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Results for “Viral Load”

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PubMed2001

Baseline CD4(+) cell count, not viral load, correlates with virologic suppression induced by potent antiretroviral therapy.

OBJECTIVE: To investigate the relationship between viral load suppression and baseline viral load as well as that between viral load suppression and baseline CD4(+) cell count. DESIGN: Meta-analysis of published and presented studies. METHODS: Trials of two nucleoside analogs plus nevirapine, indinavir, nelfinavir, or efavirenz as therapy for antiretroviral treatment-naive patients with HIV infection or AIDS who were followed-up for at least 6 months were included in the meta-analysis. The proportion of patients with viral loads of <200-500 copies/ml at 6 and 12 months (total number of patients, 1619 and 761, respectively) was regressed to the mean or median baseline viral load and CD4(+) cell count. RESULTS: Thirty-six treatment arms from 30 studies were identified. Multivariate regression demonstrated a significant correlation between baseline CD4(+) cell count and virologic suppression at 6 and 12 months ( t = 2.85, p =.008; and t = 3.08, p =.010, respectively) but not between baseline viral load and virologic suppression ( t = 0.92, p =.365; and t = 1.31, p =.215, respectively). The same pattern was seen in a subanalysis of trials of nevirapine-containing therapy (CD4(+) cell count: t = 2.89, p =.014 at 6 months; viral load suppression: t = 0.84, p =.415). CONCLUSIONS: Baseline CD4(+) cell count was a better predictor of virologic suppression induced by triple combination therapy than was baseline viral load.

Anti-HIV Agents↗

PubMed1997

Impaired early growth of infants perinatally infected with human immunodeficiency virus: correlation with viral load.

OBJECTIVE: To evaluate the effect of viral load on the early growth of infants infected with human immunodeficiency virus (HIV). METHODS: Plasma concentrations of p24-antigen and HIV ribonucleic acid were measured retrospectively and correlated with growth parameters for the first 18 months of life in a cohort of 47 term infants born to HIV-infected mothers prospectively enrolled in a study of perinatal HIV transmission. Comparisons of the mean weight and length of the 18 HIV-infected and 29 uninfected infants for each interval and across intervals were made. Viral load was correlated with standard deviation scores. Infants were stratified by high and low viral load during the first 6 months of life. RESULTS: At birth, no difference in weight and length was observed between HIV-infected and uninfected infants. Between birth and 6 months of age, the infected infants grew less rapidly than the uninfected infants, a finding temporally associated with an exponential increase in HIV viremia. The linear growth of infected infants remained consistently less than that of the uninfected infants after 6 months of life, although the differences were no longer statistically significant and tended to decrease with age in parallel with declines in viral load. The median plasma concentration of HIV ribonucleic acid was significantly higher at 3, 6, 12, and 18 months in infected infants in whom growth failure developed. Infants who had a high viral load in the first 6 months of life were significantly more likely to have severe growth failure. Though the mean SD for weight of the infected infants was always less than that of the uninfected infants, the differences were small and not significant. CONCLUSIONS: Our results confirm the observation that stunting is an early frequent finding in perinatal HIV infection. The deleterious effect of HIV on linear growth appears to be correlated with the level of postnatal HIV viremia, although the exact mechanism of this association remains to be elucidated.

Birth Weight↗

PubMed2006

Cross-sectional analysis of oncogenic HPV viral load and cervical intraepithelial neoplasia.

In human papillomavirus (HPV)-associated carcinogenesis, HPV infection characteristics such as viral load may play an important role in lesion development. The purpose of this study was to determine the association between quantitative assessment of oncogenic HPV viral load, and abnormal cytology among women residing along the United States-Mexico border. A cross-sectional study of 2,319 women was conducted between 1997 and 1998. Viral load of oncogenic HPV types (16, 18, 31, 39, 45, 51, 52, and 58) was measured among 173 HPV (+) women using quantitative real-time PCR. Overall, HPV 16, 31, 52 and 58 showed the highest viral load. Single type infection had higher viral loads compared to multiple type infections. HPV viral load declined significantly (p = 0.04) with age. No significant association was observed with other known HPV risk factors such as oral contraceptive use, parity, sexual and STD history. Viral load was independently associated with degree of cervical lesions. An adjusted odds ratio (AOR) of 4.7 for the association between increasing total viral load and Atypical Squamous Cells of Undetermined Significance (ASCUS)/Atypical Glandular Cells of Undetermined Significance (AGUS) was observed (p for trend <0.01). Increased risk of low-grade SIL was observed with higher viral load compared with HPV negative women (AOR = 47.7 for total viral load; AOR = 37.1 for HPV viral load not including HPV16, and AOR = 25.9 for HPV16 viral load). Likewise, increased risk of high-grade SIL with higher viral loads was observed (AOR = 58.4 for high total viral load compared with HPV negative women, AOR = 58.1 for HPV viral load not including HPV16, and AOR = 69.8 for HPV16 high viral load). Results from this study suggest a dose-response relationship between increasing oncogenic HPV viral load and risk of LSIL and HSIL.

