Reactivation of BK polyomavirus in patients with multiple sclerosis receiving natalizumab therapy.

Hdl Handle:
http://hdl.handle.net/10147/207601
Title:
Reactivation of BK polyomavirus in patients with multiple sclerosis receiving natalizumab therapy.
Authors:
Lonergan, Roisin M; Carr, Michael J; De Gascun, Cillian F; Costelloe, Lisa F; Waters, Allison; Coughlan, Suzie; Duggan, Marguerite; Doyle, Katie; Jordan, Sinead; Hutchinson, Michael W; Hall, William W; Tubridy, Niall J
Affiliation:
Department of Neurology, St Vincent's University Hospital, Elm Park, Dublin,, Ireland. roisin.lonergan@st-vincents.ie
Citation:
J Neurovirol. 2009 Sep;15(5-6):351-9.
Journal:
Journal of neurovirology
Issue Date:
1-Feb-2012
URI:
http://hdl.handle.net/10147/207601
DOI:
10.3109/13550280903131923
PubMed ID:
19670070
Abstract:
Natalizumab therapy in multiple sclerosis has been associated with JC polyomavirus-induced progressive multifocal leucoencephalopathy. We hypothesized that natalizumab may also lead to reactivation of BK, a related human polyomavirus capable of causing morbidity in immunosuppressed groups. Patients with relapsing remitting multiple sclerosis treated with natalizumab were prospectively monitored for reactivation of BK virus in blood and urine samples, and for evidence of associated renal dysfunction. In this cohort, JC and BK DNA in blood and urine; cytomegalovirus (CMV) DNA in blood and urine; CD4 and CD8 T-lymphocyte counts and ratios in peripheral blood; and renal function were monitored at regular intervals. BK subtyping and noncoding control region sequencing was performed on samples demonstrating reactivation. Prior to commencement of natalizumab therapy, 3 of 36 patients with multiple sclerosis (8.3%) had BK viruria and BK reactivation occurred in 12 of 54 patients (22.2%). BK viruria was transient in 7, continuous in 2 patients, and persistent viruria was associated with transient viremia. Concomitant JC and CMV viral loads were undetectable. CD4:CD8 ratios fluctuated, but absolute CD4 counts did not fall below normal limits. In four of seven patients with BK virus reactivation, transient reductions in CD4 counts were observed at onset of BK viruria: these resolved in three of four patients on resuppression of BK replication. No renal dysfunction was observed in the cohort. BK virus reactivation can occur during natalizumab therapy; however, the significance in the absence of renal dysfunction is unclear. We propose regular monitoring for BK reactivation or at least for evidence of renal dysfunction in patients receiving natalizumab.
Language:
eng
MeSH:
Adolescent; Adult; Antibodies, Monoclonal/administration & dosage/*adverse effects; Antibodies, Monoclonal, Humanized; BK Virus/*genetics/immunology; CD4-CD8 Ratio; DNA, Viral/blood/genetics; Female; Follow-Up Studies; Humans; Immunocompromised Host; Male; Middle Aged; Molecular Sequence Data; *Multiple Sclerosis, Relapsing-Remitting/complications/drug therapy/immunology; Phylogeny; Polyomavirus Infections/complications/*immunology/virology; Recurrence; Tumor Virus Infections/complications/*immunology/virology; Viremia/complications/immunology/virology; Young Adult
ISSN:
1538-2443 (Electronic); 1355-0284 (Linking)

