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At least 631 records · Page 35Linked to original sources

PubMed2004

Epstein-Barr virus (EBV) reactivation in allogeneic stem-cell transplantation: relationship between viral load, EBV-specific T-cell reconstitution and rituximab therapy.

BACKGROUND: Monitoring of Epstein-Barr virus (EBV) reactivation after allogeneic hematopoietic stem-cell transplantation markedly improved with quantitative real-time polymerase chain reaction amplification of EBV DNA and visualization of EBV-specific CD8+ T cells with peptide-human leukocyte antigen (HLA) class I tetramers. We decided to combine these methods to evaluate posttransplant EBV reactivation and rituximab therapy. METHODS: We followed 56 patients treated with an HLA-genoidentical sibling (n=32), an HLA-matched unrelated donor (MUD, n=19), or an unrelated cord-blood transplant (n=5). EBV DNA was quantified in plasma and in peripheral blood mononuclear cells (PBMC). Patient CD8+ T cells were stained with a panel of eight tetramers. RESULTS: EBV DNA was detected in half of the patients, mainly in the MUD group (17/19). In 19 patients, viral DNA was detected only in the cellular compartment. All patients who controlled reactivation without rituximab and despite a viral load of greater than 500 genome equivalents (gEq)/150,000 PBMC mounted an EBV-specific CD8+ T-cell response in greater than 1.4% of CD3+CD8+ T cells. Plasmatic EBV genome was found in nine patients preceded by a high cellular viral load. Three of these patients controlled the reactivation before or without the introduction of rituximab, and they all developed a significant and increasing EBV-specific T-cell response. Patients with EBV-specific T cells at the onset of reactivation controlled viral reactivation without rituximab. CONCLUSION: This study emphasizes the benefit of an early and close monitoring of EBV reactivation and CD8+-specific immune responses to initiate rituximab only when necessary and before the immune response becomes overwhelmed by the viral burden.

Adolescent↗

PubMed2002

Mother-to-infant transmission of hepatitis C virus: rate of infection and assessment of viral load and IgM anti-HCV as risk factors.

One hundred twenty-six mother-infant couples were studied and 105 exposed babies were monitored for at least 12 months to define the risk of mother-to-infant HCV transmission. Infection occurred in 5 out of 76 infants (6.6%) born to 69 viraemic mothers and in none of 29 born to 26 non-viraemic mothers. Only one child was HCV RNA positive one month after birth, while the remaining children became positive at the 3rd to 4th month. HCV genotypes of the babies matched those of their mothers. No difference was found between women who transmitted the virus and those who did not with regard to age, history of drug abuse, HIV infection, ALT abnormal values, HCV genotype, type of delivery, and breast-feeding. Four out of 5 infected infants were born to mothers with IgM anti-HCV (P = 0.04). The mean viral titre in transmitting women (10(7.2)) was higher than in non-transmitting (10(6.5)), and the proportion of mothers with viral load > or = 10(7) was statistically higher in transmitting than non-transmitting women (P = 0.03). These data show that HCV perinatal infection is a rare event and suggest that IgM positivity and high viral load (> or = 10(7)) in the mother are independent variables correlated with HCV transmission (O.R. = 14.5; 95% CI: 1.3-160.7 and O.R. = 16.3; 95% CI: 1.5-179.9, respectively).

Adult↗

PubMed1998

Comparison of 3 quantitative HCV RNA assays--accuracy of baseline viral load to predict treatment outcome in chronic hepatitis C.

