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Results for “Viral Load”

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PubMed2007

Parvovirus B19 infection in pregnancy: maternal and fetal viral load measurements related to clinical parameters.

OBJECTIVE: To correlate quantitative maternal and fetal parvovirus B19 (B19V) viral loads and antibody levels at intrauterine transfusion (IUT) as a predictor of fetal morbidity. METHODS: Prospectively collected clinical data and quantitative B19V viral load and specific IgM and IgG values in fetal and maternal blood samples taken during IUT. RESULTS: Maternal IgM and IgG levels exceeded fetal antibody levels. Fetal viral load measurements correlated positively with maternal viral loads and exceeded maternal viral load 10(5)-fold (p < 0.0001). Maternal B19V IgM and fetal B19V viral load showed a positive correlation (r = 0.840, p = 0.007). No relation was found between fetal viral load and severity of fetal anemia derived from Doppler flow measurements in the middle cerebral artery. CONCLUSIONS: Maternal and fetal B19V viral load values are highly interrelated, suggesting continuous maternal and fetal viral replication or a fetal source of maternal viremia. Maternal B19V IgM values may predict the severity of fetal infection, but the severity of B19V induced fetal anemia cannot be predicted using fetal or maternal viral loads. Fetal ultrasound remains the gold standard for identifying fetal anemia in B19V infection.

Adult↗

PubMed2002

Level and pattern of HIV-1-RNA viral load over age: differences between girls and boys?

OBJECTIVE: To estimate RNA viral load patterns over age in vertically infected children that account for between- and within-individual variation, treatment and assay cut-off detection level. To investigate possible sex-based differences. DESIGN: A total of 118 infected children with 894 RNA viral load measurements enrolled in the European Collaborative Study were prospectively followed from birth for up to 15 years. METHODS: Fractional polynomial and mixed effects models with censored data to assess the non-linear pattern of viral load over age, allowing for repeated measures. RESULTS: The RNA viral load peaked at approximately 3 months of age, and gradually declined thereafter. The sex by age interaction was significant (chi2 = 19.7, P < 0.001); viral load peaked higher for girls than boys, but after 4 years the RNA load was consistently 0.25-0.5 log10 lower for girls than boys. The effects of sex and treatment on viral load vary over age (chi2 = 6.31, P = 0.043). Sex differences in RNA viral load relating to measurement without treatment were more pronounced than those under treatment. Disease progression was more rapid for girls than for boys up to the age of 4 years, and less rapid thereafter; the overall difference was not statistically significant. CONCLUSION: Differences in RNA viral load over age between untreated boys and girls may have implications for policies for the initiation of antiretroviral therapy, but do not seem to translate into differences in progression to serious disease. The findings would suggest underlying biological explanations, which need further investigation.

Adolescent↗

PubMed2001

Viral load of human herpesvirus 8 in peripheral blood of human immunodeficiency virus-infected patients with Kaposi's sarcoma.

Viral load is an important marker of activity of viral diseases for a number of viruses. We wished to evaluate whether the viral load of human herpesvirus 8 (HHV-8) in peripheral blood was a consistent feature of Kaposi's sarcoma (KS) patients and whether the viral load correlated with human immunodeficiency virus (HIV) RNA levels, CD4 counts, and/or the HHV-8 seroreactivity. Fifty-four consecutive plasma samples from 14 patients with KS were evaluated for HHV-8 viral load by quantitative real-time PCR. Samples were analyzed at the start of highly active antiretroviral therapy (HAART) and at different intervals during treatments. The median HHV-8 DNA load before HAART treatment was 8,998 (ranging from 170 to 40,100) copies/ml and 12,270 (ranging from 40 to 142,575) copies/ml during HAART. There were both increasing and decreasing trends. There was an association between HHV-8 DNA and HIV RNA viral loads (odds ratio [OR] = 5.40; 95% confidence interval [95% CI], 1.54 to 18.98) and between HHV-8 viral load and CD4 cell counts (OR = 7.24; 95% CI, 1.30 to 40.35). High HHV-8 viral load was also correlated with the titers of antibodies to the lytic HHV-8 antigen detected with immunofluorescence (P < 0.01), but not with antibodies to the latent HHV-8 antigen. In conclusion, we found that HHV-8 viremia in KS is associated with HIV viral load, CD4 cell counts, and lytic HHV-8 serological reactivity. HHV-8 viral load monitored by real time PCR might be useful for determination HHV-8 viral load during the follow-up of KS patients.