Adolescent↗

PubMed2003

Ablation of CD8 and CD4 T cell responses by high viral loads.

To evaluate the impact of sustained viral loads on anti-viral T cell responses we compared responses that cleared acute lymphocytic choriomeningitis virus infection with those that were elicited but could not resolve chronic infection. During acute infection, as replicating virus was cleared, CD8 T cell responses were down-regulated, and a pool of resting memory cells developed. In chronically infected hosts, the failure to control the infection was associated with pronounced and prolonged activation of virus-specific CD8 T cells. Nevertheless, there was a progressive diminution of their effector activities as their capacity to produce first IL-2, then TNF-alpha, and finally IFN-gamma was lost. Chronic lymphocytic choriomeningitis virus infection was also associated with differential contraction of certain CD8 T cell responses, resulting in altered immunodominance. However, this altered immunodominance was not due to selective expansion of T cells expressing particular TCR Vbeta segments during chronic infection. High viral loads were not only associated with the ablation of CD8 T cell responses, but also with impaired production of IL-2 by virus-specific CD4 T cells. Taken together, our data show that sustained exposure to high viral loads results in the progressive functional inactivation of virus-specific T cell responses, which may further promote virus persistence.

Animals↗

PubMed2003

Iron, haptoglobin phenotype, and HIV-1 viral load: a cross-sectional study among pregnant Zimbabwean women.

BACKGROUND: Viral load is a determinant of HIV-1 progression and transmission. Iron status and the phenotype of haptoglobin, a heme-binding acute phase reactant, may be determinants of viral load. We aimed to describe the effect of iron status, haptoglobin phenotype (Hp), and other predictors on HIV-1 viral load. METHODS: Based on a cross-sectional study among 1669 antenatal care attenders (22-35 weeks) in Zimbabwe, 526 (31.5%) were found to be HIV infected. The role of season, age, gravidity, gestational age, malaria parasitemia, Hp, and elevated serum alpha(1)-antichymotrypsin (ACT) as well as serum ferritin, folate, retinol, and beta-carotene on HIV viral load among the 526 HIV-infected women was assessed using multiple linear regression analysis. RESULTS: The distribution of Hp 1-1 (32%), Hp 2-1 (48%), and Hp 2-2 (20%) was not different from that of 53 uninfected women. Mean viral load was 3.85 log(10) (95% CI: 3.77-3.93) genome equivalents (geq)/mL, ranging from 3.77 (95% CI: 3.64-3.90) geq/mL in women with Hp 1-1 to 4.05 (95% CI: 3.81-4.21) geq/mL in women with Hp 2-2. With elevated serum ACT controlled for, women with Hp 2-2 had viral loads twice (95% CI: 1.4-4.0, p =.002) that of women with Hp 1-1, whereas those with serum ferritin <6 micro g/L had viral loads less than one third (95% CI: 0.13-0.53, p =.013) that of women with serum ferritin >24 micro g/L. Viral loads were also higher in women enrolled in the early rainy season compared with the dry season, in gravidae 4+ compared with gravidae 1 through 3, and in those with moderately elevated compared with low serum alpha(1)-antichymotrypsin, but neither age, gestational age, serum folate, serum retinol, nor serum beta-carotene were predictors. CONCLUSION: Storage iron, Hp 2-2, and elevated ACT are independent positive predictors of HIV-1 viral load. The positive relationship between serum ferritin and viral load was not the result of an acute phase response or iron accumulation with advanced HIV infection. A possible detrimental role of iron in HIV infection would have serious public health implications.

Female↗

PubMed2002

Genotypic analysis of plasma HIV-1 RNA after influenza vaccination of patients with previously undetectable viral loads.

