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PubMed2003

Genital tract and plasma human immunodeficiency virus viral load throughout the menstrual cycle in women who are infected with ovulatory human immunodeficiency virus.

OBJECTIVE: The purpose of this study was to determine the vaginal, cervical, and plasma viral load through the menstrual cycle in women who are positive for human immunodeficiency virus. STUDY DESIGN: A prospective cohort study was performed on 14 women with ovulatory menstrual cycles who have human immunodeficiency virus. Duplicate cervical and vaginal viral load samples (n = 301) were taken at four stages (menstrual, follicular, periovulatory, and luteal) of two consecutive cycles. RESULTS: Participant characteristics were mean age of 32.7 years, median human immunodeficiency virus helper cell count value of 355, and median plasma viral load of 24,000 copies/mL. Through the menstrual cycle, there was no statistically significant difference in plasma viral load, but there was a significant decrease in genital tract viral load at the periovulatory phase (vagina, P =.018; cervix, P =.007). Vaginal and cervical viral load were correlated (r = 0.582, P <.001). CONCLUSION: Although the plasma viral load remained constant throughout the menstrual cycle, the genital viral load decreased at the periovulatory phase. These results suggest that local factors may affect the genital viral load compartment independent of plasma viral load.

Acquired Immunodeficiency Syndrome↗

PubMed2002

Correlates of plasma HIV-1 RNA viral load among HIV-1-seropositive women in Dar es Salaam, Tanzania.

This study was conducted to determine the predictors of plasma HIV-1 RNA viral load in HIV-1-positive pregnant women (N = 151) participating in a clinical trial in Tanzania. Viral load was measured at randomization, delivery, and approximately 7 months after delivery. The median viral load was 20,400 copies/mL at baseline, 20,216 copies/mL at delivery, and 19,100 copies/mL 7 months after delivery. The absolute CD4+ lymphocyte count had a strong negative correlation with HIV-1 RNA viral load at baseline (r = -.38), time of delivery (r = -.36), and 7 months after delivery (r = -.53). The association between CD4+ lymphocyte count and HIV-1 RNA viral load was modified by the per capita daily food expenditure in the household, although the difference in viral load became small as the food expenditure in the household increased and was marginally significant at the 75th percentile of the per capita food expenditure. The presence of malaria parasites at baseline was associated with an approximate 116% higher viral load at the three evaluation points (p =.007). Although the long-term effects of malaria on viral load are unknown, prevention of malaria among people living with HIV-1 should be given the highest priority.

Adult↗

PubMed2000

Fluctuations in HIV-1 viral load are correlated to CD4+ T-lymphocyte count during the natural course of infection.

Viral load fluctuates during the natural course of asymptomatic HIV-1 infection. It is often assumed that these fluctuations are random around a set point or underlying growth trend. Using longitudinal data, we tested whether fluctuations in viral load can be better explained by changes in CD4+ T-cell count than by a set point or trend of exponential growth. The correspondence between viral load and CD4+ T-cell count could be described by a simple mathematical relation. Using a bootstrapping approach, the hypothesis that viral load fluctuations are random around a set point was rejected with p < .00005. The hypothesis that viral load fluctuations are random around a trend of exponential growth was rejected with p < .005. Viral load data was explained better by changes in CD4+ T-cell counts than by a set point or by a trend of exponential growth. The implications of this finding for improved prognostication are discussed.

CD4 Lymphocyte Count↗

PubMed2000

Natural fluctuations of hepatitis C viral load in a homogeneous patient population: a prospective study.

