Presence of hepatitis B and C viral genomes in US blood donors as detected by polymerase chain reaction amplification

Hepatitis C virus (HCV) represents a major cause of posttransfusion hepatitis worldwide. Posttransfusion hepatitis associated with hepatitis B virus (HBV) continues to occur. HBsAg-negative donor sera from the Rhode Island Blood Center between 1987 and 1988 were screened using more sensitive techniques to assess the prevalence of low level HBV infection. Group I consists of 866 healthy blood donors without HBV serologic markers, group II consists of 377 donors with ALT elevations (>45 IU/L), group II consists of 148 donors positive for anti-HBc, and group IV consists of eight donors positive for both surrogate markers. A sensitive monoclonal immunoradiometric assay (M-IRMA) was employed for detection of HBsAg-associated epitopes (detection limit of 20 pg/ml) in serum. A subset of sera were analyzed for the presence of HBV DNA using the method of anti-HBs capture of HBV related virions in serum followed by polymerase chain reaction (PCR) amplification. Using these techniques, 0.8% and 1.7% of donors were positive for HBsAg and HBV DNA respectively in group I. In contrast, 0.9% and 9.5% in group II and 0.7% and 18.1% in group III were positive, respectively. There were eight donors with both ALT elevation and anti-HBc; and four (50%) of these were positive for HBV DNA. In the group with anti-HBc, the majority (80%) of donors with HBV DNA had either no or low (signal to noise ratio <10) anti- HBs titer. Using anti-HCV testing and reverse transcription-PCR for detection of HCV genomes, we detected evidence of HCV infection in nine of the 49 donors with low level HBV DNA. We demonstrate that low level HBV viremia otherwise undetectable by conventional method are prevalent in donor grups with either or both of the surrogate and HCV infection either alone or as co- infecting agent are also common in this population.