AIDS-Related Opportunistic Infections↗

PubMed2006

Factors influencing breast milk HIV RNA viral load among Zambian women.

In a longitudinal cohort study we investigated factors contributing to breast milk HIV RNA viral load among lactating women in Lusaka, Zambia. Detailed data from 135 HIV-infected women were collected by questionnaires concerning postpartum maternal and infant health and infant feeding practice. Maternal blood was collected during pregnancy and at 6 weeks postpartum. Milk samples collected from each breast at 10 days and 6 weeks postpartum plus a subset collected at other time points were analyzed for HIV RNA viral load. Increased milk viral load was associated in univariate analyses with maternal symptoms of poor health, raised plasma alpha(1)-acid glycoprotein (AGP) at week 6, raised milk sodium/potassium (Na/K) ratio, postpartum need for antibiotics, preterm delivery, and low birth weight infants. In a multiple regression 49% of variability in mean milk viral load was explained by milk Na/K ratio and need for antibiotics, with borderline contributions from plasma AGP and plasma viral load. Maternal blood hemoglobin or receipt of iron supplements and infant feeding variables such as changing the infant's diet by moving from exclusive to nonexclusive breastfeeding or adding solid foods were not associated with milk viral load. Thus maternal health was the main factor contributing to milk viral load. The lack of effect of feeding practices on milk viral load and the previously determined association of poor maternal health with reduced duration of exclusive breastfeeding in this cohort suggest the relation between exclusive breastfeeding and decreased HIV transmission may be secondary to poor maternal health.

Adult↗

PubMed1999

Retrospective analysis of viral load and SIV antibody responses in rhesus macaques infected with pathogenic SIV: predictive value for disease progression.

The prognostic significance of SIV plasma viral load in macaques has not been well established, primarily owing to the small numbers of animals in experimental groups. In addition, many investigators have noted that animals that fail to develop an anti-SIV humoral response develop disease rapidly. To establish the prognostic significance of viral load and seroconversion, we retrospectively analyzed the plasma viral load and serology data from 74 rhesus macaques infected with SIVmac. Viral load was analyzed at three time points: in the peak (days 7-21), acute (days 30-55), and chronic (days 80-100) periods postinfection. High viral load in the peak and acute phases was associated with more rapid development of disease (p = 0.0086, p = 0.0004, respectively). We defined clinical outcome as rapid ( <1 year) or slow (> or =1 year) progression. When peak and acute viral loads were analyzed together, acute viral load was more strongly associated with rapid progression (p = 0.03). Slow progression was strongly associated with chronic viral loads below the median of 3.47 x 10(5) RNA copies/ml. Despite having preexisting anti-SIV antibodies, 7 of 23 vaccinated animals were rapid progressors. All unvaccinated animals that mounted a humoral response to SIV were slow progressors. Animals that received a formalin-fixed, microencapsulated SIV vaccine prior to infection had lower peak viral loads than unvaccinated animals (p = 0.0005), but developed disease at the same rate. Overall, in naive animals, viral load is an important prognostic indicator of the disease progression rate. We found that viral load measured during the chronic phase (days 80-100) of infection was most closely associated with disease progression. We also found that a formalin-fixed, microencapuslated SIV vaccine reduced viral load without affecting clinical outcome. This latter finding may have implications for the evaluation of HIV-1 human vaccine trials.

Animals↗

PubMed1995

Correlation between viral load measurements and outcome in clinical trials of antiviral drugs.

BACKGROUND: As evidence is emerging that viral load can be correlated with clinical outcome in HIV-infected patients, new assays have been developed to measure viral load in vivo. These include biological assays that involve assessment of viral load by limiting dilution cultures of plasma or peripheral blood mononuclear cells and nucleic acid-based amplification techniques including RNA-based polymerase chain reaction and branched-chain DNA signal amplification. VIRAL LOAD QUANTITATION IN CLINICAL INVESTIGATION: The advent of RNA polymerase chain reaction and branched-chain DNA technology has allowed direct measurements of plasma HIV RNA levels. Several studies, including AIDS Clinical Trials Group (ACTG) 116B/117, the Veterans Administration Study VA CSP 298 and, more recently, ACTG 175, have indicated that viral load monitoring is a powerful predictor of disease progression and clinical outcome. A change in viral load of approximately 1 log unit is associated with an increase in CD4 cell count of about 85 cells/mm3. CONCLUSIONS: Viral load monitoring, particularly when combined with other laboratory markers, can be correlated with clinical outcome. In routine clinical practice, viral load monitoring may be used to assess the need for changes in antiretroviral therapy, allowing individualized therapy. Viral load monitoring may also reduce the time needed for the clinical development of new therapeutic approaches, allowing earlier patient access to promising anti-HIV therapies.