The aim of this study was to determine the variation in hepatitis C viral load over an extended period of patient follow up. Serum samples were collected from 49 female individuals who were identified as having been infected from the same source of hepatitis C-contaminated anti-D immunoglobulin during the period from 1977 (May) to 1978 (November). All patients attended the hepatitis C clinic at Cork University Hospital, Cork, Ireland. The study group was homogeneous with respect to gender, hepatitis C virus (HCV) genotype (1b), and duration of infection. None of the patients had received antiviral therapy at the time of completion of study. Viral load quantifications were assessed using the Roche Monitor (F. Hoffmann-La Roche, Ltd., Basel, Switzerland) assay. The mean age of the study group at time of infection was 30.3 years (SD +/- 6.1) with a range from 18.5 to 43 years. The mean time of follow-up was 4. 1 years (SD +/- 1.0) with a range from 1.2 to 5 years. The mean rate of change of viral load per year was 0.23 log(10) viral copies per mL serum for the study group (SD +/- 0.19) with a range of -0.18 to 0.78 that was significantly different from zero, P < 10(-10). The rate of change of viral load per year was negatively correlated with viral load at first determination, r = -.35, P =.01. Age at infection did not correlate with the slope of change of viral load, P =.10. In conclusion, most women infected with HCV 1b will have an increase in viral load over time but a few patients who acquire infection early in adult life will show a decrease in viral load.

Adolescent↗

PubMedDate not supplied

HIV viral load: the myth of the undetectable?

There is a wealth of data supporting the use of viral load measurements to monitor therapy. Indeed, clinical drug trial endpoints routinely include the proportion of patients with a plasma viral load reduction of greater than 0.5 log(10), or greater than 1 log(10). Since a higher viral load reflects increased amounts of virus replication, it would seem desirable to reduce this replication as far as possible, so that the goal of therapy has become one of viral undetectability in plasma. However, virological suppression to undetectable levels is not an absolute determinant of outcome because recent observational cohort data suggest that any significant reduction of viral load is associated with clinical benefit. There are also technical problems when attempting to measure undetectability, with lower limits of detection of 400 or 50 RNA copies/ml of plasma being driven more by the performance of commercial assays than by any inherent cut-off value with proven prognostic significance. Furthermore, the obsession with undetectability has created the concept of the 'viral blip', or 'intermittent viraemia' commonly defined as a single viral load measurement of between 50 and 400 copies/ml, preceded and followed by consistent measurements of less than 50 copies/ml, in a patient receiving therapy. Such blips should be considered in the context of frequent transient changes in viral load which occur below the lower limit of detection by existing laboratory assays. In my view, there remains a misunderstanding about the importance ascribed to these relatively minor changes in lower detection limits, when considered against the background of virus within the body as a whole. I also consider other possible uses of HIV-1 quantification in clinical practice, such as identifying the inherent potency of antiviral regimens.

Anti-HIV Agents↗

PubMed1999

The effects of HIV viral load on the phagocytic activity of monocytes activated with lipopolysaccharide from oral microorganisms.

A study was undertaken to determine whether viral load status in HIV+ patients has any potential effect on monocyte phagocytic function both before and after challenge of the monocytes with lipopolysaccharide (LPS) isolated from oral microorganisms. LPS of two putative periodontal pathogens Porphyromonas gingivalis (P. gingivalis) and Fusobacterium nucleatum (F. nucleatum) was prepared. Whole blood samples in EDTA were collected from 30 HIV+ patients presenting for dental care at the University of Maryland. Control samples were prepared from appropriate uninfected individuals. Viral load was determined using quantitative RT-PCR (Amplicor, Roche Diagnostics). Phagocytic function was determined using FITC labeled Saccharomyces species in resting isolated monocytes and in cells after 24 h stimulation with 1 microgram/ml of LPS of P. gingivalis or F. nucleatum. Immunohistochemical staining was performed for complement receptor CR-1 (CD-35) on phagocyte cells. In HIV+ patients with high viral load (> 10,000 copies/ml), 13.5% of isolated resting monocytes demonstrated phagocytic activity, while 23% of the resting control monocytes from non-infected individuals showed phagocytic function. When the monocytes were stimulated with 1 microgram/ml of LPS of F. nucleatum, phagocytic activity was observed in 18.5% of monocytes in patients with high viral load, 33.5% with moderate viral load (400-10,00 copies/ml) and 51% with low viral load (<400 copies/ml), while 62% of the control monocytes demonstrated phagocytic activity. Stimulation of monocytes with LPS of P. gingivalis showed similar results. Complement receptor CD-35 showed a 50% decrease in expression in HIV+ patients with high viral load. A progressive decrease in monocyte/macrophage phagocytic function and CD-35 expression with and without oral LPS activation occurs after HIV infection and this trend appears to be accentuated in patients with high viral load. This relationship may contribute to increased susceptibility to oral opportunistic infections in advanced HIV+ patients.

