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Results for “Viral Load”

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PubMed2004

Differences in HIV-2 plasma viral load and immune activation in HIV-1 and HIV-2 dually infected persons and those infected with HIV-2 only in Abidjan, Côte D'Ivoire.

OBJECTIVE: To determine whether blood plasma levels of HIV-2 RNA viral loads and immune activation markers differ between persons infected with HIV-2 only and those dually infected with HIV-1 and HIV-2. METHODS: Between September 1996 and February 2000, we collected, analyzed and compared levels of HIV-2 RNA in plasma and immune activation markers among 52 persons infected with HIV-2 alone and 75 with confirmed dual infection. We also compared viral load and immune activation in patients who were infected with HIV-1 only and those who were dually infected. RESULTS: When we conducted a CD4 T-cell count-stratified multivariate analysis of HIV-2 viral load, controlling for difference in CD4 T-cell counts, age and sex: at < 200 x 10 CD4 T cells/l, HIV-2 viral load was 2.0 log10 copies/ml lower in dually infected patients than in HIV-2 only patients (P < 0.0001). At CD4 T-cell counts between 200 x 10 and 500 x 10/l, HIV-2 viral load was 0.3 log10 copies/ml lower in dually infected patients (P = 0.45). However, at CD4 T-cells counts > 500 x 10/l, HIV-2 viral load was 0.9 log10 copies/ml higher in dually infected patients (P < 0.0001). Dually infected persons with undetectable HIV-2 viral loads had significantly higher median levels of CD8 T cells expressing CD38 (P < 0.001) and HLA-DR (P = 0.01) than HIV-2 only infected patients. CONCLUSION: These results suggest that in dual infection, the level of HIV-2 replication depends on the immune status of the patients, with HIV-1 out-replicating HIV-2 as disease progress.

Adult↗

PubMed2002

Quantitation of viral load in neonatal herpes simplex virus infection and comparison between type 1 and type 2.

Neonatal herpes simplex virus (HSV) infection is a severe disease with high mortality and morbidity in spite of the development of effective anti-viral therapies. The viral load in neonatal herpes simplex virus (HSV) infection was measured retrospectively in 37 patients. HSV DNA copy numbers in serum and cerebrospinal fluid (CSF) were quantified using a real-time PCR assay. Patients with disseminated infection had a higher viral load in their sera. whereas patients with central nervous system (CNS) infection exhibited a higher viral load in the CSF. The viral load was significantly higher in the serum of patients who died later. Interestingly, patients with HSV type-2 infection exhibited more CNS involvement and neurological impairment, together with a high viral load in the CSF, than did HSV type-1 patients. These results suggest that quantitation of HSV viral load may be useful for assessing the prognosis, and may provide additional information for the management of neonatal HSV infection.

Central Nervous System Viral Diseases↗

PubMed2003

Whole blood versus plasma spots for measurement of HIV-1 viral load in HIV-infected African patients.

The increasing availability of antiretroviral drugs to HIV-infected populations in developing countries highlights the need to develop field-friendly practical methods for HIV-1 viral load measurements to monitor the effects of treatment. We compared use of whole-blood spots versus plasma dried on filter paper to quantify HIV-1 viral load in 51 African patients with HIV-1. The mean log10 HIV-1 viral loads were 4.22 for dried plasma spots (DPS) and 4.20 for dried whole-blood spots (DBS). The difference between the pairs of log10 viral load for DPS and DBS were significantly correlated with their mean (Spearman's r=0.31, p=0.03). This correlation between the difference and mean of viral load was no longer evident for values of log10 DPS that were less than 5 (r=0.01, p=0.93). For the 38 paired values with log10DPS of less than 5, the mean difference (log10DPS-log10DBS) was -0.04 (SD 0.29). Dried whole blood stored on filter paper at room temperature shows potential as a field-friendly alternative to plasma for measurement of HIV-1 viral load.

Adult↗

PubMed1999

[Primary infection in vertically infected HIV-1 infants: biological characteristics of isolated virus, viral load and CD4 t-lymphocytes].