OBJECTIVE: In this study we evaluated the possibility that plasma viral load elevations secondary to influenza vaccination in HIV-1-seropositive individuals with previously undetectable viral loads (< 200 copies/ml) could develop resistance-bearing mutations in the viral reverse transcriptase (RT) and protease regions. METHODS: Thirty-four patients with undetectable viral burdens on highly active antiretroviral therapy (HAART) were evaluated for elevations in plasma viral load 2 and 4 weeks post-influenza vaccination. Plasma from patients whose viral load increased after vaccination was subject to genotypic resistance analysis by the line probe assay (LiPA) to determine whether primary resistance-bearing mutations developed during this period and at follow-up. Stored plasma was used to evaluate whether RT or protease mutations existed pre-vaccination. RESULTS: Seven out of 34 patients were found to experience elevations in their viral load after influenza vaccination. Two of the patients revealed evidence of primary RT or protease mutations not demonstrated in earlier pre-vaccination samples. One patient failed therapy after vaccination, and one patient revealed post-vaccination viral load elevations that eventually led to the progressive development of primary zidovudine mutations. CONCLUSION: Evidence is presented that supports the contention that a small subset of patients who experience viral load elevations after influenza vaccination can develop mutational changes in the RT region of the viral genome either acutely or after a failure of the viral load to return to undetectable levels.

Adult↗

PubMed2000

Predictive value of the ultrasensitive HIV viral load assay in clinical practice.

The aim of this study was to determine whether an HIV viral load of <50 copies/ml (c/ml), in the first available plasma sample to have shown a viral load of <400 c/ml, in patients on antiretroviral therapy, is correlated with longer term suppression of viral load (at <400 c/ml) compared to a viral load of 50-399 c/ml, and secondly, to compare the results obtained by ultrasensitive and standard viral load assays carried out on the same sample. A total of 98 HIV-positive patients on antiretroviral therapy with a viral load of <400 c/ml and at least one subsequent viral load measurement, were selected. For each patient, the first available specimen showing a viral load of <400 c/ml was tested using the Roche Amplicor ultrasensitive viral load assay, and patients were followed up subsequently for a median period of 52 weeks. Whether patients achieved an ultrasensitive viral load (USVL) of <50 c/ml or not made very little difference to the proportion of patients in each group showing continued response to treatment (52% vs. 45% respectively). The only variable that was shown to significantly predict longevity of response was the number of antiretroviral drugs used. Secondly, a standard viral load of <400 c/ml but with a detectable signal above background levels, was strongly predictive of a USVL of >50 c/ml. Overall, the findings suggest that the advantage in predictive value of the ultrasensitive over the standard HIV viral load assay, shown previously in clinical trials, may be limited in clinical practice.

Anti-HIV Agents↗

PubMed2003

Cytomegalovirus viral load monitoring after allogeneic bone marrow transplantation in patients receiving antiviral prophylaxis.

Cytomegalovirus viral load measurement is a powerful new tool for monitoring of CMV disease; however, the optimal strategy for use is unknown. Weekly plasma CMV viral loads and CMV-related outcomes were monitored in 46 consecutive allogeneic bone marrow transplantation (BMT) recipients receiving standardised antiviral prophylaxis. A total of 412 CMV viral loads were quantitated in the first 100 days post transplantation with 77 positive samples (19%) in 20 patients (43%). No patient with all negative CMV viral load results developed CMV disease. Two of three patients with highly positive CMV viral loads (first positive < or =30 days post transplant, maximum viral load > or =5000 copies/ml, and > or =50% of samples positive) developed CMV disease. A total of 17 patients with positive CMV viral loads, who did not meet the criteria for highly positive, did not develop CMV disease. CMV viral load detection was higher in recipients who were CMV sero-positive. In conclusion, CMV disease did not occur in the setting of a persistently negative CMV viral load. A positive CMV viral load result occurred commonly after allogeneic BMT, even in patients receiving antiviral prophylaxis.

Acute Disease↗

PubMed2000

Predictive negative value of persistent low Epstein-Barr virus viral load after intestinal transplantation in children.

