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PubMed2004

Kinetics of hepatitis B viral load during 48 weeks of treatment with 600 mg vs 100 mg of lamivudine daily.

Oral therapy for chronic hepatitis B remains suboptimal. Mathematical modelling of viral decay kinetics to rapidly assess potential antiviral regimens has proved valuable for human immunodeficiency virus and cytomegalovirus. We defined the kinetics of viral replication in 10 chronic hepatitis B patients randomized to lamivudine 100 mg vs 600 mg for 48 weeks. Viral decay kinetics conformed to a biphasic pattern in nine of 10 subjects. Persons receiving 600 mg daily of lamivudine exhibited a 1.6-fold faster decay rate in the infected cell compartment (0.028/day vs 0.017/day, P = 0.06) and a greater overall change in serum viral load when compared with those receiving 100 mg (4.06 vs 1.52 log(10) copies/mL, P = 0.08). More potent therapy appeared to result in more rapid decrease in the infected cell population. Studies using mathematical modelling of viral decay may be a useful method to evaluate single or combination therapy for HBV infection in vivo.

Adult↗
PubMed1997

[Viral load--significance for individualized therapy].

The treatment of HIV infection/AIDS has changed dramatically because of a new pathophysiological understanding of this disease. The most important laboratory parameter for the management of antiretroviral therapy is the direct measurement of virus load in plasma. In Germany 11 different medications are available to the patient for reduction of his viral load in blood and possibly tissues, i.e. lymph-nodes. The majority (about 2/3) of physicians begin to treat with double combination therapy. Protease inhibitors are an important addition to the therapeutic arsenal.

Anti-HIV Agents↗
PubMed2002

Characterization of pol, vif, vpr, and vpu genes of HIV type 1 in AIDS patients with high viral load and stable CD4+ T cell counts on combination therapy.

The success of combination therapy has also led to AIDS patients who exhibit elevated viral load without a corresponding decline in CD4+ T cells. In this study, we characterized changes in the pol gene and accessory genes vif, vpr, and vpu of HIV-1 isolated from the plasma of patients receiving highly active antiretroviral therapy. From each patient three sequences were obtained and compared with the sequence of HIV-1 from nontreated patients, revealing many substitutions that were similar in most cases. Protease and reverse transcriptase genes showed many mutations that were due to antiviral drugs. Premature termination was observed in the vif gene of one patient, leading to a protein truncated after 187 amino acids. In another patient the entire vpr open reading frame was missing, with no synthesis of Vpu protein because the 5' end of the gene was missing, including the start codon. In the same patient, the Vif protein was also truncated because of the deletion of 100 nucleotides at the 3' end of the vif gene.

Amino Acid Sequence↗
PubMed2006

Syphilis and human immunodeficiency virus (HIV)-1 coinfection: influence on CD4 T-cell count, HIV-1 viral load, and treatment response.

OBJECTIVES: To assess the effect of human immunodeficiency virus (HIV)-1 and syphilis coinfection on HIV-ribonucleic acid (RNA) viral load, CD4 cell count, and the response in rapid plasmin reagin (RPR) to treatment of the syphilis infection. STUDY DESIGN: Cases of syphilis diagnosed during 1 year in HIV-infected patients in Copenhagen were included. HIV-RNA, CD4 cell counts, and RPR-serology were measured before, during, and after syphilis. RESULTS: Forty-one patients were included. CD4 cell count decreased significantly during infection in patients with primary and secondary stages of syphilis (mean 106 cells/mm, P = 0.03). Treatment of syphilis was associated with an increase in the CD4 cell count and a decrease in HIV-RNA in the overall group (mean 66 cells/mm and -0.261 RNA log10 copies/ml, P = 0.02 and 0.04). The serological response rates for 15 patients treated with penicillin and 25 treated with doxycycline were the same. CONCLUSION: Syphilis was associated with a decrease in CD4 cell counts and an increase in HIV-RNA levels that both improved after treatment of syphilis.