OBJECTIVE: Our aim was to study the relationship between virological and/or immunological markers during the first month of life in vertically HIV-1 infected infants without prior antiviral treatment. PATIENTS AND METHODS: Thirty HIV-1 infected infants that had not received prior antiviral therapy, nor had their mother during pregnancy, were studied. Viral load was quantified using standard molecular assays. Viral isolation and phenotype were carried out by using viral co-cultures. Subpopulations of lymphocytes were determined by flow cytometry. RESULTS: We have found an inverse correlation between log10 CD4+ cells/mm3, as well as CD4+ percentage with log10 viral load, with a slope of -0.266 (CI95%: -0.459 to -0.074) and -6.648 (CI95%: -12.815 to -0.471), respectively. When the influence of viral phenotype on the log10 viral load or the percent of CD4+ T cells standardized according to age (Z-score) with the log10 of the viral load was determined, it was found that infants having syncytium inducing (SI) virus had 12.355% (CI95%: 2.336 to 22.373) less CD4+ cells and 4.530 standard deviations (IC95%: 0.448 to 8.613) than infants with non syncytium inducing (NSI) isolates. CONCLUSIONS: Our results suggest that a particular biological phenotype of viral isolates (SI and those with rapid/high replication) and high plasma viral loads have a statistically significant tendency to be associated. Viral load is the marker that shows the best inverse correlation with the level of CD4+ cells normalized according to the infant's age. This correlation shows a different value in infants with SI and NSI isolates.

CD4-Positive T-Lymphocytes↗

PubMed2003

Sequence elements correlating with circulating viral load in genotype 1b hepatitis C virus infection.

The correlation between hepatitis C virus (HCV) genomic sequences and circulating HCV RNA levels was assessed to investigate the genetic elements affecting viral load. The interferon sensitivity-determining region (ISDR) sequence and the serum viral load were strongly correlated in 226 patients examined. Analysis of the entire HCV genome from six patients (three with a high and the others with a low viral load) with similar ISDR sequences identified several candidate residues associated with viral load. The amino acid (aa) sequences of these candidate residues and flanking regions in 67 additional patients revealed that only the residue at aa 962 varied significantly between the HCV patients with low and high serum loads (P=0.042). At this position, alanine was observed more frequently in the patients with a high viral load. In conclusion, our results strongly suggest that serum HCV RNA loads are inversely correlated with amino acid substitutions in the ISDR, and aa 962 was identified as a possible second determinant of serum HCV RNA load.

Amino Acid Sequence↗

PubMed2003

Comparison of different HCV viral load and genotyping assays.

BACKGROUND: We report an interlaboratory comparison of methods for the determination of hepatitis C virus (HCV) serum load and genotype between a recently, established molecular laboratory at the Alaska Native Medical Center (ANMC) and two independent laboratories using different assays. At ANMC, a Real-time quantitative RT-PCR amplification methodology (QPCR) has been developed in which HCV viral loads are determined by interpolation of QPCR results to those of standards calibrated to the World Health Organization (WHO) First International Standard for HCV. HCV genotype is subsequently determined by direct sequencing of the DNA fragment generated from the QPCR assay. OBJECTIVES AND STUDY DESIGN: The above methods were statistically compared to results obtained for the same patient sera by two independent laboratories using different commercially available viral load assays; Quantiplex HCV RNA (Bayer Diagnostics) and Amplicor HCV Monitor (v 2.0) (Roche Molecular Systems), as well as two different genotyping assays; restriction fragment length polymorphism (RFLP) and INNO-LiPA HCV II (Innogenetics). RESULTS: ANMC's Real-time QPCR HCV viral load results compared moderately well with those obtained by the Quantiplex HCV RNA method (R2=0.3813), and compared quite well with recent lot numbers of Amplicor HCV Monitor in which viral loads are derived in IU/ml (R2=0.6408), but compared poorly with earlier lot numbers of Amplicor HCV Monitor in which viral loads were derived in copies/ml (R2=0.0913). The ANMC direct sequencing method for genotype determination compared moderately to very well with both the RFLP (84-86%) and INNO-LiPA (85-97.5%) methods. CONCLUSIONS: These viral load comparisons highlight the discrepancies that may occur when patient HCV viral loads are monitored using different types of assays. Comparison of HCV genotype by different methods is more reliable statistically and important clinically for predicting probability of response to antiviral therapy. However, viral loads are important for monitoring response once therapy has begun.