Antiviral Agents↗

PubMed1996

Predictive value of viral load measurements in asymptomatic untreated HIV-1 infection: a mathematical model.

OBJECTIVE: To model the predictive value of viral load measurements in asymptomatic patients with HIV-1 infection, who have CD4 cell counts > 500 x 10(6)/l and no prior antiretroviral therapy, when the time of seroconversion and the prior levels of viremia are unknown. DESIGN: A mathematical model was constructed for the changes in HIV RNA load over time based on data from cohorts of HIV-infected patients followed since the time of seroconversion. METHODS: For different values of viral load, the time to progression to AIDS or an equivalent state [progression to AIDS equivalent (PAE)] was calculated using a wide range of estimates for the time since seroconversion and the rate of change of the viral load over time. RESULTS: In the absence of antiretroviral treatment, patients with a viral load of 10(5) copies/ml serum are at risk for PAE in less than 3 years (0-3 years) and patients with a viral load half a log higher are at risk in less than 1 year. In contrast, patients with a viral load of 10(4.5) have at least 1.9 years and may have up to 8 years before risk of PAE. Patients with a viral load of 10(4) RNA copies/ml have at least 2.8 years and may have up to 19 years before risk of PAE. The rate of change of the viral load was an important predictor of outcome; the time since seroconversion had only a minor effect. CONCLUSIONS: The viral load in the plasma or serum has predictive value even if the time of seroconversion is unknown. The rate of change of viral load over time may also be an important predictive factor. Serial measurements of viral load over time may provide therapeutic guidance.

CD4 Lymphocyte Count↗

PubMed1998

Amplicor HIV monitor, NASBA HIV-1 RNA QT and quantiplex HIV RNA version 2.0 viral load assays: a Canadian evaluation.

BACKGROUND: HIV-1 viral load quantitation is now recognized as a useful tool to monitor the efficiency of antiviral treatment and a powerful predictor of disease outcome. Three HIV-1 viral load quantitation methods have been currently available as commercial kits in Canada since 1996. OBJECTIVE: To evaluate the ability to quantify HIV-1 RNA in plasma of the Amplicor HIV Monitor Test, the NASBA HIV-1 RNA QT Assay and the Quantiplex HIV RNA Assay, version 2.0, at comparable lower detection limits. STUDY DESIGN: Blood was collected from 50 HIV-1-infected patients at various stages of infection and therapy. CD4+ cell count were estimated by flow cytometry. Plasma was isolated and tested in duplicate on four occasions using viral load kits from a single lot. HIV RNA data, performance, sensitivity and intra- and inter-assay variability were compared. RESULTS: RNA could be quantified in 33 patients by each technique. An inverse correlation was observed between viral load level and CD4+ cell counts in patients with counts below 200. Monitor could detect RNA in 94% of patients, but it showed the greatest variability and failure rate. Quantiplex 2.0 could detect HIV-1 RNA in 78%, and NASBA in 88% of the patients at theoretically equivalent lower detection limits, suggesting that the detection limit of Quantiplex 2.0 may be higher than 500 HIV-1 RNA copies per ml. NASBA had the fewest invalid tests and good reproducibility, comparable to that of Quantiplex 2.0. The mean values from NASBA and Monitor were the most similar but the best correlation was observed between Monitor and Quantiplex 2.0 results. CONCLUSIONS: Monitor, NASBA and Quantiplex results were comparable, although those obtained by Quantiplex were significantly lower. Performing this study at comparable detection limits showed that the detection limit of Quantiplex 2.0 may be higher than stated by the manufacturer.

Adolescent↗

PubMed2004

Longitudinal comparison between plasma and seminal HIV-1 viral loads during antiretroviral treatment.