Adult↗
PubMed2003

Evaluation of the clinical sensitivities of three viral load assays with plasma samples from a pediatric population predominantly infected with human immunodeficiency virus type 1 subtype G and BG recombinant forms.

The viral load assays AMPLICOR HIV-1 Monitor Test 1.5, Nuclisens HIV-1 QT, and Quantiplex HIV RNA 3.0 (bDNA) were evaluated for their abilities to quantify human immunodeficiency virus type 1 (HIV-1) RNA in 64 plasma samples from 21 children infected in Portugal. The children were infected with HIV-1 subtypes A1, B, F1, G, and BG recombinant virus. AMPLICOR v1.5 and Quantiplex v3.0 detected all samples, and there was a good correlation of results between the two kits. Thirty-eight specimens containing HIV-1 subtype B, G, or recombinant BG, could not be detected by Nuclisens HIV-1 QT. We also evaluated the new Retina HIV-1 assay on 21 samples that were HIV-1 positive; Retina HIV-1 failed to detect 5 of 11 subtype G specimens. AMPLICOR v1.5 and Quantiplex v3.0 assays may be used for HIV-1 RNA quantification in Portugal, whereas an improvement in sensitivity for subtype G and recombinant BG is required for Nuclisens HIV-1 QT and Retina HIV-1.

Branched DNA Signal Amplification Assay↗
PubMed2006

Distribution of Epstein-Barr viral load in serum of individuals from nasopharyngeal carcinoma high-risk families in Taiwan.

The utility of EBV load as a tumor marker in nasopharyngeal carcinoma (NPC) patients suggests that it might also serve as a screening test for individuals who are at high risk for developing NPC. We previously demonstrated that unaffected individuals from high-risk families had elevated anti-EBV antibody levels compared to community controls. In this study, we measured EBV load using 2 different real-time PCR assays (targeting BamH1W and polymerase gene sequences, respectively) carried out in 2 independent research labs in serum samples from 19 untreated NPC cases, 11 healthy community controls and 100 unaffected individuals from families in which 2 or more individuals were affected with NPC. EBV genomes were detectable in 68% of NPC cases by the EBV BamH1W assay and in 74% by the EBV polymerase assay (kappa = 0.64). Patients with stage III or IV disease had significantly higher EBV load compared to those with stage I or II disease (p = 0.008). EBV DNA was detected in a single community control sample by the EBV BamH1W assay and in none of the samples by the EBV polymerase assay. Only one of 100 unaffected family members tested positive by both assays. An additional 14 were positive by only one of the 2 EBV load assays used and usually in only one of the duplicate wells tested, all with very low viral loads (3-50 copies/ml). In addition, EBV load did not correlate with EBV serology results (anti-VCA, anti-DNase, anti-EBNA-1) among these unaffected family members. In conclusion, our study suggests limited clinical utility of the EBV load test, in its current configuration, to screen individuals from high-risk families. Should a more sensitive or specific molecular assay be developed that is capable of detecting and distinguishing tumor-derived EBV genomes or gene products from true negatives, it could be evaluated as a possible screening tool for asymptomatic and early-stage NPC.

Antibodies, Viral↗
PubMed2002

Consecutive rebounds in plasma viral load are associated with virological failure at 52 weeks among HIV-infected patients.