Adult↗

PubMed2000

Problems in the interpretation of HIV-1 viral load assays using commercial reagents.

During routine monitoring of human immunodeficiency virus (HIV) viral load, two problems arose. First, a number of patients, the majority being African, were found to have low viral loads by the Chiron branched-chain DNA assay in conjunction with low CD4(+) cell numbers. In order to determine whether this was due to failure of the branched-chain DNA assay to detect non-B subtypes of HIV, selected samples were subtyped and HIV RNA quantified by branched-chain DNA, NASBA, and the Roche Monitor RT-PCR assay. Twenty-eight (97%) of 29 Africans were infected with a non-B subtype of HIV and 15 (93.7%) of 16 non-Africans with subtype B. Twenty-three samples had a low viral load by branched-chain DNA, which was confirmed by the NASBA and RT-PCR assays. All three assays detected B and non-B subtypes with similar efficiency; NASBA failed to detect HIV RNA in a small number of non-B samples. Discrepancies between viral load and CD4(+) cell numbers did not appear therefore to be related to subtype. Second, while quantification of HIV RNA was being conducted using version 2 of the branched-chain DNA assay (lower detection limit 500 HIV RNA copies/ml) the manufacturers had developed a more sensitive assay and a comparative evaluation was therefore conducted. In approximately 30% of samples the viral load was up to 10 times higher with the more sensitive assay. These experiences emphasise the importance of close collaboration between the clinic and the laboratory.

CD4 Lymphocyte Count↗

PubMed2004

Use of viral load measured after 4 weeks of highly active antiretroviral therapy to predict virologic outcome at 24 weeks for HIV-1-positive individuals.

Early prediction of suboptimal viral response to highly active antiretroviral therapy (HAART) is vital to prevent early development of drug resistance. We used logistic regression to predict the odds of achieving virologic suppression (<50 copies/mL) after 24 weeks of HAART in 656 antiretroviral-naive patients starting HAART at the J.W. Goethe University, Chelsea and Westminster, and Royal Free Hospitals according to their week 4 viral load. Therapy changes involving the switch of a single antiretroviral were assumed to have occurred for toxicity reasons and ignored. Because complete regimen changes or additions of new antiretrovirals could be due to virologic failure, patients were counted as virological failures at week 24. Three hundred sixty (84%) of 430 patients with viral loads of <1000 copies/mL, 106 (61%) of 175 with viral loads between 1001 and 10,000 copies/mL, 11 (37%) of 30 with viral loads between 10,001 and 100,000 copies/mL, and 5 (24%) of 21 with viral loads of >100,000 copies/mL at week 4 subsequently attained virologic suppression at 24 weeks. The odds of attaining virologic suppression at 24 weeks was 65% lower for every 1-log higher viral load at week 4 (odds ratio, 0.35; 95% confidence interval, 0.27-0.45). The proportion of patients with an undetectable viral load at 24 weeks among those who have not attained a viral load of <1000 copies/mL by 4 weeks is quite low. We suggest that this group of patients should be particularly closely monitored.

Adult↗

PubMed2003

Measurements of HIV viral loads from different levels of the respiratory tract.

