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RNA Viral Load (rna + viral_load)
Kinds of RNA Viral Load Selected AbstractsClose association of CD8+/CD38bright with HIV-1 replication and complex relationship with CD4+ T-cell count,CYTOMETRY, Issue 4 2009Edouard Tuaillon Abstract Background: Measuring lymphocyte activation provides information in addition to CD4+ T-cell count for immune monitoring of HIV-1 infected patients. CD38 is a well-established activation marker that is generally analyzed on the whole population of CD8+ T-cells. Focusing specifically on CD38 high expression (CD8+/CD38bright) may be an interesting surrogate gating strategy because CD38bright characterizes principally activated memory cells. Methods: CD8+/CD38bright was investigated in 1,353 HIV-1 infected patients over a one-year period to establish relevant cutoff values and clarify the relationships of this marker with HIV-1 RNA viral load (VL) and CD4+ T-cell count. Results: The CD8+/CD38bright (>8,500 CD38 binding site per cells) is well correlated with HIV-1 VL (r = 0.87, P < 0.001) in this longitudinal follow-up of nonimmunodepressed patients that initiated antiviral therapy (ART). In aviremic patients on ART, the marker was highly predictive of VL rebound (sensitivity 93%, specificity 64% for a VL level of detection >200 copies/ml). While the CD8+/CD38bright moderately correlated with CD4+ T-cell count independently of the VL (r = ,0.37, P < 0.001), it increased dramatically in aviremic patient groups that exhibited profound CD4+ T-cell depletion (median 39% for CD4+ T-cell counts <50/mm3). This result indicates that other additional immunological and/or viral factors than readily detectable HIV-1 replication appears to be involved in T-cell activation of immunodepressed individuals. Conclusions: CD8+/CD38bright is an effective marker for monitoring T-cell activation, which is a central factor of HIV-1 pathogenesis. This gating strategy requires only a single additional staining in conventional four color CD4 protocols. © 2008 Clinical Cytometry Society [source] Effect of simplification from protease inhibitors to boosted atazanavir-based regimens in real-life conditionsHIV MEDICINE, Issue 9 2010R Rubio Background Atazanavir (ATV) boosted with ritonavir (ATV/r) is a potent, well-tolerated, once-daily protease inhibitor (PI). Few data are available on this agent as a treatment simplification option for patients taking other PIs. Objective The aim of the study was to determine the effectiveness and safety of ATV-containing regimens in patients who have simplified their antiretroviral treatment. Methods SIMPATAZ was a multicentre, prospective, noninterventional study in patients who had undetectable HIV RNA on their current PI-containing therapy and who were switched to an ATV/r-based regimen. Patients underwent a routine physical examination, and data were collected on HIV RNA levels, CD4 cell counts, liver function, lipid parameters, adverse reactions, adherence to treatment and patient satisfaction. Results A total of 183 patients were enrolled in the study and included in the analysis (80% were male, 29% had AIDS, and 52% were coinfected with HIV and hepatitis B virus or hepatitis C virus). The median baseline CD4 count was 514 cells/,L. Median exposure to previous HIV therapy was 8 years, and 32% of patients had a history of PI failures. Lopinavir boosted with ritonavir was the most frequent PI replaced (62%) and tenofovir+lamivudine /emtricitabine the backbone most used during the study (29%). The study drug was discontinued early by 25 patients (14%), two of whom discontinued as a result of adverse events (Hodgkin lymphoma and vomiting). Two patients died (lung cancer and myocardial infarction). At month 12, 93% of the study population had an undetectable HIV RNA viral load. Hyperbilirubinaemia >3 mg/dL and increased alanine aminotransferase levels>200 IU/L were observed in 38.5% and 4.4% of patients, respectively. Median changes from baseline to month 12 in total cholesterol, triglycerides and low-density lipoprotein cholesterol were ,13 mg/dL (,7%; P<0.0001), ,19 mg/dL (,13%; P<0.0001) and ,7 mg/dL (,6%; P=0.021), respectively. Conclusions