The correlation between 3 assays for hepatitis C virus (HCV) RNA quantification and their respective accuracy in predicting the response to interferon and interferon/ribavirin therapy was evaluated by analysing pre-treatment sera from 100 patients. A total of 97%, 100%, and 98% of the patients tested positive by the branched DNA 2.0 assay (Quantiplex), a multi-cycle reversed transcriptase polymerase chain reaction quantitative assay (Superquant) and the Roche Amplicor Monitor assay, respectively. The correlations between the assays, in all patients and in the major genotypes 1, 2, and 3, were significant, although the levels detected by the Amplicor Monitor assay were more than 1 log lower than by the other assays. Sustained virological responders to interferon therapy, but not to combination therapy, had lower baseline viral levels than long-term non-responders (p = 0.002 by Quantiplex 2.0; p = 0.008 by Superquant; p = 0.06 by Roche Amplicor Monitor). Pre-treatment viral load greater than 3 x 10(6) Eq or copies/ml by the Quantiplex 2.0 and Superquant assays and greater than 100,000 copies/ml by the Amplicor Monitor assay predicted long-term non-response in 94%, 93% and 91% of the interferon treated patients, respectively. In conclusion, acceptable correlations between available commercial quantitative assays were found. High baseline viral load predicted long-term non-response to interferon monotherapy, whereas it did not to interferon/ribavirin combination therapy.

Antiviral Agents↗

PubMed2006

Antiviral treatment withdrawal in viremic HCV-positive liver transplant patients: impact on viral loads, allograft function and morphology.

BACKGROUND: The aim of this study was to evaluate the clinical long-term consequences of antiviral treatment discontinuation in viremic hepatitis C virus (HCV)-positive liver transplant recipients. METHODS: Twenty-five HCV-positive patients after liver transplantation were included in this study. After diagnosing recurrent hepatitis C, a combination therapy with interferon-alpha2b and ribavirin for a minimum of 12 months was initiated. Viremia levels and allograft function were monitored continuously. Allograft biopsies were performed yearly, analyzing grading of inflammation and staging of fibrosis. RESULTS: HCV recurrence rate was 100%. Up to 114 months post-transplantation, sustained virological response rate was 64%. Treatment discontinuation in virological nonresponders led subsequently to a significant increase of viral loads and deterioration of allograft function (P<0.05) within 1 month. In three patients, a fibrosing cholestatic syndrome developed, resulting in one patient death. Antiviral retherapy was maintained for a mean of 33 months, leading to a significant decline of aminotransferases (P<0.05) as well as decreasing serum levels of bilirubin and HCV-RNA within 6 months. In addition, development of severe allograft fibrosis was prevented despite persistent viral loads. CONCLUSION: Our study suggests that antiviral treatment withdrawal carries the risk of severe disease progression in persistently viremic HCV-positive liver transplant patients.

Adult↗

PubMedDate not supplied

Branched DNA for quantification of viral load.

This is a summary of a presentation made at the 13th International Convocation on Immunology. Nucleic acids in patient samples can be quantified directly using a solid phase nucleic acid hybridization assay based on branched DNA (bDNA) signal amplification technology. For example, HIV RNA is detected in a plasma sample by hybridization of multiple specific synthetic oligonucleotides to the target, 10 of which capture the target onto the surface of a microwell plate and 39 of which mediate hybridization of branched DNA molecules to the pol region of each HIV RNA molecule. Alkaline phosphatase-labeled probes bind to each arm of the branched DNA molecules. Detection is achieved by incubating the complex with a chemiluminescent substrate and measuring the light emission. The signal is directly proportional to the level of target nucleic acid, and the quantity of HIV RNA in a sample is determined by comparison with a 4-point standard curve. In order to ensure that different subtypes of HIV-1 were detected and quantified equally, in vitro RNA transcripts of the pol region of HIV subtypes A-F were purified and quantified by OD 260, phosphate analysis, and hyperchromicity. These characterized transcripts were then quantified using the bDNA assay. Comparisons were made using a ratio of signal per attomole for each transcript. Genetic subtypes A-F quantified within a factor of 1.5, indicating that the bDNA assay can be used to measure viral load in clinical samples regardless of genotype. Accuracy is important because several studies indicate that there may be a threshold level of virus which predicts progression of HIV disease. Detection of change in viral load is important in determining the efficacy of therapy. The bDNA assay for HCV RNA can be used to determine level of virus in HCV-infected individuals and assist in establishing prognosis prior to initiation of alpha-interferon therapy. Patients with lower levels of virus are more likely to have a sustained response to therapy. Patients who respond to treatment typically have a rapid decline in virus load within one to four weeks of the start of therapy. Many patients relapse when therapy is discontinued as evidenced by a rise in virus load to near pre-treatment levels. Sustained response is most often seen with patients who have lower pre-treatment levels of RNA.