BACKGROUND: The lung is a common site of disease in HIV infection. Virus has been detected in BAL fluid (BALF) and saliva. However, the relationship between viral loads detected at different levels of the respiratory tract is unknown. METHOD: We measured simultaneous HIV viral loads in parotid saliva (PS), bronchial fluid (BF), BALF, and plasma by reverse transcription polymerase chain reaction in 20 HIV-infected individuals. RESULTS: HIV was detected in 53% of BALF samples, 15% of BF samples, 5% of PS samples, and 88% of plasma samples. Viral loads in plasma and BALF samples were positively correlated. There were significantly higher levels of HIV viral load in both plasma and BALF in subjects with CD4 counts of < 200 cells/ microL compared to those with higher counts. Antiretroviral therapy (ART) was associated with lower BALF and plasma viral loads, and the effect in BALF was independent of the plasma viral load. Interestingly, smoking also was associated with lower levels of both BAL and BF viral loads, independent of the plasma viral load. CONCLUSION: These data demonstrate that while HIV can be detected in the respiratory tract, the viral load is influenced by both local factors (ie, level of the respiratory tree and cigarette smoking) and systemic factors (ie, ART and peripheral CD4 count).

Adult↗

PubMedDate not supplied

Use of bDNA testing in the immunologically nonresponding patient who has a low or undetectable viral load by RT-PCR testing.

BACKGROUND: Studies have shown that reverse transcription-polymerase chain reaction (RT-PCR) technology underquantifies viral loads in patients with non-B clades of HIV-1. Testing with bDNA technology gave higher viral loads in these subtypes. A study was conducted to determine whether virologically responding patients on HAART who were not immunologically responding would have higher viral loads using bDNA technology and whether these differences were due to non-B clades. METHOD: Forty-eight patients receiving HAART for more than 6 months who were having inappropriate immunologic responses in spite of undetectable or very low viral loads determined by RT-PCR (<3000 copies by Roche Amplicor 1.0) were studied. These patients had bDNA viral loads performed. All patients who had bDNA viral loads equivalent to >3000 by RT-PCR had clade and genotypic studies performed. RESULTS: Fifteen patients had viral loads by bDNA that were equivalent to >3000 copies by RT-PCR. Four of these were found to have non-B clades (one D clade and three AG clade). The D clade patient had multidrug resistance; none of the AG clade patients had resistance. Of the remaining 11 patients, virus could not be recovered from 2 and 9 had a B clade. Six of these nine had genotypic resistance to HAART drugs. CONCLUSION: bDNA testing may be useful in the immunologically nonresponding patient.

Adult↗

PubMed2005

Neuropsychological functioning and viral load in stable antiretroviral therapy-experienced HIV-infected children.

OBJECTIVE: Neuropsychological functioning and its correlation with viral load were investigated for previously treated HIV-infected children who underwent a change in treatment regimen. METHODS: Thirteen age-appropriate measures of cognitive, neurologic, and behavioral functioning were administered to 489 HIV-infected children who were aged 4 months to 17 years and had been treated previously for at least 16 weeks with antiretroviral therapy. These clinically and immunologically stable children were randomized onto 1 of 7 drug treatment combinations, 6 of which included a protease inhibitor (PI), and evaluated prospectively for 48 weeks with respect to changes in neuropsychological performance and viral load. RESULTS: Neuropsychological functioning was significantly poorer at baseline for the HIV-infected children as compared with established norms for their age. Children with higher viral load had poorer cognitive, both-hands fine-motor, and neurologic signs at baseline, but single-hand fine-motor and behavioral functioning were not correlated with viral load. After 48 weeks of treatment with PI-containing combination therapy, there was significant improvement in only the vocabulary score. Neuropsychological changes did not differ among the 6 PI-containing combination regimens. At week 48, even children with a viral load response below the level of detection (RNA < or =400 copies/mL) still showed poorer neuropsychological functioning compared with established norms. CONCLUSION: Poor neuropsychological functioning was seen for HIV-infected children and was worse for children with higher viral loads. Only 1 measure of neuropsychological functioning showed improvement after treatment with PI-containing combination therapy, and the extent of that improvement was relatively minor. Treatment strategies for children with HIV disease need to be reevaluated so that they consider restoration of neuropsychological functioning in addition to lowering the viral load.

