Initiation and modification of antiretroviral therapy depend, to a large extent, on plasma viral load and peripheral blood CD4+ T lymphocyte count. Although these surrogates for monitoring disease status are widely used, there are Isoshaftoside limitations. For example, the kinetics and extent of antiretroviral-mediated CD4+ T cell recovery may show great variation from child to child. Similarly, in many settings CD4+ Orphenadrine Citrate T-cell counts may correlate poorly with viral replication. There has been a search for complementary immunological markers to assess or predict response to therapy. In the pediatric setting, most reports have been generated by relatively small studies. For example, T-cell expression of HLA-DR, CD38 and CD95 has been correlated with a poor response to therapy. Functional characteristics of T-cells have also been evaluated. Predominant production of interleukin -2 by HIV-specific Tcells may be associated with a favorable response to antiretrovirals, in contrast to the poorer outcome when IFN-c production is more prevalent. Two studies in the United States of novel immunological correlates of response to therapy have involved large numbers of infants and children. Both studies found that a decrease in CD8+ T-cell percentage, and in CD8+CD38+HLA-DR+ percentage, is associated with a favorable response to therapy. The authors suggested introduction of such markers into clinical pediatric practice. More recently, numerous studies have indicated that T-cell expression of IL-7 receptor alpha may be a predictor of clinical HIV disease status in adults. These studies show that CD127 expression on T-cells is lower in HIVinfected individuals compared with uninfected controls, and that this expression correlates inversely with disease severity. Some reports have suggested that the marker may be useful for predicting response to therapy, whereas another has questioned its utility. CD127 is the receptor for IL-7, a cytokine crucial for thymopoiesis, maintenance of CD8+ memory T-cells, and peripheral T-cell homeostasis in states of T-cell depletion.