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Background: Lopinavir/ritonavir has demonstrated antiviral activity in the HIV-infected patient., Objective: To analyse virological response to lopinavir/ritonavir therapy in previously protease inhibitor (PI)-experienced HIV-1-infected children., Materials and Methods: Sixty-seven HIV-1-children on lopinavir/ritonavir were studied in a multicentre prospective cohort observational study. The outcome variables were undetectable viral load (uVL; VL < or =400 copies/mL) and virological failure after uVL with a rebound of VL >400 copies/mL. VL and genotype of HIV-1-isolates were measured using standard assays., Results: 83.5% of children had a 1 log10 VL decrease including 65.6% who reached uVL. Children with >2 changes of antiretroviral therapy (ART) or >5 drugs needed a median time of 3-4 months higher than children with < or =2 changes of ART or < or =5 drugs previous to lopinavir/ritonavir, to reach those values, and the relative proportions (RP) were 2.2 (P =0.038) and 1.9 (P=0.050), respectively. Children with CD4+>15% (P=0.122), VL < or =30,000 (P < 0.001) copies/mL, and age >12 years (P=0.096) achieved an earlier control of VL during the follow-up. The children with virological failure or rebound of VL had higher baseline VL and lower CD4+ T-lymphocytes/mm3 and had taken a greater number of drugs previous to lopinavir/ritonavir. HIV-children with a new nucleoside reverse transcriptase inhibitor (NRTI), or protease inhibitor (PI) or PI plus non-nucleoside reverse transcriptase inhibitors (NNRTI) in the current regimen had a better virological response than children without these new drugs. Also, children with <6 protease mutations had an RP of 2.31 of achieving uVL., Conclusions: Highly active antiretroviral therapy (HAART) including lopinavir/ritonavir induces beneficial effects in terms of virological outcome responses, and it is an effective option for salvage therapy in PI-experienced HIV-1-infected children.

The objective of this study was to monitor the changes in the immune system of HIV-infected children with moderate or severe immunodeficiency after highly active antiretroviral therapy (HAART), comprising a follow-up study in 14 HIV-infected children on HAART at two time points separated approximately by 11.8 +/- 0.4 (9.9; 15.4) months. HIV-infected children had significantly lower TREC levels than the control group, but 1 year after HAART the levels increased significantly (P < 0.05). In contrast, viral load (VL) did not change significantly. A positive correlation between T cell receptor excision circle (TREC) levels and both CD4(+) T cell absolute counts (r = 0.558; P = 0.05) and percentages (r = 0.625; P = 0.030) was found. During follow-up on HAART, the percentages and absolute counts of naive CD4(+) and CD8(+) T cell subsets were increased significantly (P < 0.05). CD4(+) CD45RA(hi+) CD62L(+), CD4(+) CD45RA(+) and CD4(+) CD38(+) percentages, and the CD8(+) CD45RA(hi+) CD62L(+) counts reached similar values to the control group. Also, CD8(+) CD45RO(+) CD38(+) and CD8(+) CD45RO(+) percentages, and CD8(+) CD45RO(+) CD38(+) absolute counts (P < 0.05) decreased with respect to the baseline. Lymphoproliferative responses to pokeweed mitogen (PWM) before HAART were lower in HIV-infected children than the control group, but they recovered to normal levels after a year on HAART. Tumour necrosis factor (TNF)-alpha and interferon (IFN)-gamma production by PHA-activated peripheral blood mononuclear cells (PBMC) was lower before HAART (P < 0.001), but reached similar levels to the control group 1 year after HAART. In HIV-infected children IgG, IgG(1) and IgG(3) plasma levels decreased significantly after HAART. The immune system reconstitution induced by HAART in HIV-infected children seems to be the consequence of decreased immune system activation and naive T cell reconstitution, mainly of thymic origin.

