SEN virus (SEN-V) is a recently identified single-stranded, circular DNA vi
rus. Two SEN-V variants (SENV-D and SENV-H) were assayed by polymerase chai
n reaction (PCR) to investigate their role in the causation of transfusion-
associated non-A to E hepatitis, The incidence of SEN-V infection after tra
nsfusion was 30% (86 of 286) compared with 3% (3 of 97) among nontransfused
controls (P < .001). Transfusion risk increased with the number of units t
ransfused (P < .0001) and donor-recipient linkage for SEN-V was shown by se
quence 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 o
f 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 f
rom liver tissue. In summary, SENV-D and -H were present in nearly 2% of US
donors, and were unequivocally transmitted by transfusion and frequently p
ersisted. 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 hepatit
is. The vast majority of SEN-V-infected recipients did not develop hepatiti
s.