DNA, Viral↗

PubMed2006

Comparative evaluation of the performance of the Abbott real-time human immunodeficiency virus type 1 (HIV-1) assay for measurement of HIV-1 plasma viral load following automated specimen preparation.

The performance of the new Abbott real-time human immunodeficiency virus type 1 (HIV-1) assay for HIV-1 RNA load determination in plasma was compared to that of the Abbott LCx HIV-1 RNA quantitative assay following automated RNA isolation by the Abbott m1000 extractor. The measured viral loads of 89 clinical specimens differed by mean 0.19 log10 copies/ml (95% confidence interval, 0.12 to 0.26 log10 copies/ml). Although the difference in viral load determinations was positively skewed in favor of the LCx assay, it did not reach statistical significance (P = 0.42). Results were linearly associated (R2 = 0.94) and strongly correlated (R = 0.96). Good performance was observed with HIV-1 subtypes other than B and circulating recombinant forms, although results obtained with two subtype G specimens and one H specimen showed a more substantial difference.

Automation↗

PubMed2004

Limited long-term naive CD4+ T cell reconstitution in patients experiencing viral load rebounds during HAART.

Long-term (3.5 years) immune reconstitution in relation to viral load response was determined. Plasma HIV-1 RNA was suppressed in 40 patients (full responders) up to 42 months, and 17 patients achieved partial response. The measurements of CD4(+) and CD8(+) T lymphocyte subsets (CD45RA, CD45RACD62L, CD45RO, CD28, CD38) were carried out by flow cytometry. Full responders had a significant increase of CD4(+) and all CD4(+) T subsets both up to 6 and from 6 to 42 months, while the increase for partial responders was only up to 6 months. By 6 months, higher slopes were observed in full versus partial responders in the % of CD28 on CD4(+) and the % of CD4(+) memory subset and in both naïve and memory CD4(+) subsets from 6 to 42 months. The percentage of CD8(+) and its subsets was decreased significantly in full responders both up to 6 and from 6 to 42 months (except for an increase in the CD8(+)CD45RA(+) CD62L(+) cells), while in partial responders this decrease was only up to 6 months. Lower slopes were observed in full versus partial responders from 6 to 42 months in the percentages of CD8(+), CD8(+)CD45RO(+), CD8(+)CD28(-), and CD8(+)CD38(+) T cells. In conclusion, full responders have a stronger long-term naive CD4(+) T cell subset reconstitution than partial responders.

ADP-ribosyl Cyclase↗

PubMedDate not supplied

Different outcomes in patients achieving complete or partial viral load suppression on antiretroviral therapy.

BACKGROUND: Potent combination antiretroviral therapy can reduce HIV plasma viral load (VL) to levels below the detection limit for as long as 2 years or more. A VL <500 HIV RNA copies/mL was until recently considered a reasonable therapeutic goal. However, lower levels seem necessary if VL rebounds and development of drug resistance are to be avoided. PATIENTS AND METHODS: The clinical and virologic outcome at 1 year were prospectively examined in a group of 100 patients who began a triple combination antiretroviral therapy regimen consisting of stavudine (d4T), lamivudine (3TC), and indinavir (IDV). A modified ultrasensitive VL test with a detection limit of 40 copies/mL and a point mutation nested polymerase chain reaction (PCR) assay for detecting the codon 184 mutation conferring 3TC resistance were used for testing samples collected longitudinally from these individuals. RESULTS: Overall, VL values <40 copies/mL were reached in 45% and 32% of patients at nadir and at 12 months, respectively. More than half (24 of 45 persons) who achieved a level <40 copies/mL at nadir remained with undetectable VL at 1 year, whereas this occurred in only one fourth (7 of 28 persons) of those having levels of 40 to 500 copies/mL (P < .05). However, rebounds in VL to >500 copies/mL at 1 year were seen at similar rates (26.6% and 25%, respectively) in persons achieving either complete (<40 copies/mL) or partial (40-500 copies/mL) VL suppression at nadir. In contrast, the codon 184 mutation emerged more frequently at 1 year in patients whose VL remained between 40 and 500 copies/mL at nadir than in those who reached a level <40 copies/mL (30.7% versus 0%; P < .05). CONCLUSION: Plasma VL at nadir after beginning highly active antiretroviral therapy (HAART) predicts the 1-year outcome. The achievement of levels of viremia <40 copies/mL are desirable during antiretroviral therapy if prolonged benefit is to be obtained. Because more than two thirds of persons with residual viremia do not show drug resistance, intensification strategies should be investigated for those patients with a good virologic response but without complete suppression during the first 6 months on HAART.