An observational study was performed involving 95 children with vertically transmitted human immunodeficiency virus type 1 infection to assess the sustainability of undetectable viral loads (VLs) and increased CD4+ T lymphocyte percentages after 48 months of highly active antiretroviral therapy (HAART). The median time to achieve a 10% increase in the CD4+ T lymphocyte percentage was 11.01 months. The median time to achieve an undetectable VL was 6.4 months. At the end of the study, 64.2% of the children had achieved an undetectable VL. Of the patients with an initial VL of >3.6 log10 copies/mL, 74.7% had a decrease in the VL of 1 log10 copies/mL. By contrast, of the patients who presented with an initial VL of >4.6 log10 copies/mL, 37.9% had a decrease of >2 log10 copies/mL. Higher VL at baseline, antiretroviral therapy regimens received before HAART, and multiple drug switches while receiving antiretroviral therapy were all inversely associated with an undetectable VL. A CD4+ T lymphocyte percentage of >25% was directly associated with undetectable VL during the follow-up period. In conclusion, first-line HAART induces beneficial virological and immunological outcome responses in children.

Our objective was to study the probability of achieving undetectable viral load levels in HIV-1-infected children after 36 mo of highly active antiretroviral therapy (HAART). A prospective, multicenter, longitudinal study in 41 HIV-1-infected children on HAART was undertaken. Viral load was quantified using standard molecular assay. CD4+ and CD8+ T cell subsets were determined by flow cytometry. The probability of achieving undetectable viral load was determined using Kaplan-Meier curves according to groups by percentage CD8+ at baseline (CD8+ <25% or >25%). Lower baseline CD8+ T cell levels conditioned a less effective virological response to HAART in children, independent of baseline CD4+ T cell numbers and viral load levels. A greater number of children (81%) from CD8+ >25% group than from the CD8+ <25% (40%) presented undetectable viral load levels (p = 0.013). Additionally, the CD8+ >25% group showed a 4.5-fold higher (95% confidence interval: 1.1-19.2) relative proportion for achieving viral load <400 copies/mL than the CD8+ <25% group (p = 0.039). We concluded that monitoring CD8+ T cell numbers may be valuable in deciding when to start HAART in vertically HIV-1-infected children.

Background and Objective: Our goal was to determine the probability of achieving a fall-off of viral load (VL) and an increase of CD4+T-lymphocytes by 36 months from the initiation of antiretroviral therapy (ART) in a cohort of HIV-infected children according to their baseline data., Patients and Method: This was retrospective multicenter observational study of virologic and immunologic markers in 128 HIV-1-vertically infected children on ART: 55 HIV-infected children on combination therapy (CT), and 73 HIV-infected children on highly active antiretroviral therapy (HAART). Viral load (VL) was quantified using a standard molecular assay. CD4+ and CD8+ T-cells subsets were determined by flow cytometry., Results: The median time for a 10% rise of CD4+ T-lymphocytes was 35.7 months (95% confidence interval [95% CI], 15.5-55.9) after starting CT, and 11 months (95% CI, 7,7-14.3) after starting HAART. The median time for a VL fall to < 400 copies/ml was 29.6 months (95% CI, 9.4-49.7) after starting CT, and the median time for a VL fall to < 400 copies/ml was 10.9 months (95% CI, 0-21.9) after starting HAART. A 10% increase of CD4+ T-cells over baseline was associated with HAART, low CD4+ T-cells and high VL. On the other hand, a VL fall lower than 400 copies/ml was associated with HAART and low baseline VL., Conclusions: Our data indicate that HAART was better than CT in the control of VL and CD4+ T-cell increase. Also, baseline CD4+ T-cell and VL values helped to determine the response to ART in HIV-1 infected children.

Aims: To assess the "real life" effectiveness of different antiretroviral therapies (ART)., Methods: A retrospective multicentre observational study in 150 HIV-1 vertically infected children on the progression to AIDS (study A), and in 61 HIV-1 infected children on the evolution of the most relevant markers of progression (study B). All children were categorised into four groups: untreated (NT); on monotherapy (MT); on combination therapy (dual-ART); and on potent ART (HAART)., Results: No child in the HAART group progressed to AIDS, whereas 14 children in the NT and seven in the MT groups progressed to AIDS, respectively, the differences being statistically significant. There was a mean increase of 8 units of %CD4+ per year; this was greater in the HAART group than in the other groups. The mean decrease in viral load was 0.65 log(10) copies/ml per year; this was greater in the HAART group than in the NT and MT groups. The HAART group had the lowest probability of returning to baseline %CD4+ and viral load., Conclusion: Potent ART had the greatest protective effect against progression to AIDS in this observational study.