Evaluation Studies as Topic↗

PubMed2005

Integrated human papillomavirus types 52 and 58 are infrequently found in cervical cancer, and high viral loads predict risk of cervical cancer.

OBJECTIVE: The aim of this prospective study was to analyze whether integration or high viral loads of human papillomavirus (HPV) is essential for malignant transformation of HPV types 52 and 58 as well as types 16 and 18. METHODS: Cervical swabs from 178 consecutive patients, including 81 with invasive cervical cancers and 97 with cervical intraepithelial neoplasias (CIN) II-III, were collected and examined to determine the physical status and viral load of HPV types 16, 18, 52 and 58 DNA using genechip and real-time PCR (polymerase chain reaction) analysis. RESULTS: In cervical cancer patients, the integrated form of HPV 52 and 58 DNA was found in 25.0% and 12.5% of swabs, respectively; while HPV16 and 18 DNA was found in 82.6% and 100% of swabs, respectively (P < 0.01, for pair-wise comparison of types 16, 18 versus types 52, 58). The viral loads reflected by the amount of E6 for HPV 16, 18, or 52 were significantly increased in invasive cervical cancer compared to CINII-III (P = 0.022 for type 16, P = 0.003 for type18, and P = 0.001 for type 52, respectively). Area under the receiver operating characteristic (ROC) curve for cervical cancer versus CIN II-III was 73.8%, 92.9%, and 88.5% for HPV 16, 18, and 52, respectively, indicating that real-time PCR had good diagnostic value in differentiating cervical cancer from CIN II-III. CONCLUSIONS: Infrequent integration of HPV 52 and 58 DNA in cervical cancer suggests that it is not prerequisite for progression to cervical cancer. High viral loads (E6) of HPV 16, 18, and 52 DNA may be predictive of the transition of CIN II-III to cervical cancer. Our results indicate that both viral DNA physical status and viral loads of HPV are important factors in the carcinogenesis of different HPV types.

DNA, Viral↗

PubMed1998

Do viral load and CD8 cell count at initiation of tritherapy influence the increase of CD4 T-cell count?

BACKGROUND: Tritherapies including protease inhibitors improve clinical status and usually increase CD4 T cell count. However, the dissociation between the marked decreases in viral load and the incomplete restoration of CD4 cell counts with a three-drug combination has been reported. We assessed this potential difference among our patients. METHODS: Patients were enrolled when a protease inhibitor was prescribed to them for the first time. Using a computerized medical record (ADDIS), we retrospectively assessed a potential relationship between the increase in CD4 T cells (deltaCD4) at M3, M6 and variables including sex, age, CDC staging, protease inhibitor, prior antiviral therapy, CD8 and viral load at baseline. We used Epi-Info 6.4 and BMDP software. RESULTS: Data were analyzed on 154 patients. The median CD4 T cell count was 157 at baseline, 215 at month 3 and 202 at month 6. The median viral load was 52000 copies at baseline, 530 at month 3 and 500 at month 6. In a univariate analysis, a significant relationship was found between deltaCD4 and CD8 at baseline. A statistically significant negative correlation appeared between the CD8 cell count at baseline and deltaCD4 at M6 (r=-0.28, Pearson). Moreover, we found that there also was a relationship between deltaCD4 and viral load at baseline. There was a correlation between deltaCD4 at M6 and the viral load at M0 (r=0.37, Pearson). In a multiple regression model, after CD8 count at baseline had been accounted for, we found a significant correlation between deltaCD4 and viral load at baseline (multiple r=0.33 at M3, and 0.40 at M6). CONCLUSIONS: Patients with a low viral load do not benefit from as great an increase in CD4 T cell count as others when they receive a tritherapy including protease inhibitors. These results suggest that another mechanism rather than direct viral pathogenicity leads to CD4 T cell destruction. This mechanism may not be efficiently stopped by antiviral therapy, especially protease inhibitors.