Adult↗

PubMed2000

Neuroelectric assessment of HIV: EEG, ERP, and viral load.

The effects of the human immunodeficiency virus (HIV) infection on the central nervous system function were studied with electroencephalographic (EEG) and auditory event-related brain potentials (EPRs) in patients infected with HIV and unaffected young adult control subjects (n=10/group). All subjects were assessed once every 15 min for four trial blocks at the same time of day to assess EEG/ERP changes with time on task-induced fatigue. Spectral analysis was applied to the pre- and post-stimulus EEG segments. ERP values were evaluated with respect to group differences for component amplitude and latency measures. Spectral analysis demonstrated that HIV patients evinced greater pre-stimulus delta power over frontal areas compared to control subjects, and less post-stimulus spectral power for the delta, theta, and alpha bands over the central/parietal areas. P300 amplitude was smaller, and latency was marginally longer for the HIV patients compared to control subjects. P300 latency correlated positively with increases in the patient HIV viral load. Time-on-task generally did not affect EEG or ERP measures for either group other than contributing to an overall decrease in neuroelectric responsivity. Group spectral power effects were consistent with differences in arousal/fatigue level. P300 group differences were consistent with declines in cognitive capability, and P300 latency increased with increased viral load. HIV infection negatively affected central nervous system function as measured by EEG and cognitive ERPs in a manner that suggests decreased arousal and increased fatigue in HIV patients.

AIDS Dementia Complex↗

PubMed2005

Failure time analysis of HIV vaccine effects on viral load and antiretroviral therapy initiation.

The world's first efficacy trial of a preventive HIV vaccine was completed in 2003. Study participants who became HIV infected were followed for 2 years and monitored for HIV viral load and initiation of antiretroviral therapy (ART). In order to determine if vaccination may have altered HIV progression in persons who acquired HIV, a pre-specified objective was to compare the time until a composite endpoint between the vaccine and placebo arms, where the composite endpoint is the first event of ART initiation or viral failure (HIV viral load exceeds a threshold x(vl) copies/ml). Specifically, with vaccine efficacy, VE(tau, x(vl)), defined as one minus the ratio (vaccine/placebo) of the cumulative probability of the composite endpoint (with failure threshold x(vl)) occurring by tau months, the aim was to estimate the four parameters {VE(tau, x(vl)): x(vl) is an element of {1500, 10,000, 20,000, 55,000} copies/ml} with simultaneous 95% confidence bands. A Gaussian multipliers simulation method is devised for constructing confidence bands for VE(tau, x(vl)) with x(vl) spanning multiple discrete values or a continuous range. The new method is evaluated in simulations and is applied to the vaccine trial data set.

AIDS Vaccines↗

PubMed2006

Does HAART improve renal function? An association between serum cystatin C concentration, HIV viral load and HAART duration.