In a real-world setting, switching from other PIs to ATV/r is a well-tolerated and safe option for improving the lipid profile and for retaining virological response in controlled pretreated patients. [source] Evaluation of the use of dried spots and of different storage conditions of plasma for HIV-1 RNA quantificationHIV MEDICINE, Issue 6 2007B Amellal Objectives The aim of the study was to evaluate the use of dried plasma spots to determine HIV-1 RNA viral loads. Methods The viral loads of 30 liquid plasma samples were compared with those of corresponding dried plasma spots on filter paper (DPS-FP) and in tubes (DPS-T), both of which were left for 7 days at 22°C. Also, 10 liquid plasma samples with detectable viral load were stored at 4, 22 or 37°C for 7 days and five further liquid plasma samples were air-dried for up to 54 h to assess the effects of temperature and the drying step on HIV-1 viral load. Results The viral loads of the 30 liquid plasma samples correlated significantly with those of the paired dried spots DPS-FP and DPS-T, but with median losses of 0.64 and 0.69 log10 HIV-1 RNA copies/mL, respectively, and a limit of detection of 3 log10 copies/mL. The 10 liquid plasma samples stored for 1 week at 37°C showed a weaker correlation and had a significantly reduced median viral load (,0.92 log10; P=0.005) when compared with the viral load of the matched plasma stored at ,80°C. Most of the loss happened during the drying step. Conclusions Reliable measurement of HIV-1 RNA viral load requires good plasma storage conditions. HIV RNA stability was affected by desiccation and 1 week of storage at 37°C. However, our findings suggest that liquid plasma can be kept at 4 or 22°C for a week with no effect on viral load. [source] Changes in HIV RNA viral load, CD4+ T-cell counts, and levels of immune activation markers associated with anti-tuberculosis therapy and cotrimoxazole prophylaxis among HIV-infected tuberculosis patients in Abidjan, Côte d'IvoireJOURNAL OF MEDICAL VIROLOGY, Issue 2 2005Mireille Kalou We analyzed changes in plasma human immunodeficiency virus (HIV)-1 viral load, CD4+ T-cell count, and markers of immune activation markers at start of treatment of tuberculosis and 12 months after among 44 HIV-1-infected patients with newly diagnosed, sputum-smear positive for Mycobacterium tuberculosis pulmonary in fection. All patients received a standard regimen of 6 months of rifampicin and isoniazid with first 2 months of pyrazinamid with or without cotrimoxazole. Compared with values at start of treatment, median viral load increased by a median of 0.64 log10 copies/ml after 12 months of follow-up (P,=,0.0002). Median CD4+ T-cell counts were 393 cells/L at start of treatment and 370 cells/L after 12 months of follow-up (P,=,0.61). Levels of serum activation markers decreased significantly at 12 months of follow-up of the patients for both patients on standard and cotrimoxazole treatment. Levels of viral load, CD4+ T-cell counts, and markers of immune activation were not different for patients on standard treatment of tuberculosis compared with those on standard and cotrimoxazole treatment. Levels of serum activation markers decreased significantly at 12 months of follow-up of the patients for both patients on standard and cotrimoxazole treatment. Because viral load is a predictor of disease progression, its persistent elevated levels in blood of HIV-infected patients co-infected with tuberculosis, who successfully complete TB treatment, may account for the high mortality observed in this population. J. Med. Virol. 