Unlabelled: Treatment with highly active antiretroviral therapy (HAART) has been shown to modify viral replication dynamics and lead to a significant recovery of CD4+ T-cells. A retrospective multicentre observational study was performed in a non-study population of 151 HIV-1-infected children, categorized into four groups according to therapy: untreated (NT), on monotherapy (MT) with a nucleoside inhibitor, on combination therapy (CT) with two nucleoside inhibitors, and on HAART, protease inhibitor containing regimens, to assess the "real-life" effectiveness of these different therapies on plasma viral load (VL) and CD4+ T-cells. VL was quantified using a standard molecular assay. CD4+ and CD8+ T-cells subsets were determined by flow cytometry. The HAART group showed the highest relative proportion (RP) of increases in 5, 10, 15 and 20% of CD4+ T-cells over baseline, and the earliest fall-off of VL (0.5, 1, 1.5 and 2 log10 copies ml-1). The RP of the fall-off of 0.5, 1, 1.5 and 2 log10 VL below baseline was 3-fold higher in HAART group than in the MT and CT groups. However, no differences were found among the groups of treated children in reaching undetectable VL., Conclusion: A better evolution of VL and CD4+ T-cells was evident in children on HAART, indicating a positive effect on the immune system and clinical status, inhibiting HIV-1 replication and enabling the recovery of CD4+ T-cell counts.

Unlabelled: This study measured cytokine production by mitogen-stimulated peripheral blood mononuclear cells (PBMCs) from 55 human immunodeficiency virus (HIV)-infected children born to HIV-infected mothers, and compared it with vertically exposed but uninfected age-matched children. A significant defect was observed in Th1 cytokine production [interferon-gamma and interleukin-2 (IL-2)] in HIV-infected children compared with controls, but without a concomitant increase in Th2 cytokines. Indeed, IL-5 and IL-10 production was even lower in HIV-infected children than in controls, with the decrease in IL-5 being the best predictive marker of immunodeficiency. In addition, an increased release of tumour necrosis factor-alpha (TNF-alpha) that correlated well with CD4+ levels, and a positive correlation of the TNF-alpha/IL-10 ratio with disease progression was observed. A correlation between AIDS-free status and higher %CD4+ and %CD8+ T-lymphocytes and RANTES (regulated on activation, normal T-cell expressed and secreted) production was also found., Conclusion: A dysfunctional cytokine production of PBMCs was observed in HIV-infected children in both Th1 and Th2 cytokines due to quantitative and qualitative defects induced by HIV-1. An important observation was an increased RANTES production associated with viral isolates of NSI/R5 phenotype and S/L kinetics.

The objective of this study was to investigate the relationship between peripheral blood CD4+ T cell subsets and routine viro-immunological markers in vertically HIV-1-infected children undergoing highly active antiretroviral therapy (HAART). CD4+ and CD8+ T cell subsets were examined by three-colour flow cytometry. Plasma viraemia was quantified by a standardized molecular assay. A negative correlation between the %CD4+ T cells and both viral load and the %CD8+ T cells was observed. A strong positive correlation between the %CD4 T cells and naïve, CD38+ and non-activated CD4+ T cell subsets was found, whereas the %CD4 T cells correlated negatively with the numbers of memory, activated and memory-activated CD4+ T cell subsets. Elevated percentages of CD8 T cells were associated with increased memory and CD4+ CD62L-T cell subsets, whereas the naïve and CD4+ HLA-DRCD38+ subsets negatively correlated with the CD8%. Co-expression of CD62L on memory CD4+ cells and high expression of HLA-DR (but not of CD38) were associated with high viral load. No association between viral load and naïve CD4+ T cells was observed. Specific CD4+ T cell subsets may be more informative than routine surrogate markers in defining the evolution of HIV infection and immune reconstitution in children.

In contrast to adults, there is no information about children concerning the effects of the new antiretroviral therapy on the chronic activation and expansion of CD8+ T cells. We have investigated the relationship between blood CD8(+) T cell subsets, with percent CD4+ cells (%CD4), percent CD8+ cells (%CD8), and plasma viral load (VL), in 39 vertically HIV-1-infected children receiving highly active antiretroviral therapy (HAART) (mean age, 7.6 years; range, 2-15.6 years). CD8+ subsets were examined by three-color multiparametric flow cytometry, and VL was quantified by standard assays. There was a strong positive correlation between activated CD8+ T cells and VL. An increase in memory and memory-activated CD8+ T cells correlated with increased VL, whereas nonactivated memory cells and CD28+ CD8+ T cells correlated negatively with VL. Naive and effector cells did not correlate with VL, although the CD8+ CD45RA -CD62L- subset correlated with increased VL. Activated CD8(+) T cells did not correlate with %CD4, but an increase in memory-activated and effector CD8+ T cells was associated with lower %CD4. Increased naive CD8+ and CD28 +CD8+ T cells showed a positive correlation with %CD4 and a negative correlation with %CD8. In conclusion, in HIV-1-infected children receiving HAART, the activation of CD8+ T cells is associated with high VL, whereas CD8 +CD28+ and nonactivated CD8+ memory cells are associated with lower viral load. Naive CD8+ and CD28 +CD8+ T cells are associated with an improved immunological status.