Adult↗

PubMed2001

HLA class II genes determine the natural variance of hepatitis C viral load.

The aim of this study was to investigate the relationship between human leukocyte antigen (HLA) class II genes and the natural fluctuations in hepatitis C viral load in a homogeneous patient population. The study group consisted of 57 viremic (hepatitis C virus [HCV] 1b) women for whom HLA class II DRB1 and DQB1 haplotyping, virologic, histologic, and biochemical markers of disease activity were available. All patients were infected with HCV 1b from the same source of hepatitis C-contaminated anti-D immunoglobulin during the period from May 1977 to November 1978. The mean slope of change of viral load was 0.34 (SD +/- 0.73) log(10) viral copies/mL/year, which is significantly different from zero, P < 10(-9). Analysis of the relationship between the slope of change of viral load and HLA class II haplotype indicated a significantly different slope of change of viral load between the alleles of (1) DRB1(*)15 and DRB1(*)0701, and (2) DQB1(*)0602 and DQB1(*)0201, P(c) =.036 and P(c) =.026 after Bonferroni correction for multiple comparisons, respectively. Significant differences for grade and stage of disease at liver biopsy were observed for DQB1(*)0501 and DQB1(*)0201 alleles; P =.019, r(s) =.64, and P =.047, r(s) =.57, respectively. In addition, significant differences in stage of disease were found to exist between DRB1(*)13 and DRB1(*)0701, P =.031, r(s) = -.71. Our results define an association between the slope of change of viral load and HLA class II haplotype in patients infected with genotype 1b of HCV. This suggests a role for host immunogenetic factors in HCV infection in this homogeneous group.

Adult↗

PubMedDate not supplied

Support group participation, HIV viral load and sexual-risk behavior.

OBJECTIVE: To examine the impact of participation in community-based support groups and human immunodeficiency virus (HIV) viral load on sexual behavior among gay men. METHODS: Using self-administered questionnaires, 46 seropositive support-group participants and 20 seropositive comparison subjects were asked about viral load and frequency of unprotected anal intercourse in 1996 and 1997 following the XI International Conference on AIDS. RESULTS: Support group participants reported less unprotected receptive anal sex at follow-up than did comparison subjects. Overall, study participants with undetectable viral loads reported more unprotected anal intercourse at follow-up than did participants with detectable viral loads. CONCLUSION: Among HIV-seropositive gay men, knowledge of an undetectable viral load may contribute to high-risk sexual-risk behavior.

Adult↗

PubMed1998

Sex differences in HIV-1 viral load and progression to AIDS.

BACKGROUND: Plasma HIV-1 RNA measurements are used for initiation of antiretroviral treatments. Whether the viral-load association with prognosis is similar in women and men is unknown. METHODS: We studied 812 specimens from 650 injection-drug users (IDUs) participating in a continuous observational study of patients based in a community clinic. HIV-1 load was measured by branched-chain DNA on samples from 527 IDUs from the baseline visit, and by reverse-transcriptase PCR and quantitative microculture on samples from 285 IDUs at a follow-up visit 3 years later. FNDINGS: Women had lower median viral-load measurements than men by branched-chain DNA (3365 vs 8907 copies/mL; p=0.001), reverse-transcriptase PCR (45416 vs 93130 copies/mL; p=0.02), and quantitative microculture (5 vs 8 infectious units per million peripheral blood mononuclear cells; p=0.015). This association remained even after adjustment for CD4 cell count, race, and drug use within the previous 6 months. Time to AIDS was statistically similar for men and women in a univariate proportional-hazards model and in a model adjusting for CD4 cell count. Proportional-hazards models showed that women with the same viral load as men had a 1.6-fold higher risk of AIDS (95% CI 1.10-2.32); or, equivalently, that women with half the viral load of men had a similar time to AIDS as men. INTERPRETATION: Although a biological mechanism remains unclear, these data suggest that current recommendations for HIV-1 viral-load thresholds to initiate antiretroviral therapy should be revised downwards for women.