This study was designed to investigate the impact of anti-retroviral therapy on both plasma and seminal HIV-1 viral loads and the correlation between viral loads in these compartments after treatment. Viral load, CD4+ and CD8+ T-cell counts were evaluated in paired plasma and semen samples from 36 antiretroviral therapy-naive patients at baseline and on days 45, 90, and 180 of treatment. Slopes for blood and seminal viral loads in all treated patients were similar (p = 0.21). Median HIV-1 RNA titers in plasma and semen at baseline were 4.95 log10 and 4.48 log10 copies/ml, respectively. After 180 days of therapy, the median viral load declined to 3.15 log10 copies/ml (plasma) and 3.2 log10 copies/ml (semen). At this timepoint 22 patients presented HIV-1 viral load below 400 copies/ml in either plasma or semen, but only 9 had viral loads below 400 copies/ml in both compartments.

Adult↗

PubMed2006

Human T-lymphotropic virus type 1-associated myelopathy/tropical spastic paraparesis: viral load and muscle tone are correlated.

Human T-lymphotropic virus type 1 (HTLV-1) infections are associated with varying degrees of HTLV-1 viral load and spasticity. Increased viral load is associated with higher risk of developing HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP). The authors performed a cross-sectional study of 24 people with HAM/TSP in Lima, Perú, to determine if higher HTLV-1 viral load was correlated with increased muscle tone, measured with a device providing quantitative spasticity assessment (QSA). Median HTLV-1 viral load was 17.0 copies/100 peripheral blood mononuclear cells and QSA value was 39.9 Newton-meters/radian. HTLV-1 viral load was significantly correlated with QSA value (Spearman rho = .48, P = .02), suggesting viral load may play a role in expression of symptomatic neurologic disease. Longitudinal studies are needed to determine if treatments that reduce viral load will reduce muscle tone.

Cross-Sectional Studies↗

PubMed1999

Misdiagnosis of HIV infection by HIV-1 plasma viral load testing: a case series.

BACKGROUND: The availability of sensitive assays for plasma HIV viral load and the trend toward earlier and more aggressive treatment of HIV infection has led to the inappropriate use of these assays as primary tools for the diagnosis of acute HIV infection. OBJECTIVE: To describe limitations in the use of plasma viral load testing for the diagnosis of HIV infection. DESIGN: Case series. SETTING: Academic medical centers in Providence, Rhode Island, and Worcester, Massachusetts. PATIENTS: Three persons in whom HIV infection was falsely diagnosed by plasma viral load testing. MEASUREMENTS: Laboratory measures and clinical outcomes. RESULTS: Two cases of false-positive results obtained by using branched-chain DNA plasma viral load assays and one case of a false-positive result obtained by using reverse transcriptase-polymerase chain reaction plasma viral load assay are reported. All three plasma viral load tests yielded positive results with low values (1254 copies/mL, 1574 copies/mL, and 1300 copies/mL). Infection with HIV was initially diagnosed in all three patients, but each patient subsequently tested negative by HIV-1 enzyme-linked immunosorbent assay and repeated plasma viral load testing. CONCLUSION: Physicians should exercise caution when using plasma viral load assays to detect primary HIV infection, particularly when the pretest probability of infection is low.

Adult↗

PubMed2003

Growth, survival and viral load in symptomatic childhood human immunodeficiency virus infection.

BACKGROUND: The relationships among weight and height growth, viral load and survival in HIV-infected children remain unclear. OBJECTIVES: To determine whether weight or height growth velocity independently predicts survival and to investigate associations of weight, height and head circumference growth velocities with viral loads in symptomatic HIV-infected children. METHODS: We analyzed data from a prospective antiretroviral study utilizing clinical endpoints (PACTG 152). Viral load [log(RNA PCR)] and anthropometric measures 12 weeks before and after viral load measures were available in 494 of 831 children. Interval changes during 24 weeks in z-scores for weight-for-age (DeltaWAZ), height-for-age (DeltaHAZ) and head circumference-for-age (DeltaHCZ) were used as growth velocity surrogates. Logistic regression determined whether DeltaWAZ and/or DeltaHAZ correlated with survival when age, viral load and CD4+ cell count were controlled. Bivariate analysis assessed correlation among viral load and DeltaWAZ, DeltaHAZ and/or DeltaHCZ. RESULTS: Survival related significantly to height growth velocity (P = 0.03, n = 434) but not to weight growth velocity (P = 0.84, n = 446) or head circumference growth velocity (P = 0.67, n = 148). Viral load was not significantly associated with changes in weight-, height-, or head circumference-for-age z scores (P = 0.86, n = 235; P = 0.07, n = 226; and P = 0.09, n = 165, respectively) in children <30 months of age or with changes in weight- or height-for-age z scores (P = 0.27, n = 259; P = 0.11, n = 251) in older children. CONCLUSIONS: Height growth velocity predicted survival independently of age, viral load and CD4+ cell count. Weight, height and head circumference growth velocities were not significantly associated with viral load in symptomatic HIV-infected children in this large prospective trial of nucleoside reverse transcriptase therapy.