In order to investigate the correlation among cytokine production and antiretroviral therapy (ART), viral load, CD4(+) and CD8(+) T lymphocytes, 55 human immunodeficiency virus (HIV)-1-infected children on ART or not, and 16 uninfected controls were studied. Peripheral blood mononuclear cells (PBMCs) of HIV-1-infected children and controls were cultured and spontaneous and mitogen-stimulated cytokines production was quantified in the supernatants. Viral load was quantified using standard molecular assay. CD4 and CD8 T-lymphocyte counts were determined by flow cytometry. Cytokine production by mitogen-stimulated PBMCs showed different profiles in HIV-1 children whether treated or not. The tumour necrosis factor (TNF)-alpha production was higher and the interleukin (IL)-10 production was lower in the HIV-1-untreated group than in the HIV-1-treated children and controls. The IL-2 production was reduced and the RANTES production was higher in both HIV-1 groups compared with the controls. The interferon (IFN)-gamma and the IL-5 production was significantly reduced in the HIV-1-treated children compared to the controls. Interestingly, the analysis of the correlation of HIV-1 phenotype with cytokine production indicated an increased RANTES production in relation to nonsyncytium-inducing viral phenotype with slow/low replication profile, whereas decreased IL-10 levels was associated to syncytium-inducing (SI) strains and rapid/high replication. Our findings suggest that AVT changes on the cytokine and chemokine production play an important role in the HIV pathogenesis.

Background: To study the prognostic AIDS progression value of the percentage of CD4+, CD8+, and plasma viral load (VL) (copies/ml) in HIV-1-vertically infected children., Patients and Method: We study a cohort of 115 HIV-1 infected children older than 12 months of age. The VL was quantified using standard molecular assay. CD4 and CD8 T lymphocytes were determined by flow cytometry., Results: The children with a median of VL > 4.5 log10 (p < 0.001) and percentage of CD8+ < 25% (p = 0.05) during follow-up, progressed faster to AIDS than children with a median of VL < 4.5 log10 and CD8 > 25%. The relative risk (RR) of AIDS progression was 7-fold higher in children with median VL above 4.5 log10. When considering VL as a continuous variable, risk of progression to AIDS is 3.5-fold higher for each increase of one log10 of VL. The percentage of CD8+ T-cells had a RR of AIDS progression of 0.95/% CD8+ at entry to the study and of 0. 19/% CD8+ during follow-up, indicating protection against progression to AIDS., Conclusions: Our results indicate that each basal values at entry in the study and during the follow-up of the percentage of CD8+ and VL helps to determine the risk of AIDS progression in HIV-1-infected children. More interestingly, the use of the two predictive markers together had higher predictive value.

Objective: To study the relationship among clinical symptoms and biological markers as predictive value of progression to death in HIV-1 vertically infected infants., Patient and Methods: We carry out a prospective study in 43 HIV-1 infants with a mean age of 4.27 (range: 0-11.8 months). None of the infants' mothers had received any antiviral treatment during pregnancy. None of the infants were breastfed. They were routinely assessed for clinical symptoms during follow-up., Results: Cox regression analysis was used to study the hazard ratio (HR) of progression to death. For the median viral load > 5 log10, the HR was 6.42 (95% CI, 1.28-32.03) (p = 0.023) and 6.84 (95% CI, 1.52-30,69) (p = 0.012) for biological phenotype of viral isolates with rapid replication and high titter (R/H-X4). We also study the predictive value of the clinical symptoms and we observe that the symptoms with more HR of progression to death were the progressive encephalopathy (3.60 [95% CI, 0.92-14.06; p = 0.065]) and the cardiopathy (6.29 [95% CI, 1.59-24.85; p = 0.008])., Conclusions: Our data indicate that viral load > 5 log10 and biological phenotype R/H-X4 of virus isolates along the study are predictive markers of progression to death. In addition, the progressive encephalopathy and cardiopathy were also markers of progression death.

