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JNCI Journal of the National Cancer Institute 2003 95(17):1330-1335; doi:10.1093/jnci/djg039
© 2003 by Oxford University Press
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© 2003 Oxford University Press

ARTICLE

Human Herpesvirus 8 Infection and Transfusion History in Children With Sickle-Cell Disease in Uganda

Sam M. Mbulaiteye, Robert J. Biggar, Paul M. Bakaki, Ruth M. Pfeiffer, Denise Whitby, Anchilla M. Owor, Edward Katongole-Mbidde, James J. Goedert, Christopher M. Ndugwa, Eric A. Engels

Affiliations of authors: S. M. Mbulaiteye, R. J. Biggar, R. M. Pfeiffer, D. Whitby, J. J. Goedert, E. A. Engels, Viral Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD; P. M. Bakaki, A. M. Owor, E. Katongole-Mbidde, C. M. Ndugwa, Makerere University Medical School and Mulago Hospital, Kampala, Uganda.

Correspondence to: Sam M. Mbulaiteye, MD, 6120 Executive Blvd., EPS Rm. 8007, Rockville, MD 20852 (e-mail: mbulaits{at}mail.nih.gov).

Background: Although human herpesvirus 8 (HHV-8), the etiologic agent for Kaposi’s sarcoma, can be detected in peripheral blood, blood-borne transmission of this virus has not been demonstrated. We studied the association between HHV-8 seropositivity and transfusion history among children with sickle-cell disease in Uganda, where HHV-8 infection is common in blood donors. Methods: We studied 600 children (aged 0–16 years) with sickle-cell disease at Mulago Hospital, Kampala, from November 2001 through April 2002. By design, about half had previously been transfused. HHV-8 serostatus was determined using enzyme-linked immunosorbent assays for antibodies against HHV-8 proteins K8.1 and orf 73. We used logistic regression to test for an association between HHV-8 serostatus and transfusion history and a Markov model to estimate the transmission risk per transfusion and the cumulative risk from community (i.e., nontransfusion) sources. Statistical tests were two-sided. Results: HHV-8 antibodies were detected in 117 of 561 (21%) children with unambiguous K8.1 results. HHV-8 seroprevalence among the never-transfused children increased with age from 7% in children aged 0–2 years to 32% in those aged 13–16 years (Ptrend<.001). HHV-8 seropositivity was more frequent in transfused than never-transfused children (24% versus 17%, odds ratio = 1.48, 95% confidence interval [CI] = 0.97 to 2.26; P = .07). Seropositivity increased with number of reported transfusions, with age-adjusted odds ratios of 0.97 (95% CI = 0.54 to 1.75), 1.13 (95% CI = 0.59 to 2.17), 1.76 (95% CI = 0.81 to 3.83), and 2.17 (95% CI = 1.18 to 3.99) for children with one, two, three, or four or more transfusions, respectively (Ptrend = .007). Overall, the estimated HHV-8 transmission risk was 2.6% per transfusion (95% CI = 1.9% to 3.3%), whereas the annual risk of infection unrelated to transfusion was 2.7% (95% CI = 1.7% to 3.7%). Conclusion: Our study suggests that blood transfusion is associated with a small risk of HHV-8 transmission. In Uganda, this risk is approximately equivalent to the 1-year cumulative risk of infection from community sources.


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