OBJECTIVES: To describe the characteristics and predictors of transient plasma viral load (pVL) rebounds among patients on stable antiretroviral therapy and to determine the effect of one or more pVL rebounds on virological response at week 52. METHODS: Individual data were combined from 358 patients from the INCAS, AVANTI-2 and AVANTI-3 studies. Logistic regression models were used to determine the relationship between the magnitude of an increase in pVL and the probability of returning to the lower limit of quantification (LLOQ: 20-50 copies/ml) and to determine the odds of virological success at 52 weeks associated with single and consecutive pVL rebounds. RESULTS: A group of 165 patients achieved a pVL nadir < LLOQ; of these, 85 patients experienced pVL rebounds within 52 weeks. The probability of a pVL rebound was greater among patients who did not adhere to treatment (68% vs 49%; P < 0.05). The probability of reachieving virological suppression after a pVL rebound was not associated with the magnitude of the rebound [odds ratio (OR), 0.86; P = 0.56] but was associated with triple therapy (OR, 2.22; P = 0.06) or non-adherence (OR, 0.40; P = 0.04). The probability of virological success at week 52 was not associated with an isolated pVL rebound but was less likely after detectable pVL at two consecutive visits. CONCLUSIONS: An isolated pVL rebound was not associated with virological success at 52 weeks but rebounds at two consecutive visits decreased the probability of later virological success. Given their high risk of short-term virological failure, patients who present with consecutive detectable pVL measurements following complete suppression should be considered ideal candidates for intervention studies.

Antiretroviral Therapy, Highly Active↗
PubMed2007

Estimating the benefit of an HIV-1 vaccine that reduces viral load set point.

Vaccines designed to induce cell-mediated immune responses against human immunodeficiency virus (HIV)-1 are being developed. Such vaccines are unlikely to provide sterilizing immunity but may be associated with reduced viral set points after infection. We modeled the potential impact of a vaccine that reduces viral set point after infection, using natural history data from 311 HIV-1 seroconverters. Log-normal parametric regression models were used to estimate the log median time to events of interest. Relative times were estimated for those with viral load set points of 30,000 copies/mL (reference group) versus those with lower viral set points. The time to key clinical events in the course of HIV-1 disease progression was significantly extended for those with viral set points 0.5-1.25 log(10) copies/mL lower than the reference group. By quantifying the anticipated clinical benefits associated with a reduction in viral set point, these findings support the use of virologic end points in HIV-1 vaccine trials.

AIDS Vaccines↗
PubMed2003

Characterization of gag gene of plasma HIV type 1 in combination therapy-treated AIDS patients with high viral load and stable CD4+ T cell counts.

Many AIDS patients retain a high CD4+ T cell count despite a significant increase in polymerase chain reaction (PCR)-determined viral load after various periods of treatment by combination therapy. Our study involved 10 such AIDS patients who showed this discordance. In this study, we characterized changes in the gag gene of HIV-1 isolated from the plasma of such patients. Viral RNA was extracted from plasma samples and the gag gene was amplified by reverse transcription-PCR. The PCR product was cloned and three clones from each patient were sequenced. All the sequences were aligned and compared with similar HIV-1 isolated from nontreated AIDS patients. Several kinds of changes were observed in the sequences including substitutions, frameshifts, and deletions. One patient showed a frameshift due to a missing G residue in the capsid-encoding region of the gene whereas another patient had virus with two different deletions. Such changes are probably due to combination therapy.

Amino Acid Sequence↗
PubMed1994

Early stages of simian immunodeficiency virus infection in lymph nodes. Evidence for high viral load and successive populations of target cells.

Lymph nodes obtained from 14 macaques sacrificed at early time points following experimental inoculation with simian immunodeficiency virus were analyzed by in situ hybridization for virus load and virus cellular tropism. The lymph nodes presented a remarkably high viral load during the early phase of infection, as viral RNA was detected in as many as 2% of lymph node cells 1 week after inoculation. At this stage, macrophages and T4 lymphocytes were identified by combined immunohistochemistry and in situ hybridization as the target cells of the virus. Simian immunodeficiency virus-positive macrophages concentrated in the subcapsular sinuses, suggesting an entry of infected cells via the afferent lymphatics. A shift in the pattern of viral infection was observed at 2 weeks after inoculation, with a concentration of viral RNA in the germinal centers of the developing lymphoid follicles. Follicular dendritic cells were found to be the major target of the virus at this stage. Follicular dendritic cells were associated with high levels of viral RNA but little or no detectable viral DNA, suggesting that the virus was present mostly in the form of viral particles trapped at the cell surface. Follicular dendritic cell-associated virus persisted at high levels for 2 months before subsiding, indicating that follicular dendritic cells constituted a major reservoir of the virus during the early stages of simian immunodeficiency virus infection.