Introduction: it is known that in early-stage HIV-induced disease there is a discrepancy between the levels of viral burden and virus replication in peripheral blood versus lymphoid organs. HIV disease is active in the lymphoid tissue throughout the period of clinical latency. However, it is not known how long term progression of HIV infection is influenced by short-term changes in the adenoidal size., Objective: To assess the reliability of adenoidal-nasopharyngeal (AN) ratio in predicting clinical evolution of pediatric HIV infection., Methods: lateral radiographs of the nasopharynx in 94 Caucasian children born to HIV-1-infected mothers ranged from 6 months to 15 years (60 children infected with HIV-1 and 34 without HIV infection), and in a control group of 692 normal children were evaluated to obtain the AN ratio in order to identify the relationship of AN profiles with different stages of the disease. Patients were rated regarding their clinical and immunological status according to the Center for Disease Control Classification., Results: statistically significant differences between the groups of HIV-1-infected children, seroreverters and controls in the AN ratio were found (P < 0.001). Moreover, significant differences were also found in individual children that correlated with clinical progression., Conclusion: examination of radiographic changes in adenoidal size by AN ratio in relation to clinical status during one year period in the whole group showed strong prognostic value. These findings may have important implications in the design of therapeutic strategies.

Objectives: To assess the immunological and virological markers as potential predictors of progression to death in HIV-1 infected < 12 months of age., Patients and Methods: Forty-three HIV-1 infants < 12 months of age were evaluated. None of the children received antiviral treatment, neither their mothers during pregnancy. Plasma viremia was quantified by standardised molecular assay. Virus isolation, evaluation of the non-syncytia-inducing (NSI) or syncytia-inducing (SI) phenotype and kinetic of replication was performed in parallel cultures., Results: Regarding viral load cut off levels of 5 log10 copies/ml appeared to be the best predictors of progression to death. The mean times of progression to death estimated by Kaplan-Meier method were 61.08 months fir children with viral load below that limit, and 19.16 months above this limit (p < 0.013). When the first viral isolate was NSI the mean time of progression to death was of 73.9 months, whereas it was of 26.7 months when was SI (p < 0.003). When the first viral isolate was slow/low (S/L) the mean times of progression to death was 71.8 months, whereas it was of it was of 19.8 months when was rapid/high (R/H) (p < 0.0003). When the first viral isolate was S/L-NSI the mean times of progression to death was of 73.9 months, whereas it was of 19.4 months when was R/H-SI (p < 0.0004). The hazard rate of progression to death in infants with viral load > 5 log10 copies/ml was 4.7, whereas was of 8.07 in those with SI isolates and of 9.32 in those with R/H kinetics., Conclusions: Initial HIV-1 biological characteristics are better predictors of progression to death than viral load in untreated infants under 12 months of age. Nevertheless, a correlation exists between viral load over 5 log10 copies/ml and progression to death.

To assess the predictive power of immunological and virological markers for the development of neurological syndromes, 39 HIV-1-infected infants with a mean age of 4.05+/-0.5 months and without neurological manifestations at enrolment were studied. They had neither been previously treated with antiretroviral therapy, nor had their mothers been given such treatment during pregnancy. They were routinely assessed for signs of neurological impairment during follow-up (19.54+/-3.37 months). Cox regression analysis was used to evaluate the risk of appearance of neurological signs, associated to viral load and T-lymphocyte subsets. A HR > 1 for viral load, and <1 for CD8+, but not for CD4+T-lymphocyte percentage, was observed, indicating that higher viral load and lower CD8+ T-lymphocytes percentages are risk factors for developing neurological signs. By applying the Kaplan-Meier method we found that infants with viral load > 5 1og10 copies/ ml or <20% CD8+T lymphocyte had higher relative risk for developing neurological impairment than those with these two parameters below or above these values, respectively. Finally, CD8+ T lymphocyte had a stronger prognostic value to predict neurological manifestations than viral load. Our data strongly suggest that in the early postnatal period viral load and CD8+ percentages are useful markers in predicting neurological impairment. To our knowledge, this is the first time that CD8+ T-lymphocyte levels are related to development of neurological disorders in AIDS.