AIM: The prevalence of renal disease in human HIV-infected individuals varies between 2% and 10%. Many reports have demonstrated the beneficial effect of antiretroviral (ARV) therapy on slowing the progression of renal diseases. The aim of our cross-sectional study was to determine serum cystatin C concentration in different stages of HIV infection and the relationship between cystatin C concentration and ARV treatment. METHODS: Cystatin C concentration was measured in the sera of 77 HIV-1-infected individuals and 18 HIV-seronegative volunteers. The glomerular filtration rate (GFR) was estimated using the Modification of Diet in Renal Disease Study formula. RESULTS: HIV infection resulted in a significant increase in serum cystatin C concentration compared with healthy individuals (933.4 +/- 32.1 vs 621.1 +/- 56.8 ng/ml, P < 0.001). There were no significant differences in urea, creatinine and GFR between those groups. On multivariate analyses serum cystatin C was independently associated with highly active antiretroviral therapy (HAART) duration (beta = -0.34, P = 0.04) and HIV viral load (beta = 0.33, P = 0.04), whereas there were no significant relationships with age, body mass index, HIV duration, CD4+ and CD8+ T-cell counts and serum high sensitivity C-reactive protein concentration. CONCLUSIONS: Our initial observations indicate that serum cystatin C, which may reflect mild renal dysfunction, is increased during HIV-infection and is associated with HIV viral load. Long-lasting HAART seems to decrease cystatin C concentration, thus potentially improves renal function.

Adult↗

PubMed2002

Entrapment of recent thymic emigrants in lymphoid tissues from HIV-infected patients: association with HIV cellular viral load.

OBJECTIVE(S): Depletion of thymus derived naive T-cells is a feature of HIV infection. Here the impact of HIV infection on the compartmentalization of recent thymic emigrants of (RTE) and naive T-cells was examined. METHODS: Peripheral blood mononuclear cells (PBMC) and lymphoid tissue (LT) from 43 HIV-infected patients and 12 controls were examined for RTE distribution by measuring coding joint T-cell receptor excisional circles (cjTREC) by PCR and naive and memory T-cell subsets and adhesion molecules (L-selection, LFA-1) by flow cytometry. RESULTS: In HIV-infected patients, the RTE as quantified by cjTRECs in CD4 LT cells were significantly higher than in PBMC. Their values, however, were less than in control subjects, in both the LT and PBMC compartments. This was associated with an increase in L-selectin and LFA-1 expression on LT derived T cells. In PBMC, a significant positive relationship between TREC and naive CD4 cells and an inverse relationship between TREC and cellular viral load (CVL) was observed. Whereas in LT, there was a positive relationship between cjTREC and both naive CD4 cell percentage and CVL. CONCLUSIONS: Collectively, the data suggests that LT is a significant reservoir for RTE. The RTE appeared to be entrapped in LT from HIV-infected subjects. Such entrapment is probably a response to the high viral load in these tissues. These observations may partially explain the decline in RTE observed in the peripheral blood of HIV-infected patients, and the delay in recovery of naive cells in blood after initiation of HAART.

Adult↗

PubMed1997

Genotype, viral load and age as independent predictors of treatment outcome of interferon-alpha 2a treatment in patients with chronic hepatitis C. Construct group.

Patients with chronic hepatitis C respond differently when treated with interferon. We randomized 116 patients with chronic hepatitis C in order to compare two dosage regimens of recombinant interferon alpha 2a:3 MIU x 3 per week for 6 months (arm A) or 6 MIU x 3 per week for 3 months and then 3 MIU x 3 per week for 3 months (arm B). There were no significant differences concerning outcome between the two dose regimens: sustained clearance of HCV viremia 6 months after the end of treatment was obtained in 12/59 (20%) in group A compared with 18/57 (32%) in group B (p = 0.24). In patients with genotype 1a, 4/31 (13%), in genotype 1b, none of 9 (0%), 9/15 (60%) in genotype 2, and 17/58 (29%) in genotype 3, showed sustained clearance of HCV viremia 6 months after the end of treatment (p = 0.002). In a stepwise logistic regression analysis, only pretreatment viral load (p = 0.0001), genotype (p = 0.001) and age (p = 0.04) were identified as independent predictors of sustained clearance of HCV viremia. Liver histology as assessed by Knodell index was significantly improved in patients with sustained HCV RNA response 6 months after the end of treatment (5.2 +/- 2.2 vs 2.6 +/- 2.2, p < 0.001), but not in responders with relapse or in non-responders. In conclusion, stepwise logistic regression analysis showed that viral load, HCV genotype and age were the only independent predictors for sustained HCV RNA response.

Age Factors↗

PubMed1995

Viral load in peripheral blood mononuclear cells as surrogate for clinical progression.