Adolescent↗

PubMed2000

High viral eradication with a daily 12-week natural interferon-beta treatment regimen in chronic hepatitis C patients with low viral load. IFN-beta Research Group.

Virological sustained response (SR) is achieved in 31-49% of patients with chronic hepatitis C with combination therapy using interferon (IFN)-alpha and ribavirin for 24-48 weeks. However, as a period of 24-48 weeks is a burden for patients, we investigated the effect of daily intravenous administration of natural IFN-beta for 12 weeks in this study. In all, 112 patients were enrolled and received a daily administration of 6 MU of natural IFN-beta intravenously for 12 weeks. Serum HCV-RNA before treatment was assessed by the competitive reverse-transcription polymerase chain reaction assay. The patients were divided into two groups according to pretreatment viral load: the low viral load group (N = 25, <6.3 x 10(5) copies/ml), and the high viral load group (N = 87, > or =6.3 x 10(5) copies/ml) who were additionally administered IFN-beta thrice weekly for subsequent 14 weeks at the patients' request. Virological SR was obtained in 37% (41/112) of all the patients; 88% of those with a low viral load, and 22% of patients with a high viral load. Virological SR was attained in 21% of patients with HCV subtype 1, and in 67% of those with subtype 2a. In patients with HCV subtype 1b, virological SR was obtained in patients with the mutant-type (> or =4 amino acid mutations in the NSSA2209-48) having a low viral load (4/4), but not in those having a high viral load (0/3). The results suggest that a daily intravenous administration of natural IFN-beta for 12 weeks showed high therapeutic efficacy in patients with a low viral load despite the shorter treatment period and that the therapeutic efficacy depends on viral load rather than on the number of NS5A2209-48 amino acid mutations.

Adolescent↗

PubMed1999

Plasma HIV viral load in patients with hemophilia and late-stage HIV disease: a measure of current immune suppression. Multicenter Hemophilia Cohort Study.

BACKGROUND: For patients infected with HIV, plasma HIV viral load in early disease predicts long-term prognosis. However, the implications of viral load measurements late in HIV disease are uncertain. OBJECTIVE: To evaluate the relation between plasma HIV viral load and subsequent risk for disease progression in patients with late-stage HIV disease. DESIGN: Retrospective cohort study. SETTING: 16 treatment centers for patients with hemophilia. PATIENTS: 389 patients with hemophilia and late-stage HIV disease (CD4 count < 200 cells/mm3). MEASUREMENTS: Plasma HIV viral load was measured at baseline. Patients were followed for AIDS-related illnesses (primary outcome) and, specifically, Pneumocystis carinii pneumonia (secondary outcome). RESULTS: HIV viral load strongly predicted AIDS-related illness. For patients with viral loads less than 4.00 log10 copies/mL, the 1-year actuarial risk was 0% and the 5-year risk was 25%. For patients with viral loads of at least 6.00 log10 copies/mL, the 1-year actuarial risk was 42% and the 5-year risk was 78%. A linear relation existed between viral load and risk for AIDS-related illness (hazard ratio, 2.37 per 1og10 copies/mL; P < 0.001). In addition, viral load most strongly predicted risk for illness immediately after viral load testing; this predictive relation attenuated over time (P = 0.002). These findings changed little after adjustment for CD4 cell counts that were updated during follow-up. In the first year after viral load was measured, it predicted occurrence of P. carinii pneumonia (hazard ratio, 4.69 per 1og10 copies/mL; P < 0.001). CONCLUSIONS: In patients with hemophilia and late-stage HIV disease, viral load predicts disease progression independently of CD4 cell counts. Because viral load most strongly predicts progression immediately after load is measured, it seems to reflect the current level of immunosuppression.