Acquired Immunodeficiency Syndrome↗

PubMed2006

Hepatitis C virus recurrence after liver transplantation: influence of immunosuppressive regimens on viral load and liver histology.

Cyclosporine has recently been reported to produce in vitro suppression of hepatitis C virus replication driven by blockade of cyclophilins, an effect not shown for tacrolimus. However, the clinical consequence of this in vitro finding have not been well studied in vivo. We compared viral load and fibrosis in transplanted patients receiving monotherapy with tacrolimus or cyclosporine. Patients with recurrent hepatitis C after transplantation were selected from two tertiary centers with the following inclusion criteria: monotherapy with tacrolimus or cyclosporine for more than 12 months before viral load measurement, no antiviral treatment, corticosteroids stopped within 12 months after transplantation. HIV, hepatitis B, and active infection by cytomegalovirus were excluded. Patient characteristics, viral load, and fibrosis were compared by univariate analysis between the cyclosporine and tacrolimus groups. Significant variables, viral load, and fibrosis were included in a multivariate model. Sixty-six patients were included, 46 on tacrolimus and 20 on cyclosporine. Fifty-six were male, and the mean age was 55.3 +/- 10.1 years. Fibrosis (Ishak score) was 3.9 +/- 1.9 in the cyclosporine group and 2.7 +/- 1.9 in the tacrolimus group (P = .019). Viral load (log(10)IU/mL) was 5.8 +/- 0.5 and 5.9 +/- 0.5, respectively (P = .7) and time since liver transplantation was 95.3 +/- 47.7 and 41.1 +/- 16.8 months (P = .0001). In the multivariate model, viral load (P = .65) and fibrosis (P = .24) were not significantly different and only time since transplantation remained significant (P = .0001). In conclusion, viral load was not different in patients with tacrolimus as compared with cyclosporine, and the lower fibrosis observed in the cyclosporine group lacked significance when considered together with time since liver transplantation.

Aged↗

PubMed2000

Quality of human immunodeficiency virus viral load testing in Australia.

This study determined the proficiencies of laboratories measuring human immunodeficiency virus type 1 (HIV-1) viral loads and the accuracies of two assays used for HIV-1 viral load measurement in Australia and investigated the variability of the new versions of these assays. Quality assessment program panels containing (i) dilutions of HIV-1 subtype B, (ii) replicates of identical samples of HIV-1 subtype B, and (iii) samples of subtype E and B were tested by laboratories. Total variability (within and between laboratories) was tested with quality control samples. The coefficients of variation (CVs) for the Roche AMPLICOR HIV-1 MONITOR version (v) 1.0 and Chiron Quantiplex bDNA 2.0 assays ranged from 53 to 87% and 22 to 31%, respectively. The widespread occurrence of invalid runs with the AMPLICOR HIV-1 MONITOR 1.0 assay was identified. The CVs of the new versions of the assays were 82 to 86% for the AMPLICOR HIV-1 MONITOR v 1.5 assay and 16 to 23% for the Quantiplex bDNA 3.0 assay. For virus dilution samples, all but 5 of 19 laboratories obtained results within 2 standard deviations of the mean. The Quantiplex bDNA 2.0 assay reported values lower than those reported by the AMPLICOR HIV-1 MONITOR version 1.0 assay for samples containing HIV-1 subtype B, whereas the reverse was true for subtype E. Identification and resolution of the problem of invalid runs markedly improved the quality of HIV-1 viral load testing. The variability observed between laboratories and between assays, even the most recent versions, dictates that monitoring of viral load in an individual should always be by the same laboratory and by the same assay. Results for an individual which differ by less than 0.5 log(10) HIV-1 RNA copy number/ml should not be considered clinically significant.

Australia↗

PubMed2006

HPV viral load determination during pregnancy as a possible cervical cancer risk.