Animals↗
PubMed2004

Comparison of versions 1.0 AND 1.5 of the UltraSensitive AMPLICOR HIV-1 MONITOR test for subjects with low viral load.

We compared the performance of two UltraSensitive AMPLICOR HIV-1 MONITOR kits (version 1.5 [v1.5] versus v1.0) by retesting 404 plasma samples with low viral loads (<3,000 copies/ml) with both kits. With 292 samples that initially had <50 copies/ml by the v1.0 kit, the v1.5 assay was more sensitive than the v1.0 assay for samples with human immunodeficiency virus type 1 RNA near the 50-copy/ml cutoff (P = 0.0146). Median numbers of copies per milliliter were similar for 112 samples with 50 to 3,000 copies/ml with no difference in sensitivity with a 200-copy/ml cutoff.

HIV-1↗
PubMed2000

Full suppression of viral load is needed to achieve an optimal CD4 cell count response among patients on triple drug antiretroviral therapy.

OBJECTIVE: To characterize the relationship between plasma viral load (pVL) suppression and triple drug antiretroviral therapy, and the accompanying changes in CD4 cell counts. METHOD: Retrospective study of 465 participants in a HIV/AIDS Treatment Program who initiated triple drug therapy between August 1996 and May 1998. Participants were divided into three groups according to their pVL response: (i) non-responders (NR; n = 112) exhibited pVL persistently > 500 copies/ml over the study period; (ii) partial responders (PR; n = 100) achieved a pVL < 100 copies/ml at least once and subsequently rebounded to > 500 copies/ml; and (iii) full responders (FR; n = 253) achieved a pVL < 500 copies/ml and sustained this level for the remainder of the study period. For each group, the accompanying changes in absolute and fractional CD4 cell counts were evaluated. RESULTS: The median net change in pVL per person from baseline to the end of the observation period was -0.37, -2.27, and -2.56 log10 copies/ml for NR, PR and FR, respectively. During weeks 68-83, the median CD4 cell count (x 10(6) cells/l) was 150 [interquartile range (IQR) 90-370], 380 (IQR 300-480) and 525 (IQR 305-705) for NR, PR and FR, respectively. Median changes in CD4 cells (x 10(6) cells/l) were -20 (IQR -90 to 40), 150 (IQR 30-250) and 240 (IQR 110-365) for NR, PR, and FR, respectively. The net percentage change in CD4 cells per person was 0% (IQR -34-31), 54% (IQR 6-160), and 83% (IQR 39-173) for NR, PR, and FR, respectively. By weeks 68-83, the median fractional CD4 cells was 0.16 (IQR 0.07-0.22), 0.22 (IQR 0.15-0.28), and 0.26 (IQR 0.17-0.34) for NR, PR and FR respectively. CONCLUSIONS: An optimal CD4 cell count response appears to be coupled with continued pVL suppression. Our data indicate that maximal suppression of viral replication should remain the primary goal of therapy.

Adult↗
PubMedDate not supplied

Short-term interferon therapy for chronic hepatitis C patients with low viral load.

BACKGROUND/AIMS: To evaluate the usefulness of high-dose short-term interferon therapy prospectively in 32 chronic hepatitis C patients with a low viral load showing the rapid disappearance of hepatitis C virus RNA after the start of interferon therapy. METHODOLOGY: Each patient was confirmed with a low hepatitis C virus RNA level less than 1.0 Meq/mL before the start of interferon therapy regardless of hepatitis C virus genotypes. High-dose short-term interferon therapy was defined as administration of natural interferon alpha 10 MU/day for 14 weeks (daily for 4 weeks then three times a week for 10 weeks). This course of treatment was carried out only in cases with the rapid disappearance of hepatitis C virus RNA at 2 weeks after the start of interferon. RESULTS: Sustained virological response was observed in 30 of 32 patients (93.8%) who received high-dose short-term interferon therapy. One patient who received 24 weeks interferon administration relapsed and became a non-responder. One patient refused to continue this therapy. CONCLUSIONS: High-dose short-term interferon therapy might be useful when combining the selection of patients according to pretreatment hepatitis C virus RNA levels and testing virus presence at an early point after the start of interferon therapy.