Adolescent↗

PubMed2005

Discordance between viral loads determined by Roche COBAS AMPLICOR human immunodeficiency virus type 1 monitor (version 1.5) Standard and ultrasensitive assays caused by freezing patient plasma in centrifuged becton-dickinson vacutainer brand plasma preparation tubes.

The Roche COBAS AMPLICOR human immunodeficiency virus type 1 (HIV-1) Monitor (version 1.5) standard and ultrasensitive viral load assays often gave discordant results, with viral loads from the standard assay exceeding those from the ultrasensitive assay by more than 0.5 log(10) for approximately 20% of specimens received. We began studies to determine the extent, magnitude, and reproducibility of the discordance between the assays and to discover and eliminate the cause of this discordance. Until then, we revised our standard operating procedure to include both standard and ultrasensitive testing on all specimens submitted for viral load determinations. Discordant results usually recurred on retesting. They were most prevalent for specimens with ultrasensitive viral loads of <1,000 and rare for specimens with viral loads of >10,000. Often, standard assay results exceeded those of the ultrasensitive assay by 50- to 100-fold. At higher viral loads, the difference between the standard and ultrasensitive assays persisted, but the percent difference was smaller and rarely caused discordance. The proportion of discordant results was significantly higher in specimens from pediatric patients than in specimens from adults. The ultrasensitive viral load determinations generally agreed with the results of the B-DNA (Bayer) viral load assays. If the plasma was transferred from the centrifuged plasma preparation tubes before freezing, standard and ultrasensitive results were concordant with each other and with values determined on plasma from lavender-topped EDTA tubes.

Adolescent↗

PubMed2006

Past HBV viral load as predictor of mortality and morbidity from HCC and chronic liver disease in a prospective study.

BACKGROUND AND AIMS: In a prospective cohort study with 11 yr of follow-up, we assessed the relationship between past hepatitis B virus (HBV) viral load and mortality. Surviving cohort members were evaluated for current liver disease. METHODS: We measured HBV viral load by real-time polymerase chain reaction on stored samples from cohort entry (1992-1993) in 2,763 hepatitis B surface antigen (HBsAg)-positive adults. Major end points were death from hepatocellular carcinoma (HCC) or chronic liver disease (CLD). There were 447 deaths. In the 1,683 survivors, we assessed severity of liver disease on a return visit in 2003. Viral load was divided into three categories: undetected (<1.6 x 10(3) copies/mL); low titer (<10(5) copies/mL); and high titer (> or =10(5) copies/mL). RESULTS: For HCC, there was a significant increase in mortality across viral load categories (p(trend) < 0.001). Compared to the HBV undetected category, the relative risk (RR) for HCC mortality in the low viral load group was 1.7 (95% confidence interval [CI] 0.5-5.7) and 11.2 (3.6-35.0) in the high viral load group. For CLD mortality, the RRs were 1.5 (0.2-12.1) and 15.2 (2.1-109.8), respectively (p(trend) < 0.001). The RR associated with high viral load did not change with increased follow-up time. In surviving cohort members evaluated for liver disease in 2003, there was also a significant association of viral load with disease severity. CONCLUSION: In this prospective study, viral load is associated with increased mortality from HCC and CLD in HBV-infected subjects. Viral load may be a useful prognostic tool in HBV infection, and interventions aimed at its reduction should be explored.

Adult↗

PubMed1997

High viral load in semen of human immunodeficiency virus type 1-infected men at all stages of disease and its reduction by therapy with protease and nonnucleoside reverse transcriptase inhibitors.

