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Tytuł:
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CD34+ progenitor cells mobilized by natalizumab are not a relevant reservoir for JC virus.
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Autorzy:
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Warnke C; Department of Neurology, Heinrich-Heine-University, Düsseldorf, Germany. bernd.kieseier@uni_duesseldorf.de
Smolianov V
Dehmel T
Andrée M
Hengel H
Zohren F
Arendt G
Wiendl H
Haas R
Hartung HP
Adams O
Kieseier BC
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Źródło:
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Multiple sclerosis (Houndmills, Basingstoke, England) [Mult Scler] 2011 Feb; Vol. 17 (2), pp. 151-6. Date of Electronic Publication: 2010 Nov 15.
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Typ publikacji:
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Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
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Język:
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English
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Imprint Name(s):
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Publication: 2006- : London : SAGE Publications
Original Publication: Houndmills, Basingstoke, Hampshire, UK : Stockton Press, c1995-
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MeSH Terms:
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Antibodies, Monoclonal/*adverse effects
Antigens, CD34/*analysis
Cell Movement/*drug effects
Hematopoietic Stem Cells/*drug effects
Immunologic Factors/*adverse effects
JC Virus/*genetics
Leukoencephalopathy, Progressive Multifocal/*chemically induced
Multiple Sclerosis, Relapsing-Remitting/*drug therapy
Adolescent ; Adult ; Antibodies, Monoclonal, Humanized ; Cytomegalovirus/genetics ; DNA, Viral/metabolism ; Female ; Germany ; Hematopoietic Stem Cells/immunology ; Hematopoietic Stem Cells/virology ; Humans ; Leukoencephalopathy, Progressive Multifocal/blood ; Leukoencephalopathy, Progressive Multifocal/virology ; Male ; Natalizumab ; Risk Assessment ; Risk Factors ; Time Factors ; Young Adult
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Substance Nomenclature:
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0 (Antibodies, Monoclonal)
0 (Antibodies, Monoclonal, Humanized)
0 (Antigens, CD34)
0 (DNA, Viral)
0 (Immunologic Factors)
0 (Natalizumab)
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Entry Date(s):
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Date Created: 20101117 Date Completed: 20110527 Latest Revision: 20151119
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Update Code:
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20240104
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DOI:
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10.1177/1352458510385834
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PMID:
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21078695
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Background: Progressive multifocal leukoencephalopathy (PML) is associated with natalizumab treatment in patients with multiple sclerosis (MS). It has been hypothesized that natalizumab mobilizes JC virus (JCV)-infected haematopoietic progenitor cells mediating viraemia and subsequently this disease.
Objective: The objective of this study was to investigate peripheral haematopoietic progenitor cells for evidence of JCV DNA in MS patients treated with natalizumab.
Methods: We assessed JCV and cytomegalovirus (CMV) DNA in magnetically separated CD34+ haematopoietic progenitor cells, peripheral blood mononuclear cells and plasma of 67 natalizumab-treated patients with MS and six PML patients.
Results: Viral DNA was not detectable in CD34+ haematopoietic progenitor or peripheral blood mononuclear cells from any sample. Two plasma samples from patients with MS while undergoing natalizumab treatment were JCV-positive. In one case clinically manifest PML developed 8 months thereafter.
Conclusions: Our findings do not support the hypothesis that natalizumab mobilizes JC virus-infected CD34+ cells from the bone marrow mediating JC viraemia. Notably, JC viraemia was detected in one patient with MS prior to developing clinical PML. This warrants further study.