BACKGROUND: The correlation between an elevated Epstein-Barr virus (EBV) viral load in the peripheral blood and the subsequent development of EBV-associated posttransplant lymphoproliferative disease (PTLD) is the basis for strategies using serial measurements of the EBV viral load to guide preemptive therapy (PT). Neither the frequency, duration of monitoring, nor the predictive negative value of viral load monitoring for asymptomatic patients with persistent low or nondetectable viral loads against the development of PTLD has been established. METHODS: Since April 1994, children undergoing intestinal transplantation (ITx) underwent serial monitoring of the EBV viral load in their peripheral blood using a quantitative competitive EBV polymerase chain reaction assay (PCR). Samples were obtained every 2 weeks for the first 3 months and then every 1-3 months depending on the patients clinical condition. EBV viral loads > or =40 (for patients who were EBV seronegative pre-ITx) and > or =200 (for those who were seropositive) genome copies/10(5) peripheral blood lymphocytes were felt to identify patients at increased risk for PTLD and generally prompted PT. RESULTS: A total of 30 ITx recipients were compliant with our monitoring protocol; 23/30 are alive 6-59 months post-ITx. A total of 12/30 never had a viral load >40 and did not receive PT. In contrast, 18/30 had > or =1 high viral load (> or =200); the first high viral load was measured a median of 59 days post-ITx (range 1-440). A late rise (>6 months post-ITx) was seen in only 2/18 children. A total of 0/12 patients with persistently low viral loads received PT and none developed PTLD. In contrast, 5/18 with > or =1 one high viral load (including 2/14 who received and 3/4 who did not receive PT) developed PTLD. All five children with PTLD were EBV seropositive pre-ITx and experienced their first high EBV PCR within the first 3 months after ITx. CONCLUSIONS: The predictive negative value of persistently low or nondetectable EBV viral loads was 100% in this study. Patients with nondetectable or low viral loads for the first 6 months after ITx did not develop PTLD regardless of their pretransplant EBV serological status. The frequency of viral load monitoring can be safely decreased for patients whose viral loads remain low for the first 6 months ITx.

Antiviral Agents↗

PubMed2002

Viral load as a surrogate end point in HIV disease.

OBJECTIVE: To examine the role of viral load as a surrogate end point for HIV disease progression and death. DATA SOURCES: A MEDLINE search was conducted for the years 1990-March 2001. In addition, relevant articles were cross-referenced to screen for additional information. STUDY SELECTION AND DATA EXTRACTION: Data regarding the validity of viral load as a surrogate end point for disease progression or death are cited. Emphasis was placed on randomized, controlled trials, but descriptive studies are also included. DATA SYNTHESIS: Recently, viral load has emerged as an important biomarker for monitoring HIV disease and antiretroviral therapy. Both baseline viral load and changes in viral load with time predict HIV disease progression and death. In fact, disease progression increases consistently once viral load exceeds 10,000 copies/mL, and AIDS and death primarily occur in patients with viral loads > 100,000 copies/mL. Changes that occur in viral load after initiation of antiretroviral therapy, however, do not fully explain the entire treatment effect. Also, separate comparisons of antiretroviral regimens may demonstrate similar differences in viral load changes but not similar differences in disease progression. CONCLUSIONS: Viral load is an important monitoring parameter for HIV disease and antiretroviral therapy. However, changes in viral load do not explain the entire clinical improvement that occurs after initiation of therapy. Although viral load is a clinically important surrogate end point for HIV disease, it cannot fully account for all associated treatment effects.

Antiretroviral Therapy, Highly Active↗

PubMed1999

Comparative analysis of quantification of viral load in patients infected with hepatitis C virus: quantiplex HCV RNA assay and amplicor monitor assay.

OBJECTIVE: two standardized techniques, Quantiplex HCV RNA 2.0 (bDNA) and Amplicor Monitor, were evaluated for the quantification of hepatitis C virus (HCV) load. Our objectives were: 1) to determine the relationship between viral load and genotype, and 2) to evaluate viral load in serial serum samples and in patients with normal or slightly elevated liver enzyme values in an area with a high prevalence of genotype 1. RESULTS: the viral loads detected with the two methods correlated significantly (r = 0.7, p < 0.0001), but viral load was smaller with the Monitor than with the Quantiplex assay, and was independent of genotype. The Monitor/Quantiplex ratio was lower in patients with a non-1 genotype than in patients with genotype 1b. Virological characteristics were similar in patients with normal or slightly elevated enzyme levels and in patients with elevated enzyme values. Neither method showed a relationship between viral load and age, sex, duration of the infection, mode of transmission, or histological activity index. CONCLUSION: viral load was not dependent on genotype. Measurement of viral load in a single serum sample adequately reflected the viral load measured in several serum samples from patients with chronic HCV infection. Patients with normal liver enzyme levels are not good candidates, in virological terms, for treatment with interferon.

Adolescent↗

PubMed2002

Predictors of undetectable plasma viral load in HIV-positive adults receiving antiretroviral therapy in Southern Brazil.