During the symposium on surrogate markers of HIV, the Scientific Advisory Committee posed the following question: "Which surrogate markers currently deserve the greatest commitment of investigative resources to validate them in a clinical setting?" The Committee concluded that for antiretroviral drugs measurements of HIV RNA in plasma deserve the greatest priority, and for immune-based therapies assessing viral load still had the highest priority. But it was recognized that assessing viral load should not be restricted to plasma RNA because the primary mechanisms of action are different from antiretroviral drugs. Thus, the Committee voted that based on current knowledge, investigating the clinical relevance of changes in HIV-1 DNA and RNA copy number in peripheral blood mononuclear cells (PBMCs) with validated assays should be given equal focus for immune-based therapies. This article reviews the rationale for using HIV-1 DNA and RNA load in PBMCs for the monitoring of clinical trials and presents recent data that indicate that the postseroconversion level and the dissemination of proviral DNA in the blood cells have prognostic value, i.e., high levels correlate with disease progression. In addition, longitudinal studies show that an increase in proviral DNA and/or HIV mRNA load correlates with disease progression. We present evidence that these markers are relevant activity markers for anti-HIV therapies. Changes in both DNA and RNA load can be achieved using either antiretroviral drugs or immune-based therapies. These results suggest that these markers should be evaluated in clinical studies to firmly establish their value as surrogates of clinical progression.

Biomarkers↗

PubMed2006

Correlation between gag-specific CD8 T-cell responses, viral load, and CD4 count in HIV-1 infection is dependent on disease status.

BACKGROUND: It still remains controversial which kind of relationships exist between HIV-1-specific CD8 T-cell responses and HIV RNA load or CD4 count over the course of the infection. This study was designed to investigate the role of HIV-specific CD8 responses in patients with different disease status. METHODS: Three cohorts of patients were selected according to CD4 count levels: long-term nonprogressors (LTNPs, n = 19), asymptomatic progressors (CD4 counts between 500 and 350 cells/mm(3), n = 14), and progressors (CD4 counts <350 cells/mm(3), n = 23). Six of the LTNPs experiencing a quick loss of CD4 T-cells and another 6 LTNPs with stable CD4 counts were followed up. T-cell responses were studied using interferon (IFN) gamma-ELISpot assay against HIV p24 and 11 pools of HIV-Gag peptides. RESULTS: No significant differences were found in Gag-specific CD8 responses among the 3 cohorts. However, inverse correlations were identified between CD8 responses and CD4 counts in asymptomatic progressors and between CD4 responses and viral loads in progressors. In addition, the sequential dynamics of CD8 responses in 6 LTNPs showed that with a quick loss of CD4 T-cells around the range of 500 to 300 cells/mm(3), more vigorous CD8 responses were induced simultaneously, and plasma viremia was still kept relatively stable. CONCLUSIONS: These data suggest that the relationship between CD8 response and viral load or CD4 count is not universally consistent throughout the entire course of HIV-1 infection. Gag-specific CD8 responses may play differential roles in different stages of HIV-1 infection, and the maintenance of a threshold level of CD4 T-cells may contribute to mediate effective HIV-specific responses in natural control of HIV-1 infection.

Adult↗

PubMed2002

Chronic hepatitis C infection: influence of the viral load, genotypes, and GBV-C/HGV coinfection on the severity of the disease in a Brazilian population.

