SENV-H viremia and liver transplantation: significant increase of the prevalence

SEN virus H (SENV-H) is a novel circular single-stranded DNA virus that has been assumed to be associated with posttransfusion hepatitis.1 A recent investigation revealed that in about 2% to 10% of healthy Japanese blood donors, SENV-H viremia can be detected by polymerase chain reaction (PCR).1,2 To determine the risk for SENV-H transmission by blood and blood products, we examined 26 patients (8 women and 18 men; mean age 47) who underwent liver transplantation (LTX) between 1995 and 1998 in a retrospective study. These patients are at high risk for acquiring transfusion-transmitted agents due to the numerous units of blood and blood products administered to them during surgery. All patients had liver cirrhosis due to chronic hepatitis C virus (HCV) infection. At least one sample from before and after LTX was available from all patients. Additional follow-up samples were available from 12 patients over a period of up to 3 years.

SENV-H infection was investigated by nested PCR using primers directed against a conserved region within the postulated open reading frame 1.3 Before LTX, SENV-H DNA was detectable in 3 (11.5%) of the 26 patients. Postoperatively, one of the initially SENV-H viremic and 11 additional patients (46%) had detectable viremia in sera drawn between days 6 and 14 after transplantation. Additional follow-up samples were available from 8 viremic and 4 negative patients; 6 of the viremic patients became negative within 1 year of infection. In the other patients, viremia became undetectable within 2 and 3 years, respectively. The 4 patients who were initially negative remained negative during the entire follow-up period.

Since transfusion of blood and blood products is supposed to be a major route of SENV-H transmission,1 we examined the number of blood products (blood plasma, erythrocyte, and thrombocyte concentrates) administered to the patients in connection with the LTX. There was no significant difference between the number of blood products administered to the patients who became SENV-H PCR–positive postoperatively (median, 108 U) and to the ones who remained PCR negative (median, 140 U).

The prevalence of SENV-H viremia in Japanese blood donors was shown to vary from 2% to about 10%.1,2 Based on these data, each patient should have received 2 to 14 SENV-H–positive units of blood products. This could explain the observed increase in viremia after transplantation, which is similar to the data previously obtained with GB virus-C/Hepatitis G virus (GBV-C/HGV), where an increase of the prevalence from 6% before to 41% after transplantation was observed.4 In contrast, the prevalence of TTV, a virus that is distantly related to SENV-H, did not significantly increase from 17.3% to 24% after LTX.5 One reason for the unexpected low increase of TTV prevalence in the LTX recipients might be the presence of protective antibodies in the majority of the patients. It was described earlier that reinfection with different SENV-H isolates seems to be common in populations at high risk for blood-borne diseases.6 This would lead to the assumption that no protective immunity is established after SENV-H infection. Although SENV-H has been assigned a possible causative agent of posttransfusion hepatitis, no clinical impact or biochemical differences caused by SENV-H could be observed in this study. Likewise, no significant difference regarding viral titers of HCV were observed between SENV-H viremic and nonviremic patients.