Adult↗
PubMed2003

Continued indinavir versus switching to indinavir/ritonavir in HIV-infected patients with suppressed viral load.

OBJECTIVE: To compare continued indinavir (IDV) 8-hourly (q8h) with switching to indinavir/ritonavir (IDV/RTV) 12-hourly (q12h) in HIV-positive patients having suppressed viral load with IDV q8h plus two nucleoside reverse transcriptase inhibitors (NRTI). DESIGN: Multicentre, international, randomized, open-label study enrolling HIV-1 infected patients on IDV 800 mg q8h plus two NRTI with CD4 cell counts > or = 100 x 106/l and plasma HIV RNA < 500 copies/ml for > or = 3 months. METHODS: Patients were randomized to continue on the same regimen or to switch to IDV plus liquid RTV (IDV/RTV 800 mg/100 mg q12h). Primary endpoint was the proportion of patients remaining < 500 copies/ml at 48 weeks. RESULTS: A total of 323 patients (IDV/RTV, 162; IDV, 161) were evaluable. At 48 weeks, the proportions of patients with plasma HIV RNA < 500 copies/ml were 93%, 88% and 58% in the IDV/RTV arm versus 92% (P = 1), 86% (P = 0.87) and 74% (P = 0.003) in the IDV arm using on-treatment (OT) and intent-to-treat (ITT) [switches included (ITT, S = I) and switches = failure (ITT, S = F)] analyses respectively. Mean increase in CD4 cell count was 88 x 106/cells/l (IDV/RTV arm) and 60 x 106 cells/l (IDV arm) (P = 0.08). More patients discontinued study medication due to adverse events in the IDV/RTV arm than in the IDV arm (P < 0.001). CONCLUSIONS: Equivalence of continuing IDV q8h versus switching to IDV/RTV (liquid) q12h in suppressed stable patients was demonstrated by OT and ITT S = I analyses. However, the IDV q8h arm performed better when discontinuations were classified as failures. IDV/RTV q12h can be convenient and equally effective for patients able to tolerate it.

Adult↗
PubMed2025

Patterns of HIV-1 viral load suppression and drug resistance during the dolutegravir transition: a population-based longitudinal study.

BACKGROUND: Data on the population-scale impact of dolutegravir (DTG)-based HIV regimens in sub-Saharan Africa are extremely limited. We used data from a surveillance cohort in southern Uganda to assess viral suppression and antiretroviral (ART) resistance over 10-years alongside DTG scale-up. METHODS: Consenting participants in the population-based Rakai Community Cohort Study between August 2011 and March 2023 aged 15-59 completed questionnaires and provided samples for HIV testing, viral load quantification, and viral deep-sequencing. We collected data on DTG-utilization at HIV care clinics. We estimated the prevalence of HIV suppression (<1,000 copies/mL) and ART resistance using robust Poisson regression. Bayesian logistic regression quantified associations between resistance and individual-level suppression across surveys. FINDINGS: Among 20,383 people living with HIV (PLHIV), suppression increased from 57.1% (95% confidence interval [CI]: 55.4%-58.8%) to 90.3% (95%CI: 89.2%-91.4%) between 2014 and 2022. By 2020 84.4% (95%CI: 83.7%-85.2%) and 64.6% (95%CI: 63.9%-65.3%) of men and women were on DTG regimens. Among treatment-experienced viremic PLHIV, overall resistance decreased from 51.1% (95%CI: 40.7%-64.1%, 2014) to 27.9% (95%CI: 21.3%-36.5%, 2022). Only two participants harbored intermediate/high-level DTG resistance, attributable to inQ148R, inE138K, and inG140A. Low-level INSTI resistance (inS153Y) was observed in 23/207 (7.5%) of viremic individuals, with putative evidence of transmission. By 2022, suppression was unrelated to prior history of NNRTI/NRTI resistance (risk ratios: 1.14, 95%HPD: 0.96-1.32 and 1.12, 95%HPD: 0.88 - 1.35). INTERPRETATION: Viral suppression increased during the DTG-transition with minimal emerging intermediate/high-level resistance. Falling resistance among treatment-experienced PLHIV underscores the role of ART adherence in reducing viremia. The emergence of inS153Y justifies continued genomic surveillance of ART resistance. FUNDING: National Institutes of Health and the Gates Foundation.