Pregnancy may be a risk factor for cervical human papillomavirus (HPV) infection due to associated increased hormonal level and immunosuppression. Although a majority of such infections are transient, persistent infection may lead to premalignant/malignant cervical lesion. The viral burden is thought to be an indicator for persistence of the infection and malignant transformation. To assess pregnancy as a risk factor for cervical HPV infection, we compared HPV prevalence and viral load among 25 pregnant women to those of 24 non-pregnant and 28 cervical cancer cases. HPV DNA was detected in the cervical cells by PCR using MY09/MY11 primers. HPV positive cases were retested with a low stringency PCR method to ascertain the viral load. HPV prevalences of 68%, 25% and 89% were observed among pregnant women, non-pregnant women and in the cervical cancer cases, respectively. High viral load was frequently (40%) observed in cervical cancer patients. Median viral copy number/cell did not vary much between the non-pregnant and pregnant women. However, pregnant women had a predominantly moderate viral load whereas the low viral load was more frequent in non-pregnant women. High viral load was found to be associated with the presence of HPV 16 in the cervical cancer cases as compared to pregnant/non-pregnant HPV infected women.

Adult↗

PubMed2005

Associations of high-risk HPV types and viral load with cervical cancer in China.

BACKGROUND: Cervical cancer is the second most common cancer in women worldwide. Infection with some genotypes of human papillomavirus is the most important risk factor associated with cervical cancer. OBJECTIVE: The aim of this study was to determine the prevalence and genotypes of HPV in China, and to evaluate the correlation between viral load of high risk HPV and cervical cancer and its precursors. STUDY DESIGN: A cross-sectional study was carried out, wherein cervical samples were collected from 541 patients with cervical cancer, 262 with CIN, 139 with cervicitis and 68 age-matched healthy controls. Hybrid Capture 2 was employed to detect HPV DNA. Specimens from HPV DNA positive cervical cancer were tested for HPV types by using type specific PCR and general primer PCR with sequence-based typing (GP PCR-SBT). RESULTS: Overall high risk HPV prevalence was 68.8% in CIN1, 80.3% in CIN2, 90.2% in CIN3, 90.9% in cervical cancer in situ, 89.9% in invasive cervical cancer and 25% in healthy controls from China. The most common HPV DNA type found in patients with cervical cancer was HPV16 (79.6%), followed by HPV58 (5.92%), HPV33 (3.29%), HPV18 (1.97%), HPV6 (1.97%), HPV31 (1.31%), HPV39 (1.31%), HPV68 (1.31%) and other HPV types (3.3%). It was found that there was a significantly increased risk of increasing CIN stage with high viral load. Frequency of low viral load found in the controls was 13.2% and 22.9% of CIN1, obtaining an OR of 4.2 (1.5-12.0). Associations (OR) among low viral load and CIN2/3, CIS, and CC were 6.7 (2.9-15.6), 9.4 (2.7-32.3) and 8.3 (3.7-18.4), respectively. While high viral loads were found in 5.9% of controls, 27.1% of CIN1, 42.1% of CIN2/3 and 48.5% of CIS, demonstrating increasing odds ratios with severity of disease (OR for CIS=68.0, 95% CI=17.8-259.7). CONCLUSIONS: HPV16 was the most common genotype in central China. The developing cervical cancer precursors were associated with elevated high-risk HPV viral load.

Adolescent↗

PubMed2005

Mortality during the first 24 months after delivery in relation to CD4 T-lymphocyte levels and viral load in a cohort of breast-feeding HIV-1-infected women in Dar es Salaam, Tanzania.

