摘要
Aim: To investigate the role of IL- 7 in HIV- infected children on highly a ctive antiretroviral therapy (HAART) and its association with laboratory paramet ers related to disease progression. Patients and methods: A cross- sectional study in 31 vertically HIV- infected children (median age 8.4 y) t reated with HAART, and a longitudinal study in four of those same children was c arried out. In both studies, viral load, CD4+ T- cell counts, thymic producti on of T cells by TCR rearrangement excision circles (TRECs), IL- 7 plasma level s and viral phenotype were determined. Results: IL- 7 levels were higher in HIV - infected children than in age- matched, uninfected controls. In addition, HI V children with CD4+ T cells between 200 and 500 T cells/mm3 had higher IL- 7 levels and lower TREC values than HIV- infected children with CD4+ T cells > 500 T cells/mm3. IL- 7 levels were higher in children with syncytium- inducin g (SI) phenotype than in those with nonsyncytium- inducing (NSI) variants. Duri ng the follow- up of four HIV children, the decrease in viral load after HAART was always associated with a recovery of CD4+ T cells and TRECs, which was fol lowed by a decrease in IL- 7 returning to the levels present prior to the drop in CD4+ Tcells. The four HIV- infected children had SI/X4 isolates in PBMC be fore HAART, and the viral phenotype switched to NSI/R5 after HAART. Conclusion: Our data suggest that IL- 7 plays a key role in the maintenance of T- cell hom eostasis in HIV- infected children on HAART, both through peripheral expansion and through a thymus- dependent mechanism.
Aim: To investigate the role of IL- 7 in HIV- infected children on highly a ctive antiretroviral therapy (HAART) and its association with laboratory paramet ers related to disease progression. Patients and methods: A cross- sectional study in 31 vertically HIV- infected children (median age 8.4 y) t reated with HAART, and a longitudinal study in four of those same children was c arried out. In both studies, viral load, CD4+ T- cell counts, thymic producti on of T cells by TCR rearrangement excision circles (TRECs), IL- 7 plasma level s and viral phenotype were determined. Results: IL- 7 levels were higher in HIV - infected children than in age- matched, uninfected controls. In addition, HI V children with CD4+ T cells between 200 and 500 T cells/mm3 had higher IL- 7 levels and lower TREC values than HIV- infected children with CD4+ T cells > 500 T cells/mm3. IL- 7 levels were higher in children with syncytium- inducin g (SI) phenotype than in those with nonsyncytium- inducing (NSI) variants. Duri ng the follow- up of four HIV children, the decrease in viral load after HAART was always associated with a recovery of CD4+ T cells and TRECs, which was fol lowed by a decrease in IL- 7 returning to the levels present prior to the drop in CD4+ Tcells. The four HIV- infected children had SI/X4 isolates in PBMC be fore HAART, and the viral phenotype switched to NSI/R5 after HAART. Conclusion: Our data suggest that IL- 7 plays a key role in the maintenance of T- cell hom eostasis in HIV- infected children on HAART, both through peripheral expansion and through a thymus- dependent mechanism.