AIDS-Related Opportunistic Infections↗

PubMed1993

Determination of plasma viral load in HIV-1 infection by quantitative competitive polymerase chain reaction.

OBJECTIVES: To better characterize viral load profiles through the course of HIV-1 disease and in response to treatment, and to further evaluate quantitative competitive polymerase chain reaction for measurement of viral load, we extended our comparative evaluation of this and other viral load measurements to a total of 118 patients, representing all stages of HIV-1 disease. DESIGN: For cross-sectional analysis across the spectrum of HIV-1 disease, plasma viral load was evaluated in 112 HIV-1-infected patients by quantitative competitive polymerase chain reaction analysis, plasma p24 antigen assay, plasma immune complex-dissociated p24 antigen assay and an endpoint dilution viral culture. Longitudinal specimens from six additional patients were analyzed, extending from the time of presentation with symptomatic acute HIV-1 infection through up to more than 2 years of follow-up. Longitudinal specimens were also studied for three patients over the period of initiation of zidovudine treatment, for 6 weeks of treatment and following temporary withdrawal of the treatment. METHODS: All measurement techniques were assessed in replicate aliquots of plasma. RESULTS: Quantitative competitive polymerase chain reaction was the most sensitive measure of viral load, and was best correlated with CD4+ T-cell counts. In longitudinally studied patients, this technique also allowed measurement of plasma virus levels throughout the period of follow-up, even when culture and p24 assays became negative following resolution of acute HIV-1 infection. The quantitative competitive polymerase chain reaction was also able to detect rapid and substantial changes in viral load associated with initiation and temporary withdrawal of antiviral treatment. CONCLUSIONS: The quantitative competitive polymerase chain reaction is promising as a sensitive and accurate method for measuring plasma viral load in HIV-1-infected patients, and is useful for following changes in viral load over the natural history of infection and following treatment intervention. The technique is particularly useful for patients with > 200 x 10(6) CD4+ T cells/l, in whom other viral markers are typically negative.

Biomarkers↗

PubMed2004

[Factors predicting detectable viral load in patients with highly active antiretroviral treatment].

BACKGROUND AND OBJECTIVE: Knowledge of the variables predicting detectable viral load in patients with highly active antiretroviral treatment. PATIENTS AND METHOD: Observational and cross-sectional study in patients with antiretroviral treatment receiving two nucleoside reverse transcriptase inhibitors and one protease inhibitor. Several sociodemographic and clinic variables were registered. Two models were designed in order to assess the adherence: I. combining self-report and pharmacy criteria, and II. including drug plasma levels in adherent patients with the two former criteria and detectable viral load. Logistic regression analysis with variables found to be associated with detectable viral load in the univariate analysis, diagnostic algorithm and ROC statistics were performed in order to select the best model to predict detectable viral load. RESULTS: Among of 136 patients studied, 39 (28.7%) had detectable viral load. Patients less than 35 years old (OR = 2.68), intravenous drug users or heterosexual contacts as the way of HIV infection (OR = 6.42), patients not fully convinced of the capacity of mutation of the HIV by poor adherence (OR = 3.25) and patients considered non-adherent according to the drug plasma levels criteria (OR = 6.91) had more frequently detectable viral load. The best model to predict detectable viral load would include patients considered non-adherent according to the two models used, and moreover, patients where another of the factors of risk were detected; the prevalence of detectable viral load in these was of 10% versus 43%. CONCLUSION: Adherence to HAART is a key factor to predict detectable viral load, specially in young patients, infected by intravenous drug use or heterosexual contacts, and patients not convinced of the importance of the adherence.

Adolescent↗

PubMed2002

Oral candidiasis as a clinical marker related to viral load, CD4 lymphocyte count and CD4 lymphocyte percentage in HIV-infected patients.