The objective of this study was to analyze the mortality during the first 24 months after delivery in relation to CD4 T-lymphocyte levels and viral load at enrollment (36 weeks of gestation) in a cohort of HIV-1-seropositive breast-feeding women at the Dar es Salaam site of the multicenter Petra trial (a mother-to-child HIV-1 transmission intervention trial using antiretroviral therapy). Antiretroviral treatment was not available in this setting apart from the short treatment given within the trial around delivery to prevent mother-to-child transmission of HIV. T-lymphocyte subsets were determined by flow cytometry. Plasma HIV-1 RNA was quantified by the Amplicor HIV-1 RNA Monitor v 1.5 assay. Mortality after delivery was analyzed using the life-table technique and Cox regression. The analysis included 266 mothers. The CD4 cell counts at enrollment were <200 cells/mm in 14.5% of the mothers. The viral load at enrollment was >100,000 RNA copies/mL in 33.6% of the mothers. The mortality 24 months after delivery was 6.7% (95% CI = 3.1-10.1%). The mortality 24 months after delivery was 29.9% (95% CI = 13.1-46.9%) for mothers with <200 CD4 cells/mm at enrollment, 3.3% (95% CI = 0-6.6%) for mothers with 200-499 CD4 cells/mm, 2.9% (95% CI = 0-7.1%) for mothers with >500 CD4 cells/mm (P = 0.0000), 15.0% (95% CI = 6.6-23.4%) for mothers with viral load >100,000 copies/mL at enrollment, and 2.8% (95% CI = 0-5.6%) for mothers with viral load <100,000 copies/mL (P = 0.0000). In the multivariate analysis CD4 cell counts and viral load were both independent risk factors for mortality (P < 0.001 and P = 0.004, respectively). In conclusion, the mortality was high among women with severe immunosuppression or high viral load at enrollment, but not in the rest of the women. CD4 lymphocyte count in late pregnancy was a better predictor of death within 2 years than was viral load. The results support the World Health Organization recommendation to initiate antiretroviral treatment in resource-limited settings in HIV-1-infected adults with CD4 cell counts <200/mm and show that this is appropriate also among perinatal women.

Acquired Immunodeficiency Syndrome↗

PubMed1999

Cerebrospinal fluid viral load, intrathecal immunoactivation, and cerebrospinal fluid monocytic cell count in HIV-1 infection.

To assess the association between cerebrospinal fluid (CSF) viral load, intrathecal immunoactivation, and immunosuppression in HIV-1-infected individuals with no antiretroviral treatment experience a cross-sectional study of stored frozen CSF and plasma samples were conducted. The study population included a total of 120 antiretroviral-naive HIV-1-infected patients, 110 neuroasymptomatic patients, and 10 with neurologic complications. HIV-1 RNA was quantified in cell-free CSF and plasma using polymerase chain reaction (PCR; Roche Amplicor HIV-1 Monitor version 1.5, Roche Diagnostic Systems, Hoffmann-La Roche, Inc., Base, Switzerland). Immunoactivation was measured by CSF-serum IgG index, CSF neopterin concentrations, and CSF monocytic cell count. The CSF HIV-1 RNA load did not differ significantly between patients with or without neurologic complications. In patients without neurologic symptoms, the CSF monocytic cell counts were correlated to the CSF viral load (r(s) = 0.40, p < .001), whereas IgG index and CSF neopterin concentrations were correlated to the viral load only in the subgroup of patients with CD4 counts > or =200 x 10(6) cells/L. In this subgroup of patients, the peripheral CD4 cell count was, as expected, inversely correlated to the CSF viral load (r. = -0.36, p < .01), whereas in patients with CD4 counts <200 x 10(6) cells/L, an unexpected, significant positive correlation (r(s) = 0.43, p < .01 ) was found. In HIV-1-infected patients with neurologic complications, no significant correlations were found between immune activation, CSF viral load, and immunosuppression.

AIDS Dementia Complex↗

PubMed2005

The effect of highly active antiretroviral treatment on viral load and antiretroviral drug levels in breast milk.

Viral load and drug levels were measured in the plasma and breast milk of nine mothers treated with highly active antiretroviral therapy (HAART) and one woman treated only with zidovudine during delivery. In all HAART-treated women after delivery the viral load was less than 400 copies/ml in plasma and breast milk. Compared with the plasma concentration, the breast milk concentration was between 68 and 90% for nevirapine, 6 and 24% for nelfinavir and 90 and 540% for indinavir.

Adult↗