Full metadata record

DC FieldValue Language
dc.contributor.authorLonergan, Roisin Men_GB
dc.contributor.authorCarr, Michael Jen_GB
dc.contributor.authorDe Gascun, Cillian Fen_GB
dc.contributor.authorCostelloe, Lisa Fen_GB
dc.contributor.authorWaters, Allisonen_GB
dc.contributor.authorCoughlan, Suzieen_GB
dc.contributor.authorDuggan, Margueriteen_GB
dc.contributor.authorDoyle, Katieen_GB
dc.contributor.authorJordan, Sineaden_GB
dc.contributor.authorHutchinson, Michael Wen_GB
dc.contributor.authorHall, William Wen_GB
dc.contributor.authorTubridy, Niall Jen_GB
dc.date.accessioned2012-02-01T10:32:33Z-
dc.date.available2012-02-01T10:32:33Z-
dc.date.issued2012-02-01T10:32:33Z-
dc.identifier.citationJ Neurovirol. 2009 Sep;15(5-6):351-9.en_GB
dc.identifier.issn1538-2443 (Electronic)en_GB
dc.identifier.issn1355-0284 (Linking)en_GB
dc.identifier.pmid19670070en_GB
dc.identifier.doi10.3109/13550280903131923en_GB
dc.identifier.urihttp://hdl.handle.net/10147/207601-
dc.description.abstractNatalizumab therapy in multiple sclerosis has been associated with JC polyomavirus-induced progressive multifocal leucoencephalopathy. We hypothesized that natalizumab may also lead to reactivation of BK, a related human polyomavirus capable of causing morbidity in immunosuppressed groups. Patients with relapsing remitting multiple sclerosis treated with natalizumab were prospectively monitored for reactivation of BK virus in blood and urine samples, and for evidence of associated renal dysfunction. In this cohort, JC and BK DNA in blood and urine; cytomegalovirus (CMV) DNA in blood and urine; CD4 and CD8 T-lymphocyte counts and ratios in peripheral blood; and renal function were monitored at regular intervals. BK subtyping and noncoding control region sequencing was performed on samples demonstrating reactivation. Prior to commencement of natalizumab therapy, 3 of 36 patients with multiple sclerosis (8.3%) had BK viruria and BK reactivation occurred in 12 of 54 patients (22.2%). BK viruria was transient in 7, continuous in 2 patients, and persistent viruria was associated with transient viremia. Concomitant JC and CMV viral loads were undetectable. CD4:CD8 ratios fluctuated, but absolute CD4 counts did not fall below normal limits. In four of seven patients with BK virus reactivation, transient reductions in CD4 counts were observed at onset of BK viruria: these resolved in three of four patients on resuppression of BK replication. No renal dysfunction was observed in the cohort. BK virus reactivation can occur during natalizumab therapy; however, the significance in the absence of renal dysfunction is unclear. We propose regular monitoring for BK reactivation or at least for evidence of renal dysfunction in patients receiving natalizumab.en_GB
dc.language.isoengen_GB
dc.subject.meshAdolescenten_GB
dc.subject.meshAdulten_GB
dc.subject.meshAntibodies, Monoclonal/administration & dosage/*adverse effectsen_GB
dc.subject.meshAntibodies, Monoclonal, Humanizeden_GB
dc.subject.meshBK Virus/*genetics/immunologyen_GB
dc.subject.meshCD4-CD8 Ratioen_GB
dc.subject.meshDNA, Viral/blood/geneticsen_GB
dc.subject.meshFemaleen_GB
dc.subject.meshFollow-Up Studiesen_GB
dc.subject.meshHumansen_GB
dc.subject.meshImmunocompromised Hosten_GB
dc.subject.meshMaleen_GB
dc.subject.meshMiddle Ageden_GB
dc.subject.meshMolecular Sequence Dataen_GB
dc.subject.mesh*Multiple Sclerosis, Relapsing-Remitting/complications/drug therapy/immunologyen_GB
dc.subject.meshPhylogenyen_GB
dc.subject.meshPolyomavirus Infections/complications/*immunology/virologyen_GB
dc.subject.meshRecurrenceen_GB
dc.subject.meshTumor Virus Infections/complications/*immunology/virologyen_GB
dc.subject.meshViremia/complications/immunology/virologyen_GB
dc.subject.meshYoung Adulten_GB
dc.titleReactivation of BK polyomavirus in patients with multiple sclerosis receiving natalizumab therapy.en_GB
dc.contributor.departmentDepartment of Neurology, St Vincent's University Hospital, Elm Park, Dublin,, Ireland. roisin.lonergan@st-vincents.ieen_GB
dc.identifier.journalJournal of neurovirologyen_GB
dc.description.provinceLeinster-

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