this HHV-6 subtype. 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Malignant lymphomas. Malignant reticulosis. Myelofibrosis</topic><topic>Medical sciences</topic><topic>Molecular Sequence Data</topic><topic>Polymerase Chain Reaction</topic><topic>Restriction Mapping</topic><topic>Viremia</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Drobyski, William R.</creatorcontrib><creatorcontrib>Dunne, W. Michael</creatorcontrib><creatorcontrib>Burd, Eileen M.</creatorcontrib><creatorcontrib>Knox, Konstance K.</creatorcontrib><creatorcontrib>Ash, Robert C.</creatorcontrib><creatorcontrib>Horowitz, Mary M.</creatorcontrib><creatorcontrib>Flomenberg, Neal</creatorcontrib><creatorcontrib>Carrigan, Donald R.</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>The Journal of infectious diseases</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Drobyski, William R.</au><au>Dunne, W. 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Analysis of the clinical courses of these 16 patients revealed otherwise unexplained posttransplant marrow suppression in 5 patients. Idiopathic marrow suppression occurred more frequently in patients with concurrent HHV-6 viremia (4/6) than in those from whom HHV-6 was not isolated from peripheral blood (1/10, P &lt; .05). An etiologic role for the virus was also supported by isolation of HHV-6 from the bone marrow of all 4 patients at the time of marrow suppression and by in vitro colony-forming unit (cfu) assays that demonstrated that HHV-6 could inhibit cfu-granulocytemacrophage and burst-forming unit-erythroid growth from human bone marrow. By restriction enzyme mapping, all clinical isolates were type B, suggesting that bone marrow transplant recipients may be preferentially infected with and reactivate this HHV-6 subtype. This study implicates HHV-6 as a novel cause of bone marrow suppression in marrow transplant recipients.</abstract><cop>Chicago, IL</cop><pub>The University of Chicago Press</pub><pmid>8382723</pmid><doi>10.1093/infdis/167.3.735</doi><tpages>5</tpages></addata></record>
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subjects Adult
Base Sequence
Biological and medical sciences
Bone Marrow - microbiology
Bone Marrow - physiopathology
Bone Marrow Transplantation
Cohort Studies
Colony-Forming Units Assay
Fever - etiology
Foscarnet - therapeutic use
Ganciclovir - therapeutic use
Hematologic and hematopoietic diseases
Hematopoiesis
Herpesviridae Infections - drug therapy
Herpesviridae Infections - etiology
Herpesviridae Infections - physiopathology
Herpesvirus 6, Human - classification
Herpesvirus 6, Human - isolation & purification
Humans
Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis
Medical sciences
Molecular Sequence Data
Polymerase Chain Reaction
Restriction Mapping
Viremia
title Human Herpesvirus-6 (HHV-6) Infection in Allogeneic Bone Marrow Transplant Recipients: Evidence of a Marrow-Suppressive Role for HHV-6 In Vivo
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