Seminal viral load is likely to be directly related to the sexual transmissibility of human immunodeficiency virus type 1 (HIV-1). However, it is not clear whether the level of HIV-1 in semen varies with the stage of infection and whether antiretroviral therapy reduces seminal viral load. A nucleic acid sequence-based amplification (NASBA) technique was used to quantify HIV-1 RNA as an indicator of infectious viral load in semen and blood plasma of homosexual men with different stages and durations of HIV-1 infection. The median viral load in a cross section of 34 men was 11,000 HIV-1 RNA copies/ml (range, <400 to 1.3 x 10(7) copies/ml) in whole semen and 5,238 HIV-1 RNA copies/ml (range, <400 to 2.8 x 10(5) copies/ml) in seminal plasma, which is 10- to 1,000-fold higher than previous estimates. Viral loads in whole semen and seminal plasma were strongly correlated with blood plasma viral load (P < 0.001) but not with blood CD4+ T-cell count (P = 0.420). Longitudinal analysis of eight subjects who progressed to AIDS showed that seminal viral load increased in most cases, with viral load consistently higher in blood plasma than in semen. Viral loads in semen and blood plasma decreased markedly in six other patients following initiation of potent combination therapy with a protease inhibitor (indinavir) and a nonnucleoside reverse transcriptase inhibitor (DMP-266). These findings have important implications for the biology of sexual transmission of HIV-1 and its potential reduction by antiretroviral therapy.

Acquired Immunodeficiency Syndrome↗

PubMed2005

Hydroxychloroquine, hydroxyurea and didanosine as initial therapy for HIV-infected patients with low viral load: safety, efficacy and resistance profile after 144 weeks.

OBJECTIVES: To evaluate the long-term safety and efficacy of the combination of hydroxychloroquine, hydroxyurea and didanosine. METHODS: We recruited antiretroviral-naive patients with viral loads less than 100 000 HIV-1 RNA copies/mL and CD4 counts greater than 150 cells/microL. All patients received hydroxychloroquine (200 mg), hydroxyurea (500 mg) and didanosine (125-200 mg) twice daily. Clinical and laboratory safety assessments and measurements of viral load and CD4 count were made at regular intervals, and genotypic resistance testing was performed on samples with detectable viral load at 48, 96 and 144 weeks. RESULTS: Fourteen of the 17 patients who commenced therapy remained on treatment at 144 weeks. Treatment was well tolerated but caused neutropenia, usually mild and transient, in 12 patients (71%). Mean viral load was reduced by 1.6 log(10) copies/mL below baseline (P<0.001), eight patients (47%) had undetectable viral load (<400 copies/mL), and two patients (12%) had detectable viral load but no detectable resistance mutations at week 144. Four patients (24%) had detectable viral load together with major resistance mutations (three with both 74 V and 184 V, and one with both 62 V and 65R) at week 144, but still had viral load suppression below baseline. Mean CD4 count was increased by 106 cells/microL above baseline (P=0.07) at week 144. CONCLUSIONS: This novel and well-tolerated combination controls viral replication during long-term follow up, with development of few resistance mutations. With careful monitoring it may be a useful strategy for delaying highly active antiretroviral therapy (HAART) and associated toxicity in selected patients with low initial viral loads.

Adult↗

PubMed1997

The effect of maternal viral load on the risk of perinatal transmission of HIV-1. New York City Perinatal HIV Transmission Collaborative Study Group.