Background: Multiple viral subpopulations coexist in an HIV infected patient with dynamics of selection established between them. In order to get insight on the phenotype of these subpoblations, and its relation with disease progression, we have studied the biological variability of HIV-1 in 113 patients. Variability was related with CD4+ T lymphocyte counts, clinical status, way of viral transmission and antiretroviral treatment., Patients and Methods: 113 patients (80 adults and 33 children) were studied for HIV-1 isolation in cocultures of infected and non infected lymphocytes. Viral replication was evaluated as rapid (R)/slow (S) or high (H)/low (L). Syncytia formation was estimated in MT2 cell line (SI/NSI). The tropism toward lymphocytes and monocytes (LM) was studied on H9 and U937 cell lines., Results: Up to 86.7% of viral isolates were R, 56.6% were H and 49.6% were SI. These percentages increased with disease progression. Eight viral strains were R/H/NSI cocultivated in MT2 cells and SI in cocultured lymphocytes (NSI/SI), which may be considered as a new phenotype. All the SI isolates and all the R/H (SI and NSI) isolates were LM. Three categories were established: R/H/SI/LM, R/H/NSI/LM and S/L/NSI/NLM. The first two categories corresponded to patients with CD4+ T lymphocytes <200 x 10(6)/I (56%, 50%). The third category corresponded to patients with > 500 x 10(6)/I (53.3%)., Conclusions: Viral replication and SI phenotype, independently, are useful markers for severity of HIV infection. The biological differences among NSI of the 3 viral phenotype categories, including the new subgroup NSI/SI, may indicate the existence of more pathogenic NSI subpopulations.

We have studied sera from 44 children with Human Immunodeficiency Virus infection and Acquired Immunodeficiency Syndrome using immunoblotting, radioimmunoassay, enzymoimmunoassay and indirect immunofluorescence. We have detected a low incidence of antinuclear (2.9%), anti-reticulin (2.9%) and anti-smooth muscle (14.7%) antibodies by indirect immunofluorescence. By enzymoimmunoassay we have detected anti-dsDNA (20.5%) and anti-ENA [anti-nRNP (61.3%), anti-Sm (29.5%), anti-Ro (47.7%) and anti-La (18.1%)] antibodies. Tests for anti-dsDNA by radioimmunoassay were negative, suggesting the presence of low-avidity anti-DNA antibodies. By immunoblotting we have detected anti-C (nRNP) (33.3%), anti-BB' (Sm) (33.3%), anti-Ro (60 KD) (4.5%) and anti-La (11.3%) antibodies. The presence of anti-Ro antibodies was associated with progressive neurological disease. Long-term follow-up studies with larger numbers of patients are necessary to evaluate the clinical significance of the presence of anti-dsDNA and anti-ENA antibodies in children infected with Human Immunodeficiency Virus.

Abstract Background Variation of percentageCD4+ T cells may accurately reflects the kinetics of a comprehensive immune recovery independently of the antiretroviral (ART) regimen. To test this we have investigated the relationship among peripheral blood T-cell subsets with the variation of percentageCD4+ T cells during follow up in 49 HIV-infected children. Methods Children were divided into two groups according to the sign of slope percentageCD4+ T cell during follow up: Ps-group (positive slope) and Ns-group (negative percentageCD4 slope) indicative of immunological recovery or not, respectively. CD4+ and CD8+ T-cell subset percentages were examined by three-colour flow cytometry. Results We found higher memory CD4+ and CD8+ T-cell percentages in the Ns-group than in the Ps-group, and inversely, higher naive CD4+ and CD8+ T cells in the Ps-group than in the Ns-group. CD4+ and CD8+ subsets in the Ps-group expressed higher levels of CD38+ and lower levels of HLA-DR+ compared with the Ns-group. We found a very strong positive correlation among the slope of percentageCD4+, CD4+ CD38+, whereas a negative correlation among the slope of percentageCD4+, the CD8+ CD28+ CD57+ and CD8+ CD57+ T-cell subsets. Conclusion Recovery of the CD4+ T-cell percentage induced by ART reflects a reduction in the chronic immune activation and a measurable reconstitution of the immune system and depends on naive CD4+ T cells. [ABSTRACT FROM AUTHOR]