75:202,208, 2005. © 2004 Wiley-Liss, Inc. [source] Lack of effect of chemokine receptor CCR2b gene polymorphism (64I) on HIV-1 plasma RNA viral load and immune activation among HIV-1 seropositive female workers in Abidjan, Côte d'IvoireJOURNAL OF MEDICAL VIROLOGY, Issue 4 2001Christiane A. Adjé Abstract The prevalence of the CCR2b,V64I mutation among human immunodeficiency virus (HIV)-seropositive and -seronegative female workers and the potential effect of heterozygosity of this mutation on HIV-1 plasma RNA viral load and markers of immune activation were assessed. CCR2b,V64I was detected by polymerase chain reaction, followed by restriction enzymes analysis; plasma viral load was measured by the Amplicor HIV-1 monitor assay and CD4+ T-cell counts and markers of immune activation by standard three-color FACscan flow cytometry. Of the 260 female workers, 56 (21.5%) were heterozygous for CCR2b,V64I, and 8 (3%) were homozygous. Of the 99 HIV-seronegative female workers, 19 (19.2%) were heterozygous for the CCR2b,V64I mutation compared with 37 (23%) of the 161 HIV-seropositive FSW (P,=,0.47). In a univariate analysis of viral load among HIV-seropositive FSW, no difference was noted between those heterozygous for or without the mutation; both groups had plasma viral loads of 5.0 log10 copies/ml. After controlling for the effects of CD4+ T-cell counts in a multivariate analysis, no significant difference was observed between the groups in viral load or in markers of immune activation. The data suggest that the presence of the CCR2b mutation has no effect on HIV-1 plasma viral load and markers of immune activation in our study population. The finding that the frequency of this mutation is similar in HIV-seropositive and -seronegative female workers suggests that its presence is not associated with increased risk of HIV infection. J. Med. Virol. 64:398,401, 2001. © 2001 Wiley-Liss, Inc. [source] How to use virological tools for optimal management of chronic hepatitis CLIVER INTERNATIONAL, Issue 2009Stéphane Chevaliez Abstract Chronic hepatitis C is a global health problem that may cause cirrhosis and progression to hepatocellular carcinoma. Currently available antiviral treatments are moderately effective. Several virological assays are available to help diagnose and manage patients infected with the hepatitis C virus (HCV). These include the anti-HCV antibody assays, measurement of HCV RNA viral load and HCV genotyping. HCV RNA can be assayed by two types of molecular biology-based techniques: target amplification as in polymerase chain reaction methods and signal amplification such as the branched DNA assay. Monitoring of viral kinetics during the early phases of antiviral treatment is crucial in making treatment decisions such as early stopping rules and also in optimizing the length of treatment. The HCV genotype can be determined by several methods. Whatever the method, pretreatment determination allows treatment length and ribavirin dose to be optimized and also offers prognostic information on treatment outcomes as certain genotypes respond more favourably to treatment. Thus, virological assays are indispensable in the diagnosis and management of individuals infected with the HCV. [source] The model for end-stage liver disease score is the best prognostic factor in human immunodeficiency virus 1,infected patients with end-stage liver disease: A prospective cohort study,,LIVER TRANSPLANTATION, Issue 9 2009Javier Murillas End-stage liver disease (ESLD) has become the main cause of mortality in patients coinfected by human immunodeficiency virus (HIV) and hepatitis B virus or hepatitis C virus in developed countries. The aim of this study was to describe the natural history of and prognostic factors for ESLD, with particular attention paid to features affecting liver transplantation. This was a prospective cohort study in 2 Spanish community-based hospitals performed between 1999 and 2004. One hundred four consecutive patients with cirrhosis and a first clinical decompensation of their chronic liver disease or hepatocellular carcinoma were included in the study. During a median follow-up of 10 months (endpoint: death, liver transplantation, or the last checkup date), 61 patients (59%) died. The probability of mortality (Kaplan-Meier method) at 1, 2, and 3 years was 43% [95% confidence interval (CI), 34%,60%], 59% (95% CI, 48%,70%), and 70% (95% Cl, 59%,81%), respectively. In a multivariate analysis, the Model for End-Stage Liver Disease (MELD) score and the inability to reach an undetectable plasma HIV-1 RNA viral load at any time during follow-up were the only variables independently associated with the risk of death (P < 0.001). Fifteen (14%) of the 104 patients were accepted for liver transplantation, although only 5 underwent