The distributions of the different genotypes of the hepatitis C virus (HCV) and GBV-C virus (GBV-C/HGV) vary geographically and information worldwide is still incomplete. In particular, there are few data on the distribution of genotypes (and their relationship to the severity of liver disease) in South America. Findings are described in 114 consecutive patients from Northeast Brazil (median age 52 years, range 18-72 years) who had abnormal levels of serum aminotransferases and seropositivity for HCV RNA. The patients were recruited from an outpatient clinic between November 1997 and April 1998. Quantitative HCV RNA and GBV-C/HGV RNA estimations were carried out by double-nested polymerase chain reaction (PCR) using primers from the 5'-untranslated regions (UTRs) of the genomes. HCV genotypes were determined by restriction fragment length polymorphism (RFLP) analysis with 5'-UTR primers and by PCR with type-specific 5'-UTR primers. GBV-C/HGV-RNA genotypes were determined by RFLP with specific 5'-UTR primers and phylogenetic trees were constructed using the Neighbour-Joining and Drawtree programs. Histological features were graded and staged according to international criteria. Of the 114 patients, 35 (30.7%) patients had cirrhosis and 22 (27.8%) had mild, 51 (64.6%) had moderate, and 6 (7.6%) had severe chronic hepatitis. Median HCV viral load was 10(6) genome equivalents per millilitre (range 10(4)-10(9)/ml). Frequencies of genotypes were 5.3% type 1a, 44.7% type 1b, 3.5% type 2, 41.2% type 3, and 5.3% mixed types. GBV-C/HGV-RNA was detected in the sera of 12 (10.5%) patients and was distributed among three phylogenetic groups. There were no significant differences between patients with the predominant HCV genotypes (1b and 3) with respect to gender, age group, viral load, severity of liver disease, or coinfection with GBV-C/HGV.

Adolescent↗

PubMed1998

HIV-1 viral load and CD4 cell count in untreated children with vertically acquired asymptomatic or mild disease. Paediatric European Network for Treatment of AIDS (PENTA).

BACKGROUND: Plasma HIV-1 RNA levels are high in vertically infected infants. Information in older children is limited, particularly in those who have not received antiretroviral therapy. OBJECTIVES: To describe the relationships between HIV-1 RNA, age and CD4 cell count in untreated vertically infected children. DESIGN: HIV-1 RNA was measured in 70 children [median age, 3.5 years (range, 0.4-11.9 years); median CD4 cell count, 881 x 10(6)/l (interquartile range, 576-1347 x 10(6) cells/l)] enrolled in a randomized placebo-controlled trial comparing immediate with deferred zidovudine in asymptomatic or mildly symptomatic vertically infected children (PENTA-1 trial). Short-term variability was assessed by comparing HIV-1 RNA at -2 and 0 weeks (prior to randomization). The relationship between age and HIV-1 RNA, and CD4 cell count was analysed using data from all children prior to randomization and sequential samples from 35 remaining on placebo for up to 105 weeks, by fitting mixed linear models. RESULTS: The within-individual SD in viral load was 0.26 log10 copies/ml. The median plasma HIV-1 RNA at enrollment was 4.61 log10 (range, 2.3-6.56 log10 copies/ml), significantly higher in children aged < or = 2 years (median, 5.23 log10 copies/ml) than in those aged > 2 years (4.51 log10 copies/ml; P < 0.0001). Mean HIV-1 RNA fell by 0.38 log10 copies/ml per year up to 2 years of age, by 0.21 log10 copies/ml per year from 2 to 4 years of age, and by 0.03 log10 copies/ml per year from 4 to 6 years of age reaching a nadir of 4.25 log10 copies/ml at 6 years. Mean log10 CD4 cell count declined steadily with age and was not significantly correlated with HIV-1 RNA, although there was some evidence that the rate of log10 CD4 cell decline was negatively correlated with the initial rate of HIV-1 RNA decline. No mutations associated with resistance to zidovudine were observed. CONCLUSIONS: Age is a key factor in the interpretation of both viral load and CD4 cell count in vertically infected children.

Aging↗

PubMed2004

[Variability of HIV-1 viral load in patients cared along 4 years].

BASIS: Analysis of the variations of HIV-1 viral load (VL) in a cohort of patients. MATERIAL AND METHODS: A retrospective study was designed for the calculation and analysis of the differences between two consecutive measurements of VL in a cohort of 1,336 patients along a 48 months follow-up. RESULTS: At the beginning of the follow-up period the highest proportion of patients with decreases of VL (54.2% in their first measurement, at 0-75 days) as well as the least proportion of patients both without changes (30.7%) and with increases of their VL (15.1%), were registered. The proportion of patients with decreases was declining along the study period. More than half of the patients did not experience significant variations in the measurements carried out. CONCLUSIONS: The significant decreases of VL appeared in our series at the beginning of the follow-up period, and a growing proportion of individuals showed elevations of the VL along the period studied.

Adolescent↗