Although adverse events such as severe anaemia, leucopenia, neutropenia, and lymphopenia were uncommon, they should not be taken lightly because of their life-threatening potential. Yet the rate of women who were transfused was of the same magnitude as has been seen in other studies of HIV-uninfected women not receiving zidovudine. No woman stopped the study treatment because of haematological toxicity, although one woman exposed to zidovudine from 28 wk of gestation developed severe anaemia and delivered a stillborn. This woman presented at pre-entry biological parameters known to be associated with anaemia, such as low CD4 count and high HIVRNA viralload. Women in the study were provided with iron supplementation, according to the national recommendation. However, we had no information about adherence to this recommendation. As the duration of zidovudine exposure was assigned randomly, supplementation is likely to be balanced among the randomized groups in each site and should not have been a source of bias. Our Orientin result is consistent with this notion. Beside E-boxes, there are a number of other transcription factor binding sites in the ADAMTS5 enhancer with invariant arrangement of spacing and orientation across human, mouse, and rat genomes. Laboratory assessment of HIV disease status is indispensable for managing antiretroviral therapy in infected children. Progressive HIV infection is associated with increased circulating levels of IL-7, however memory T-cells are not expanded and homeostasis is not maintained. IL-7 has been proposed for use as an immunotherapeutic agent for the treatment of HIV, but the finding of immunologic failure despite high levels of circulating IL-7 has suggested that this type of therapy may not be beneficial. Dysfunctional CD127 expression suggests that failure of the IL-7/IL-7 receptor system may contribute to the loss of memory T-cell maintenance in HIV infection. Our results confirmed and expanded on previous observations in 4-Hydroxyisoleucine HIV-infected individuals, which have suggested that loss of CD127 expression on CD8+T-cells may be a correlate of disease progression.