the procedure, and 10 died while on the waiting list. The waiting list mortality rate in patients with a MELD score < 20 and in patients with a MELD score >20 was 58% and 100%, respectively (median follow-up, 5 months). In conclusion, HIV-1,infected patients with ESLD, especially those with poorly controlled HIV and a high MELD score, have a poor short-term outcome. The MELD score may be useful in deciding whether to indicate liver transplantation in these patients. However, because only a small proportion of the patients in this study were considered candidates for liver transplantation and most died while on the waiting list, few received a transplant. Liver Transpl 15:1133,1141, 2009. © 2009 AASLD. [source] HIV-1 DNA proviral load in treated and untreated HIV-1 seropositive patientsCLINICAL MICROBIOLOGY AND INFECTION, Issue 6 2010M. C. Re Clin Microbiol Infect 2010; 16: 640,646 Abstract As proviral human immunodeficiency virus type 1 (HIV-1) DNA can replenish and revive viral infection upon activation, its detection might offer significant therapeutic information, complementing the input provided by plasma RNA determination in the follow-up of infected individuals. A selected group of acutely infected subjects was studied to verify both total and 2-long terminal repeat (2-LTR) DNA proviral load during the acute phase of infection and thereafter. Patients were divided in two sex- and age-matched groups: 19 naive individuals who did not receive antiretroviral therapy during the observation period and 20 subjects treated according to current guidelines. Total and 2-LTR HIV-1 DNA proviral load, in addition to RNA viral load and CD4 cell count, were determined in peripheral blood mononuclear cells (PBMC) at baseline, 6 and 12 months after the first sampling. Total and 2-LTR HIV-1 DNA proviral load exhibited no significant variation at any time in the naive patients (total HIV-1 DNA ranging from 896 ± 731 to 715 ± 673 copies/105 PBMC and 2-LTR HIV-1 DNA ranging from 94 ± 105 to 65 ± 44 copies/105 PBMC), whereas a significant reduction in both total HIV-1 DNA (ranging from 997 ± 676 to 262 ± 174 copies/105 PBMC) and 2-LTR HIV-1 DNA proviral load (ranging from 116 ± 55 to 26 ± 35 copies/105 PBMC) was detected in highly active antiretroviral therapy (HAART) patients, together with a CD4+ T cell count increase and RNA load decrease. HAART negatively affects both the labile HIV burden and the integrated proviral DNA, at least in the initial period of successful treatment, suggesting that quantification of HIV-1 DNA proviral load may be an important parameter in monitoring HIV infection. [source] Evaluation of the use of dried spots and of different storage conditions of plasma for HIV-1 RNA quantificationHIV MEDICINE, Issue 6 2007B Amellal Objectives The aim of the study was to evaluate the use of dried plasma spots to determine HIV-1 RNA viral loads. Methods The viral loads of 30 liquid plasma samples were compared with those of corresponding dried plasma spots on filter paper (DPS-FP) and in tubes (DPS-T), both of which were left for 7 days at 22°C. Also, 10 liquid plasma samples with detectable viral load were stored at 4, 22 or 37°C for 7 days and five further liquid plasma samples were air-dried for up to 54 h to assess the effects of temperature and the drying step on HIV-1 viral load. Results The viral loads of the 30 liquid plasma samples correlated significantly with those of the paired dried spots DPS-FP and DPS-T, but with median losses of 0.64 and 0.69 log10 HIV-1 RNA copies/mL, respectively, and a limit of detection of 3 log10 copies/mL. The 10 liquid plasma samples stored for 1 week at 37°C showed a weaker correlation and had a significantly reduced median viral load (,0.92 log10; P=0.005) when compared with the viral load of the matched plasma stored at ,80°C. Most of the loss happened during the drying step. Conclusions Reliable measurement of HIV-1 RNA viral load requires good plasma storage conditions. HIV RNA stability was affected by desiccation and 1 week of storage at 37°C. However, our findings suggest that liquid plasma can be kept at 4 or 22°C for a week with no effect on viral load. [source] | |||||||||||||