Journal Article↗
PubMed2001

Intrapartum zidovudine infusion alone failed to reduce both maternal HIV-1 viral load and HIV-1 infection in infant.

A pilot clinical trial to assess the efficacy of intrapartum zidovudine (ZDV) infusion alone in the reduction of maternal viral load and its potential role in preventing vertical transmission of HIV-1. Twenty six, asymptomatic antiretroviral naïve HIV-1 infected pregnant women who had no prior antenatal care and were in labor were enrolled. Each patient received ZDV infusion at the rate of 2 mg/kg within the first hour. ZDV was then continuously infused at 1 mg/kg/h until delivery. Maternal plasma HIV-1 RNA prior to the commencement of ZDV infusion and within an hour after delivery were measured. HIV-1 transmission was documented by nested polymerase chain reaction in infants at six months of age. Median maternal plasma HIV-1 RNA prior to the ZDV infusion and after delivery was 29,401 and 32,555 copies/ml respectively, (p>0.05). The estimated HIV-1 transmission rate was 19.2 per cent (95% CI = 4-34). This result suggested that in asymptomatic HIV-1 infected pregnant women who were antiretroviral naïve and had no prior antenatal care, intrapartum ZDV infusion alone failed to reduce maternal HIV-1 viremia and the transmission rate of HIV-1.

Anti-HIV Agents↗
PubMed2002

Changes in plasma HIV-1-RNA viral load and CD4 cell counts, and lack of zidovudine resistance among pregnant women receiving short-course zidovudine.

OBJECTIVE: To describe changes in HIV-1 plasma viral load (VL) and CD4 cell counts and to assess zidovudine resistance associated with a short course of oral zidovudine during late pregnancy. METHODS: From April 1996 to February 1998 in Abidjan, Côte d'Ivoire, 280 HIV-1-seropositive women were randomly assigned at 36 weeks' gestation to receive zidovudine (300 mg) or placebo twice a day, and then one tablet every 3 h from the onset of labor until delivery. Blood samples obtained every 2 weeks until delivery, then at 2 and 4 weeks, and 3 or 6 months after delivery were tested from selected women based on duration of therapy for plasma VL and CD4 cell counts, and samples from 20 women in the zidovudine group were tested by DNA sequencing for the presence of zidovudine resistance mutations. RESULTS: In the zidovudine group, the median reduction in plasma VL (log(10) copies/ml) was -0.48 after 2 weeks (P = 0.02 versus placebo), -0.48 after 4 weeks (P = 0.06), -0.80 after 6 weeks (P = 0.29) of treatment, -0.12 at delivery (P = 0.11), +0.21 at 2 weeks (P = 0.83), +0.17 at 4 weeks (P = 0.69), and +0.21 at 3 months (P = 0.56) postpartum. Median CD4 cell counts were higher in the zidovudine than in the placebo group after 2, 4, and 6 weeks of treatment (P < 0.05). No mutations associated with zidovudine resistance were identified in any of the samples tested. CONCLUSION: These findings suggest that a short course of zidovudine has no adverse HIV-1 virological consequences for the mother.

Anti-HIV Agents↗