Factors associated with undetectable viral load (<80 copies/ml) were investigated among non-pregnant adults in antiretroviral treatment in a specialized service for HIV/AIDS in Southern Brazil. Use of antiretrovirals was investigated in two interviews (one month interval). Clinical data were collected from the clinical records; viral load previous to adherence measurement was defined the viral load previous to the first interview; the final viral load, the viral load subsequent to the second interview (interval between measures approximately 6 months). Undetectable final viral load occurred in 48% of the patients and was positively associated with levels of treatment adherence (p<0.001), being 19% for less than 60% of adherence and about 60% for adherence greater than 80%. In the multivariate model, the odds of undetectable final viral load was four times greater for 80-94% and > or =95% of adherence (CI 95% 1,80-13,28; CI 95% 1,73-9,53), compared with less than 60% adherence; it was greater for less than 6 months in treatment (OR = 3.37; CI 95% 1.09-10.46); and smaller for viral load previous to adherence measurement 5.2 log10 (OR = 0.19; CI95% 0.06-0.58), adjusted for these variables and sex, age, clinical status, current immune status, group of drugs and interval between the two measurements of viral load. The crude odds were lower for age 16-24 years and use of Nucleoside Analog Reverse Transcriptase Inhibitors only, but these effects were not significant in the multivariate model. There was no evidence of effect of sex, clinical status, current immune status, and changes in treatment regimen. Treatment adherence gave the largest effect. Motivational interventions directed at adherence may improve treatment effectiveness.

Adolescent↗

PubMed1998

Lack of evidence of a stable viral load set-point in early stage asymptomatic patients with chronic HIV-1 infection.

OBJECTIVE: To address the question of whether individuals with chronic HIV-1 infection have a stable viral load set-point and to assess the influence of host and viral factors on the evolution of viral load in a subset of stable asymptomatic patients with a baseline viral load below 5000 copies/ml and CD4+ T-cell count above 500 x 10(6)/l. METHODS: Medical visits were performed at least every 6 months including routine blood analysis, viral load and CD4+ T-cell count. HIV-1 RNA was measured in frozen (-70 degrees C) plasma samples using PCR. Patients were classified into three groups according to baseline viral load: group A, < 200 copies/ml (undetectable); group B, 201-2000 copies/ml; group C, 2001-5000 copies/ml. A survival analysis and a Cox regression model were performed to assess the influence of viral and host factors in the increase of baseline viral load. The endpoint was the time to increase viral load to a stable level > 0.5 log10 copies/ml above baseline viral load in groups B and C and to a stable detectable viral load (> 200 copies/ml) in group A. RESULTS: A cohort of 114 patients with viral load below 5000 copies/ml was followed for a median of 12 months (6-42 months). Overall, 22 (19%) out of 114 patients had an increase > 0.5 log10 copies/ml of baseline viral load. Baseline viral load increased in two (5%) out of 37 patients in group A, four (12%) out of 33 patients in group B, and 16 (36%) out of 44 patients in group C (survival analysis, P<0.002). Patients of group C had a eightfold higher risk of increasing baseline viral load than patients in the other two groups pooled together (hazards ratio, 8.28; 95% confidence interval, 1.78-38; P = 0.006). Patients with an increase of viral load to the virological endpoint had a threefold higher risk of decreasing baseline CD4+ T-cell counts > 100 x 10(6)/I than patients with stable viral load (hazards ratio, 2.78; 95% confidence interval, 1.12-14; P = 0.03). CONCLUSIONS: In our cohort of chronically HIV-1-infected asymptomatic patients with a baseline viral load < 5000 copies/ml and CD4+ cell count > 500 x 10(6)/l, a true viral load set-point did not seem to exist. Patients with baseline viral load of 2000-5000 copies/ml had an eightfold higher risk of increasing the level of viral load than patients with a baseline viral load below 2000 copies/ml.

Adult↗

PubMed2006

Reduced fertility among HIV-infected women associated with viral load in Rakai district, Uganda.

We assessed whether HIV-1 viral load affects the likelihood of live birth among HIV-positive women in a nested case-control study of HIV-positive women from a community cohort in Rakai District, Uganda. Cases were women who had a live birth (n = 270), and controls were sexually active women who did not use contraception and did not become pregnant during follow-up (n = 263). In women with a live birth and non-pregnant controls, median HIV viral loads were 4.12 log(10) copies/mL and 4.41 log(10) copies/mL, respectively (P = 0.001). A non-linear association was observed, and a segmented linear regression with spline knot at 4.5 log(10) copies/mL was fit. We observed a decline in the log (adjusted odds ratio [adj. OR])= -0.08 (95% confidence interval [CI]: -0.36, 0.20) between 3.0 and 4.49 log(10) viral load and -0.92 (95% CI: -1.21, -0.63) between 4.5 and 6.5 log(10) viral load. The two reductions differed significantly from one another (P < 0.001). Each increase in log(10) viral load after 4.5 log(10) resulted in an adj. OR of live birth which was 12% of the previous viral load category. Our data suggest that there may be considerable differences in the ability to produce a live birth among HIV-positive women with high viral loads.