BACKGROUND: High viral load is currently considered to be one of the main indicators of the progression of HIV-induced immunodepression, but few studies have analysed its relationship to the presence of oral candidiasis (OC). The aim of this cross-sectional study is to analyse the relationship between viral load, total CD4 lymphocyte count, and percentage of CD4 lymphocytes to the occurrence of OC. METHODS: The present cross-sectional study included 156 HIV-infected patients seen at a clinic for sexually transmitted diseases and HIV. We assessed the presence or absence of OC, and microbiological samples were obtained from the palatine mucosa and dorsal tongue for a smear stained with KOH (potassium hydroxide) and culture on Sabouraud's dextrose agar in all patients. Viral load was determined by quantification of viral RNA in peripheral blood with a minimum detectable level of 500 RNA copies/ml. CD4+ counts/CD4+ percentage were categorized as <200/<14%, 200-499/14-28%, and >500/>29%, and HIV viral loads were categorized as <500, 500-10,000, >10,000 copies/ml. RESULTS: Thirty-eight percent (37.8%) of the patients had OC. Patients with CD4+ lymphocyte counts below 200 x 10(6)/l and CD4+ percentages below 14% showed a significantly higher frequency of OC (57.9% and 48.0%, respectively). Patients with a viral load over 10,000 copies/ml also had OC more frequently (44.8%). In the multiple logistic regression analysis, OC showed a statistically significant association with high viral load [>10,000 vs <500, odds ratio (OR)=11.4], low percentage of CD4+ lymphocytes (<14% vs >28%, OR=5), and injection drug use (IDU vs heterosexual transmission, OR=10.2). In HIV-infected patients, high viral load was associated with more frequent OC, regardless of CD4+ lymphocyte level. CONCLUSIONS: These findings suggest that oral candidiasis could be a useful clinical marker of patients with high viral load. In view of these results, emphasis should be placed on the importance of systematic examination of the oral cavity in all medical follow-up examinations of HIV-infected patients.

AIDS-Related Opportunistic Infections↗

PubMed1998

Prognostic indicators for AIDS and infectious disease death in HIV-infected injection drug users: plasma viral load and CD4+ cell count.

CONTEXT: Plasma human immunodeficiency virus type 1 (HIV-1) viral load and CD4+ cell count are used to predict prognosis of persons infected with HIV. However, whether combining these markers improves prognostic accuracy and whether they predict prognosis for injection drug users (IDUs) and nonwhite persons infected with HIV has not been extensively investigated. OBJECTIVE: To evaluate plasma viral load and CD4+ cell count as prognostic indicators for the acquired immunodeficiency syndrome (AIDS) and infectious disease deaths. DESIGN: Cohort study initiated in 1988 and 1989 with follow-up for up to 7.9 years. PARTICIPANTS: Injection drug users infected with HIV recruited from the community in Baltimore, Md. MAIN OUTCOME MEASURES: Plasma HIV-1 RNA and CD4+ cell count measured at baseline compared with time to first clinical AIDS diagnosis and death due to an infectious disease. RESULTS: Of 522 subjects, 96% were African American, 80% were male, 96% injected drugs within the past 6 months, and the median age was 33 years. A total of 146 cases of AIDS and 119 infectious disease deaths were seen during a median follow-up period of 6.4 years. Time-fixed baseline levels of viral load and CD4+ cell count were independent predictors of progression to AIDS and infectious disease deaths, but in proportional hazards models, viral load had better predictive value than CD4+ cell count. Kaplan-Meier analysis of time to AIDS and to infectious disease deaths by viral load (<500, 500-9999, 10000-29 999, > or =30000 copies/mL) at 3 levels of CD4+ cell count (<0.20, 0.20-0.49, and > or =0.50x10(9)/L [<200,200-499, and > or =500/microL]) was reduced to a 5-stage classification scheme using a backward stepwise regression procedure. The 5-year cumulative probabilities for AIDS and infectious disease deaths ranged from 0% and 0%, respectively, for group I (viral load, <500 copies/mL; CD4+ cell count, 0.50x10(9)/L) to 81.2% and 76.1% respectively, for group V (viral load, > or =10000 copies/mL; CD4+ cell count, 0.20x10(9)/L). CONCLUSIONS: In this study, plasma HIV-1 viral load independently and in combination with CD4+ cell count measurements provided powerful prognostic information for progression to AIDS and death caused by infectious disease in a population of predominantly African American IDUs. Combining categories of both markers provided a simple method for prognostically staging HIV disease.

AIDS-Related Opportunistic Infections↗