Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2001-5-8
pubmed:databankReference
http://linkedlifedata.com/resource/pubmed/xref/GENBANK/AB049170, http://linkedlifedata.com/resource/pubmed/xref/GENBANK/AB049171, http://linkedlifedata.com/resource/pubmed/xref/GENBANK/AB049172, http://linkedlifedata.com/resource/pubmed/xref/GENBANK/AB049173, http://linkedlifedata.com/resource/pubmed/xref/GENBANK/AB049174, http://linkedlifedata.com/resource/pubmed/xref/GENBANK/AB049175, http://linkedlifedata.com/resource/pubmed/xref/GENBANK/AB049176, http://linkedlifedata.com/resource/pubmed/xref/GENBANK/AB049177, http://linkedlifedata.com/resource/pubmed/xref/GENBANK/AB049178, http://linkedlifedata.com/resource/pubmed/xref/GENBANK/AB049179, http://linkedlifedata.com/resource/pubmed/xref/GENBANK/AB049180, http://linkedlifedata.com/resource/pubmed/xref/GENBANK/AB049181, http://linkedlifedata.com/resource/pubmed/xref/GENBANK/AB049182, http://linkedlifedata.com/resource/pubmed/xref/GENBANK/AB049183
pubmed:abstractText
SEN virus (SEN-V) is a recently identified single-stranded, circular DNA virus. Two SEN-V variants (SENV-D and SENV-H) were assayed by polymerase chain reaction (PCR) to investigate their role in the causation of transfusion-associated non-A to E hepatitis. The incidence of SEN-V infection after transfusion was 30% (86 of 286) compared with 3% (3 of 97) among nontransfused controls (P < .001). Transfusion risk increased with the number of units transfused (P < .0001) and donor-recipient linkage for SEN-V was shown by sequence homology. The prevalence of SEN-V in 436 volunteer donors was 1.8%. Among patients with transfusion-associated non-A to E hepatitis, 11 of 12 (92%) were infected with SEN-V at the time of transfusion compared with 55 of 225 (24%) identically followed recipients who did not develop hepatitis (P < .001). No effect of SEN-V on the severity or persistence of coexistent hepatitis C virus (HCV) infection was observed. In 31 infected recipients, SEN-V persisted for greater than 1 year in 45% and for up to 12 years in 13%. SEN-V-specific RNA (a possible replicative intermediate) was recovered from liver tissue. In summary, SENV-D and -H were present in nearly 2% of US donors, and were unequivocally transmitted by transfusion and frequently persisted. The strong association of SEN-V with transfusion-associated non-A to E hepatitis compared with controls raises the possibility, but does not establish that SEN-V might be a causative agent of posttransfusion hepatitis. The vast majority of SEN-V-infected recipients did not develop hepatitis.
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0270-9139
pubmed:author
pubmed:issnType
Print
pubmed:volume
33
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1303-11
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
2001
pubmed:articleTitle
SEN virus infection and its relationship to transfusion-associated hepatitis.
pubmed:affiliation
The Department of Transfusion Medicine, Warren Grant Magnuson Clinical Center, National Institutes of Health, Bethesda, MD 20892-1184, USA.
pubmed:publicationType
Journal Article