Adolescent↗

PubMed2000

The impact of protease inhibitor-containing highly active antiretroviral therapy on progression of HIV disease and its relationship to CD4 and viral load.

OBJECTIVE: To compare the rate of disease progression according to viral load and CD4 cell count in patients receiving or not receiving highly active antiretroviral therapy (HAART), defined as protease inhibitor-containing regimens. DESIGN: An observational study, with prospectively collected data. METHODS: All patients attending the HIV Outpatient clinic as of 1 January 1995 (n = 2083) were included. Follow-up was until the first AIDS-defining event or death. Associations between viral load or CD4 cell count and disease progression were assessed using a person-years approach. Event rates were compared using Poisson regression analysis; a multivariate model was used to assess the independent effects of CD4, viral load and treatment group on event rates and to consider interactions between these variables. RESULTS: The event rates increased with lower CD4 cell count and higher viral load for both treatment groups and were generally lower in the HAART group. In a multivariate analysis, lower CD4 cell counts and higher viral loads remained significantly associated with disease progression, irrespective of treatment group. However, the event rate was significantly lower for the HAART group compared with the control group (relative rate 0.53, P < 0.001). CONCLUSIONS: HAART-treated patients with high viral loads and CD4 cell counts experienced reduced disease progression compared with individuals with the same CD4 cell count and viral load not receiving HAART. Consequently, the short-term prognosis associated with viral load levels and CD4 cell counts may differ in patients on HAART. Whether this effect will be observed with non-protease-inhibitor-containing HAART is not known at this time.

Adolescent↗

PubMed1996

Viral Load and Neuropsychological Functioning in HIV Seropositive Individuals:A Preliminary Descriptive Study.

We have theorized a direct relationship between viral burden and deleterious effects on the central nervous systems. It was hypothesized that HIV+ individuals would manifest poorer neuropsychological functioning after increased viral load. To address this, we compared viral burden to neuropsychological performance in subjects who participated in ACTG 116-118. Plasma samples and neuropsychological assessments completed at the same time were available for 64 observations on 21 subjects. Subjects who had a viral peak of over 1000 TCID per ml were classified as high viral load, those who did not as low viral load. Mean performances of the high viral load subjects were poorer, even though baseline performances were slightly poorer in the low viral load group. Mean post-viral peak performances were poorer than pre-viral peak performances. Declines in neuropsychological performance were found significantly more often in the high viral load group. These findings support the viral load hypothesis.

HIV Infections↗

PubMed2004

Viral loads in clinical specimens and SARS manifestations.

A retrospective viral load study was performed on clinical specimens from 154 patients with laboratory-confirmed severe acute respiratory syndrome (SARS); the specimens were prospectively collected during patients' illness. Viral load in nasopharyngeal aspirates (n = 142) from day 10 to day 15 after onset of symptoms was associated with oxygen desaturation, mechanical ventilation, diarrhea, hepatic dysfunction, and death. Serum viral load (n = 53) was associated with oxygen desaturation, mechanical ventilation, and death. Stool viral load (n = 94) was associated with diarrhea, and urine viral load (n = 111) was associated with abnormal urinalysis results. Viral replications at different sites are important in the pathogenesis of clinical and laboratory abnormalities of SARS.

Adult↗

PubMed2001

[Cerebrospinal fluid viral load in HIV-1 positive hemophilic patients treated with HAART].

As HIV seropositive patients with undetectable CSF viral load have a lower likelihood of developing neurologic disease, the determination of CSF viral load levels may be useful to evaluate the efficacy of HAART. We compared plasma viral load levels with HIV-1 RNA CSF levels in 18 hemophilic patients without neurocognitive involvement under HAART. We detected a significant correlation between plasma viral load levels and CSF viral load levels. Fourteen patients with undetectable plasma viral load had undetectable RNA HIV-1 CSF levels as well. Four patients with detectable plasma viral load had detectable HIV-RNA in CSF, but the latter were significantly lower. Viral load is usually lower in non-blood fluids and HAART decreases the viral load in CSF as well as in blood.

Antiretroviral Therapy, Highly Active↗