This research was supported by a grant from National Blood Foundation.
Human herpesvirus 8 genomes and seroprevalence in United States blood donors
Version of Record online: 15 JAN 2010
© 2010 American Association of Blood Banks
Volume 50, Issue 5, pages 1050–1056, May 2010
How to Cite
Qu, L., Jenkins, F. and Triulzi, D. J. (2010), Human herpesvirus 8 genomes and seroprevalence in United States blood donors. Transfusion, 50: 1050–1056. doi: 10.1111/j.1537-2995.2009.02559.x
- Issue online: 28 APR 2010
- Version of Record online: 15 JAN 2010
- Received for publication September 21, 2009; revision received November 9, 2009, and accepted November 10, 2009.
BACKGROUND: Human herpesvirus 8 (HHV-8) is a gamma-herpesvirus that causes Kaposi's sarcoma. The prevalence of HHV-8 genomes in US blood donors has not been systemically studied.
STUDY DESIGN AND METHODS: A sensitive and quantitative real-time polymerase chain reaction (PCR) assay was used to detect HHV-8 DNA from purified CD19+ B lymphocytes from randomly selected US whole blood donors. Cellular target for the GAPDH gene was used to quantify cell-equivalent DNA. HHV-8 PCR was run in duplicate for each donor specimen along with an HHV-8 genomic copy standard. HHV-8 antibodies were detected by an indirect immunofluorescence assay.
RESULTS: Specimens were obtained from 962 blood donors. DNA from more than 3 × 105 B-cell equivalents were obtained from 684 donors. No HHV-8 DNA was detected from any of the blood donor specimens. For the 684 donors, HHV-8 genomes were not detected in the DNA equivalent of 3 × 105 to 6 × 105 CD19+ B cells with real-time PCR, which has a detection limit of eight copies (95% confidence interval, 0-3/684). Negative results from the remaining 220 donors were potentially confounded by insufficient input DNA into the PCR procedures. Antibodies to HHV-8 were detected in 7.3% (70/962) of the donors. HHV-8 genomes were not detected from 40 of 70 HHV-8–seropositive donor B-cell DNA samples.
CONCLUSION: The results indicate that the prevalence of detectable HHV-8 genomes in healthy blood donors is very low.