OBJECTIVE: To determine the effect of maternal viral load at delivery on the risk of perinatal transmission of HIV-1. DESIGN: A nested case-control study within a prospectively followed cohort of HIV-1-infected pregnant women and their infants. SETTING: The multicenter New York City Perinatal HIV Transmission Collaborative Study. PARTICIPANTS: Fifty-one women who gave birth to HIV-1 infected infants were frequency-matched within CD4+ cell count quintiles with 54 non-transmitting mothers. MAIN OUTCOME MEASURES: Maternal quantity of HIV-1 viral RNA was assayed in plasma obtained near delivery using the nucleic acid sequence-based amplification assay system. RESULTS: Viral RNA was detected in 73 (70%) out of 105 women and the median viral load was 16,000 RNA copies/ml in transmitters and 6,600 in non-transmitters (P < 0.01). When adjusted for maternal CD4+ count near delivery, women with measurable viral load were nearly sixfold more likely to transmit HIV-1 than women with viral load below detection [adjusted odds ratio (AOR), 5.8; 95% confidence interval (CI), 2.2 15.5]. The odds ratio for perinatal transmission of log10 viral load, adjusted for CD4 count was 2.7 (95% CI, 1.5-5.1). When stratified by the stage of HIV-1 disease, the only group with significant association between log10 viral load and transmission were AIDS-free women with CD4+ count > 500 x 10(6)/l (AOR, 9.1; 95% CI, 2.6-31.5). CONCLUSIONS: High maternal viral load increases the likelihood of perinatal transmission of HIV-1 in women without AIDS and advanced immunosuppression. HIV-1 infected pregnant women without advanced disease, shown by others to have the lowest risk of perinatal transmission, may benefit the most from efforts to identify and decrease viral load at delivery.

Adult↗

PubMedDate not supplied

Efficacy of nevirapine-based HAART in HIV-1-infected, treatment-naive persons with high and low baseline viral loads.

PURPOSE: The objective of this analysis was to assess the efficacy of nonnucleoside reverse transcriptase inhibitor (NNRTI)-containing, protease inhibitor (PI)-sparing, three-drug highly active antiretroviral therapy (HAART) in HIV- 1-infected, treatment-naive patients with high and low baseline viral loads. METHOD: A composite analysis was performed of clinical studies including the NNRTI nevirapine that were presented at international conferences between 1998 and October 2000. In all of the studies, nevirapine was administered in combination with two nucleoside reverse transcriptase inhibitors (NRTIs). For a study to be included in the analysis, more than 25% of participants must have had baseline viral loads >100,000 copies/mL, and more than 25% of participants must have had viral loads <100,000 copies/mL. RESULTS: After 6 months, 139 of 156 (89%) and 82 of 99 (83% ) patients in the low and high baseline viral load groups, respectively, had on-treatment viral loads <200 to 500 copies/mL (depending on assay used). After 12 months, 95 of 124 patients (77%) with lower baseline viral loads and 63 of 76 patients (83%) with high baseline viral loads had on-treatment viral loads below the limit of quantification. CONCLUSION: Baseline viral load does not affect virologic outcome in HIV-1-infected, antiretroviral-naive participants treated with nevirapine-containing, PI-sparing HAART.

Anti-HIV Agents↗

PubMed2005

Nonfinancial factors associated with decreased plasma viral load testing in Ontario, Canada.

OBJECTIVE: To examine whether individual characteristics were associated with differential use of viral load testing when testing is available without charge to all HIV-positive patients with provincial health insurance. METHODS: Individuals enrolled in the HIV Ontario Observational Database with complete medication records and health insurance numbers for linkage were studied. Generalized estimating equation regression models were used to examine the relationship between time-varying covariates such as plasma viral load levels, CD4 counts, and antiretroviral regimen characteristics and the number of days between viral load tests and the occurrence of an interval of >or=6 or 9 months between tests. RESULTS: A total of 1032 individuals were included in the analysis with a median follow-up of 4.6 years and a median of 18 viral load tests. In multivariate analyses, clinically important gaps in viral load testing were more likely among injection drug users (odds ratio [OR]=1.86, P<0.0001), in more recent years (P<0.01) and for individuals not using antiretrovirals (OR=1.70, P<0.0001) and less likely among individuals using >4 antiretrovirals (OR=0.62, P<0.0001). Results were similar when the outcome was the number of days between tests. CONCLUSIONS: Injection drug users, younger individuals, and residents of Toronto used fewer viral load tests than other individuals, even when financial barriers to testing were removed.

Adult↗