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Background: Undetectable HIV infection in blood banks poses a serious threat to public health. Thus, donations from high school students are preferred over adult samples in Kenyan blood banks, due to lower HIV infection prevalence within this population, as detected by conventional serology testing. However, the number of recently infected individuals remains difficult to identify, as HIV-induced immunological window periods can span months. This study focuses on the potential contribution of a novel mode of diagnostic testing in revealing early, seronegative HIV carriers. Methods and Findings: Stimmunology, an in vitro lymphocyte stimulation technique, was used to detect early HIV infection among random samples of adult and adolescent blood donors. The Stimmunology protocol unveiled a significant number of early, pre-seroconversion HIV carriers both among adult and teenage Kenyan populations, undetected by typical serological diagnostic kits. Both populations demonstrated a significant increase in HIV-specific antibody formation following activation using the Stimmunology assay. The younger population exhibited a higher proportion of early HIV infection (0.45) than the adult (0.27) population. Conclusions: While blood samples of young donors are preferred over adult donations, these data demonstrate a worrisome ratio of early, seronegative HIV carriers within this population. This simple, cost-effective, and reliable HIV-boosting antibody assay can be used in a resource-poor setting to increase blood supply safety and quality. Incorporation of Stimmunology into basic blood bank testing and into diagnostic protocols can also decrease undesirable disease transmission.

In two hemophilic brothers infected by the human immunodeficiency virus (HIV), Burkitt's leukemia developed within 1 year. Both patients were treated by aggressive chemotherapy, and both are still in complete remission for 23 and 14 months, respectively. Sera from both brothers contained anti-HIV antibodies. However, DNA extracted from the tumor cells, when analyzed by Southern blot using a cloned HIV probe, did not reveal HIV-related sequences. Hybridization experiments with an Epstein- Barr virus (EBV) probe revealed the presence of EBV-specific sequences in the tumors' DNA. In both patients' tumors rearranged c-myc genes were found. The rearrangements occurred in both genes 3′ to the third exon of c-myc, thereby suggesting that a variant chromosomal translocation took place in both cases. Indeed, karyotype analysis of the malignant cells of one of the patients revealed the variant t(2:8) translocation. In contrast to the majority of Burkitt's tumors carrying this translocation, which are kappa light-chain producers, cells of our patient expressed lambda chains. Furthermore, in both cases the lymphoblasts carried IgG on the surface, again an unusual finding in Burkitt's tumors. Finally, because both patients had an identical HLA phenotype, the role of genetic factors in the development of such tumors should be considered.

In two hemophilic brothers infected by the human immunodeficiency virus (HIV), Burkitt's leukemia developed within 1 year. Both patients were treated by aggressive chemotherapy, and both are still in complete remission for 23 and 14 months, respectively. Sera from both brothers contained anti-HIV antibodies. However, DNA extracted from the tumor cells, when analyzed by Southern blot using a cloned HIV probe, did not reveal HIV-related sequences. Hybridization experiments with an Epstein- Barr virus (EBV) probe revealed the presence of EBV-specific sequences in the tumors' DNA. In both patients' tumors rearranged c-myc genes were found. The rearrangements occurred in both genes 3′ to the third exon of c-myc, thereby suggesting that a variant chromosomal translocation took place in both cases. Indeed, karyotype analysis of the malignant cells of one of the patients revealed the variant t(2:8) translocation. In contrast to the majority of Burkitt's tumors carrying this translocation, which are kappa light-chain producers, cells of our patient expressed lambda chains. Furthermore, in both cases the lymphoblasts carried IgG on the surface, again an unusual finding in Burkitt's tumors. Finally, because both patients had an identical HLA phenotype, the role of genetic factors in the development of such tumors should be considered.

No abstract