Water, vegetation and sediment gradients in submerged aquatic vegetation mesocosms used for low-level phosphorus removal.

Gradients in phosphorus (P) removal and storage were investigated over 6 years using mesocosms (each consisting of three tanks in series) containing submerged aquatic vegetation (SAV) grown on muck and limerock (LR) substrates. Mean inflow total P concentrations (TP) of 32 µg L(-1) were reduced to 15 and 17 µg L(-1) in the muck and LR mesocosms, respectively. Mesocosm P loading rates (mean=1.75 gm(-2) year(-1)) varied widely during the study and were not correlated with outflow TP, which instead varied seasonally with lowest monthly mean values in December and January. The mesocosms initially were stocked with Najas guadalupensis, Ceratophyllum demersum, and Chara zeylanica, but became dominated by C. zeylanica. At the end of the study, highest vegetative biomass (1.1 and 1.4 kg m(-2) for muck and LR substrates) and tissue P content (1775 and 1160 mg kg(-1)) occurred in the first tank in series, and lowest biomass (1.0 and 0.2 kg m(-2)) and tissue P (147 and 120 mg kg(-1)) in the third tank. Sediment accretion rates (2.5, 1.9 and 0.9 cm yr(-1) on muck substrates), accrued sediment TP (378, 309 and 272 mg kg(-1)), and porewater soluble reactive P (SRP) concentrations (40, 6 and 4 µg L(-1)) in the first, second and third tanks, respectively, exhibited a similar decreasing spatial trend. Plant tissue calcium (Ca) near mesocosm inflow (19-30% dry weight) and outflow (23-26%) were not significantly different, and sediment Ca was also similar (range of 24 to 28%) among sequential tanks. Well-defined vegetation and sediment enrichment gradients developed in SAV wetlands operated under low TP conditions. While the mesocosm data did not reflect deterioration in treatment performance over 6 years, accumulation of P-enriched sediments near the inflow could eventually compromise hydraulic storage and P removal effectiveness of these shallow systems.

Evaluation of T cell receptor gene rearrangement excision circles after antiretroviral therapy in children infected with human immunodeficiency virus.

Immune reconstitution after antiretroviral therapy in human immunodeficiency virus (HIV)infected patients may result from the recovery of thymus function, peripheral redistribution, or decreased T cell destruction. This study investigated levels of T cell receptor gene rearrangement excision circles (TRECs) as a measure of recent thymic emigrant cells in peripheral blood lymphocytes of 50 HIV-infected infants and children who were followed-up for 40 months after the start or change of antiretroviral therapy. At baseline, patients exhibited fewer TRECs than did uninfected control subjects. The increase in TRECs after antiretroviral therapy was greater in infants than in older HIV-infected children. Of interest, patients who demonstrated discordant responses (i.e., increased CD4 T cell counts without significant virologic suppression) also had substantial gains in TRECs. Furthermore, TRECs correlated positively with the number of CD4 and naive T cells and negatively with age and virus load. Measurement of TRECs may serve as a useful tool for evaluating immune reconstitution in HIV-infected children receiving antiretroviral therapy.

Patterns of CD8 T cell clonal dominance in response to change in antiretroviral therapy in HIV-infected children.

OBJECTIVE: To examine the influence of change in antiretroviral therapy (ART) on patterns of CD8 T cell clonal dominance in HIV-infected children. DESIGN: Seventeen HIV-infected children with plasma virus loads between 3.1 and 5.7 log10 were investigated before and after changes in ART. METHODS: CDR3 spectratyping was performed in 22 T cell receptor (TCR) Vbeta subfamilies by multiplex polymerase chain reaction (PCR) in purified peripheral blood CD8 T cells in conjunction with CD4 cell counts, plasma HIV-RNA copies and lymphoproliferative assays (LPA). RESULTS: CD8 T cell clonal dominance in two or more Vbeta families was present in eight out of 17 children. After a change in therapy, 13 patients (76%) acquired new clones whereas three patients (17.6%) showed a loss in CD8 cell clones. An increase in the numbers of dominant clones correlated with an increase in percentage CD4 cell counts (P < 0.001) and with improved LPA responses to tetanus (P < 0.05) and alloantigens (P < 0.01). CD4 cell increase was associated with an initial mean gain of 3.1+/-2.1 CD8 cell clones, independent of a virological response. A loss of CD8 cell clones or failure to achieve CD4 T cell increase was associated with failure to achieve virological suppression. CONCLUSION: Children with chronic HIV infection manifest CD8 T cell clonal dominance, which appears to be dependent upon the adequacy of the CD4 cells. With optimization of therapy, a gain in clonal dominance is the predominant response, except in situations of failure to contain viral replication.

Clonal dominance patterns of CD8 T cells in relation to disease progression in HIV-infected children.

CD8 T cells are important mediators of cellular immune responses as evidenced by clonal expansions in the CD8 TCR V beta repertoire during primary HIV infection in adults. This study investigated the CD8 TCR V beta repertoire by complementarity-determining region 3 length analysis using multiplex PCR in purified peripheral blood CD8 T cells of 22 HIV-infected children (age range was 0.75-15 yr, mean was 8.2 +/- 4.1 yr). Evidence of clonal dominance in one or more V beta families was obtained in 15 of 22 children. The patterns of clonal dominance were designated as major, minor, single, and none to indicate the involvement of three or more, two, one, or no V beta families, respectively. A pattern of major or minor clonal dominance was observed in 12 children (group 1), whereas 10 children had single or no clonal dominance (group 2). In comparison with group 2, the children in group 1 had a higher percentage of CD4 cells (28.3 +/- 11.6 vs 8.6 +/- 4.8, p < 0.001); a higher stimulation index in lymphoproliferative responses to Candida (92.0 +/- 59.5 vs 12.3 +/- 14.4, p = 0.002), tetanus (76.3 +/- 51.2 vs 11.2 +/- 12.7, p = 0.002), and alloantigens (178.3 +/- 298.9 vs 32.9 +/- 35.2, p < 0.001); and a lower percentage of CD8+HLA-DR+CD38+ cells (37.4 +/- 13.1 vs 54.6 +/- 14.2, p < 0.01). The number of dominant CD8 T cell clones was significantly correlated with the percentage of CD4 T cells (r = 0.669, p < 0.001) but not with plasma HIV RNA. Compared with group 1, patients in group 2 had a 4.8 times greater probability of having < 15% CD4 cells. These findings indicate that CD8 clonal dominance in HIV-infected children reflects robustness of immune responses, regardless of time since infection and virus load.