Zur Kurzanzeige

2010-03-15Zeitschriftenartikel DOI: 10.1086/650700
Interferon Beta Modulates Endothelial Damage in Patients with Cardiac Persistence of Human Parvovirus B19 Infection
dc.contributor.authorSchmidt-Lucke, Caroline
dc.contributor.authorSpillmann, Frank
dc.contributor.authorBock, Thomas
dc.contributor.authorKühl, Uwe
dc.contributor.authorLinthout, Sophie van
dc.contributor.authorSchultheiss, Heinz-Peter
dc.contributor.authorTschöpe, Carsten
dc.date.accessioned2018-05-07T14:32:52Z
dc.date.available2018-05-07T14:32:52Z
dc.date.created2011-04-08
dc.date.issued2010-03-15none
dc.identifier.otherhttp://edoc.rki.de/oa/articles/re2hmRrfBqTY/PDF/28rQSi4QT4F8.pdf
dc.identifier.urihttp://edoc.rki.de/176904/856
dc.description.abstractBackground: In a phase 1 study, we investigated whether interferon beta reduced endothelial damage in patients with cardiac persistence of human parvovirus B19 (B19V) infection. Methods and results: In vitro, B19V infected cultivated endothelial cells (ECs), which led to a reduction in their viability (Pp.007). Interferon beta suppressed B19V replication by 63% (Pp.008) in ECs and increased their viability (Pp.021). Circulating mature apoptotic ECs (CMAECs [CD45-CD146+ cells expressing von Willebrand factor and annexin V]) and circulating progenitor cells (CPCs [CD34+KDR+ cells]) were quantified by flow cytometry in 9 symptomatic patients with cardiac B19V infection before and after 6 months of interferon beta therapy (16 MU) and were compared to levels in 9 healthy control subjects. Endothelial dysfunction was measured using flow-mediated dilatation of the forearm. Patients with B19V persistence had significantly higher (Pp.004) levels of CMAECs than did control subjects, which normalized after treatment (mean standard deviation, 0.06%-0.08% vs 0.01%-0.006%; Pp.008). Similar improvement was shown for flow-mediated dilatation (Pp.04) in the treatment group only (Pp.017 for the comparison with untreated patients with B19V persistence [np5]). There were significantly higher numbers of CPCs in patients with B19V persistence before therapy (mean standard deviation, 0.04%-0.05% vs 0.01%-0.004%; Pp.02) than in control subjects, which normalized after treatment (Pp.03). Conclusion: Thus, we present (for the first time, to our knowledge) a modulation of virally induced chronic endothelial damage specifically, EC apoptosis and endothelial regeneration.eng
dc.language.isoeng
dc.publisherRobert Koch-Institut, Infektionskrankheiten / Erreger
dc.subjectAdolescenteng
dc.subjectCell Lineeng
dc.subjectHumanseng
dc.subjectFemaleeng
dc.subjectMaleeng
dc.subjectMiddle Agedeng
dc.subjectRisk Factorseng
dc.subjectAdulteng
dc.subjectAgedeng
dc.subjectTreatment Outcomeeng
dc.subjectYoung Adulteng
dc.subjectAntiviral Agents/pharmacologyeng
dc.subjectAntiviral Agents/therapeutic useeng
dc.subjectApoptosis/drug effectseng
dc.subjectCardiovascular Diseases/prevention & controleng
dc.subjectCardiovascular Diseases/virologyeng
dc.subjectEndothelial Cells/drug effectseng
dc.subjectEndothelial Cells/pathologyeng
dc.subjectEndothelial Cells/virologyeng
dc.subjectEndotheliumeng
dc.subjectVascular/drug effectseng
dc.subjectVascular/pathologyeng
dc.subjectEndothelium Vascular/virologyeng
dc.subjectFlow Cytometryeng
dc.subjectInterferon-beta/pharmacologyeng
dc.subjectInterferon-beta/therapeutic useeng
dc.subjectParvoviridae Infections/complicationseng
dc.subjectParvoviridae Infections/drug therapy*eng
dc.subjectParvovirus B19eng
dc.subjectHuman/drug effectseng
dc.subject.ddc610 Medizin
dc.titleInterferon Beta Modulates Endothelial Damage in Patients with Cardiac Persistence of Human Parvovirus B19 Infection
dc.typeperiodicalPart
dc.identifier.urnurn:nbn:de:0257-10013927
dc.identifier.doi10.1086/650700
dc.identifier.doihttp://dx.doi.org/10.25646/781
local.edoc.container-titleJournal of Infectious Diseases
local.edoc.container-textSchmidt-Lucke, C., Spillmann, F., Bock, T., Kühl, U., Van Linthout, S., Schultheiss, H.-P., Tschöpe, C. Interferon beta modulates endothelial damage in patients with cardiac persistence of human parvovirus B19 infection (2010) Journal of Infectious Diseases, 201 (6), pp. 936-945.
local.edoc.fp-subtypeArtikel
local.edoc.type-nameZeitschriftenartikel
local.edoc.container-typeperiodical
local.edoc.container-type-nameZeitschrift
local.edoc.container-urlhttp://jid.oxfordjournals.org/content/201/6/936.long
local.edoc.container-publisher-nameUniversity of Chicago Press
local.edoc.container-volume201
local.edoc.container-issue6
local.edoc.container-year2010

Zur Kurzanzeige