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Results for “Viral Load”

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PubMed1997

Chronic hepatitis C: the viral load per liver cell before treatment as a new marker to predict long-term response to IFN-alpha therapy.

BACKGROUND/AIMS: So far, there are no reliable parameters that can predict the long-term sustained response to treatment with interferon-alpha in patients with chronic hepatitis C. In this study, we have developed a semi-quantitative method to determine the viral load per liver cell and have correlated this factor with the outcome of hepatitis C patients treated with interferon-alpha. METHODS: Hepatitis C virus RNA levels were measured in serum, peripheral blood mononuclear cells and liver cells of randomly chosen hepatitis C patients before treatment with interferon-alpha (n=37). The number of cells present in the liver biopsies was determined by a polymerase chain reaction-based quantitation of the housekeeping gene beta-globin. The patients were divided into a responder ("R", n=15, 41%) and a non-responder ("NR", n=22, 59%) group, as defined by normal liver enzymes and negative hepatitis C virus-polymerase chain reaction 6 months after treatment. RESULTS: Long-term sustained responders had a significantly lower viral load per liver cell (median: 5 vs. 650 copies/1000 liver cells, p-value: 0.0001), lower age (median: 32 vs. 54 years, p-value: 0.006) and lower percentage of geno- or serotype 1 (46% vs. 91%). Regarding viral load in serum and peripheral blood mononuclear cells, alanine aminotransferase levels, gamma-globulin levels and histological changes, no statistically significant differences were observed. CONCLUSIONS: In chronic hepatitis C infection, a high viral load per liver cell represents a new marker to predict long-term response to therapy with IFN-alpha.

Adult↗

PubMed2006

Influence of peak viral load on the extent of CD4+ T-cell depletion in simian HIV infection.

Simian HIV (SHIV) infection of macaques with CXCR4 tropic viruses results in early and profound CD4 T-cell depletion in the first few weeks of infection. Analyzing data from a large study of vaccination and SHIV-89.6P challenge, we observe a strong correlation between peak viral load and the extent of CD4 T-cell depletion in acute infection, consistent with a simple kinetic model of viral infection of CD4 T cells. We have modeled the dynamics of the interaction of virus and CD4 T cells over time to investigate the rate of CD4 T-cell infection and death. This analysis indicates that up to 80% of CD4 T cells are infected at peak viremia and that the proportion of CD4 T cells destroyed is correlated with the peak viral load. The simple relation between viral load and CD4 T-cell depletion allows prediction of the level of viral control required to prevent CD4 T-cell depletion in acute SHIV infection. Whether such a simple relation also holds for HIV or simian immunodeficiency virus infections remains to be determined, particularly in the gut and other anatomic sites in which most early T-cell depletion occurs.

Animals↗

PubMed2006

The effect of antioxidant supplementation on hepatitis C viral load, transaminases and oxidative status: a randomized trial among chronic hepatitis C virus-infected patients.

OBJECTIVE: To assess the effect of antioxidant supplementation on hepatitis C viral load, transaminases and oxidative status. METHODS: We performed a randomized, placebo-controlled, double-blind trial to assess the effect of antioxidant supplementation on serum alanine aminotransferase, plasma hepatitis C viral load as well as oxidative and antioxidant markers in patients with hepatitis C virus infection. The participants received a daily dose of ascorbic acid (500 mg), D-alpha-tocopherol (945 IU) and selenium (200 microg) or placebo tablets for 6 months. RESULTS: Twenty-three patients were included. During supplementation, the antioxidant group had significantly higher levels of plasma ascorbic acid and alpha-tocopherol than the placebo group and the activity of erythrocyte glutathione peroxidase had significantly increased from baseline to month 6. No differences were observed in serum alanine aminotransferase and log10-transformed plasma hepatitis C virus-RNA between the groups or changes from the baseline at any time. No consistent differences between groups or changes from the baseline with respect to erythrocyte activities of antioxidative enzymes (glutathione reductase, superoxide dismutase and catalase) or plasma levels of oxidative markers (malondialdehyde and 2-amino-adipic semialdehyde) were found. CONCLUSION: Supplementation with vitamin C, E and selenium increased the antioxidant status, but had no effects on alanine aminotransferase, viral load or oxidative markers.

Adult↗

PubMed2004

Design and performance testing of quantitative real time PCR assays for influenza A and B viral load measurement.

BACKGROUND: The antiviral effect of anti-influenza drugs such as zanamivir may be demonstrated in patients as an increased rate of decline in viral load over a time course of treatment as compared with placebo. Historically this was measured using plaque assays, or Culture Enhanced Enzyme Linked Immunosorbent Assay (CE-ELISA). OBJECTIVES: to develop and characterise real time quantitative PCR (qPCR) assays to measure influenza A and B viral load in clinical samples, that offer improvements over existing methods, in particular virus infectivity assays. STUDY DESIGN: The dynamic range and robustness were established for the real time qPCR assays along with stability of the assay components. Cross validation of the real time PCR assays with CE-ELISA was performed by parallel testing of both serial dilutions of three different subtypes of cultured virus and a panel of influenza positive throat swab specimens. RESULTS: the assays were specific for influenza A and B and the dynamic ranges were at least seven logs. The assay variability was within acceptable limits but increased towards the lower limit of quantification, which was 3.33 log(10) viral cDNA copies/ml of virus transport medium (ten viral RNA copies/PCR). The components of the assay were robust enough to withstand extended storage and several freeze-thaw cycles. For the real time PCR assays the limit of quantification was equivalent to the virus infectivity cut off, which equates to a 93-fold increase in sensitivity. CONCLUSION: Well characterised real time PCR assays offer significant improvements over the existing methods for measuring the viral load of strains of influenza A and B in clinical specimens.

DNA, Complementary↗

PubMed2005

Rapid viral load suppression following generic highly active antiretroviral therapy in Southern Indian HIV-infected patients.

We prospectively studied the initial results of 6 months of generic efavirenz-based therapy on the plasma viral load in 40 patients at YRG Centre for AIDS Research and Education, a tertiary HIV referral centre in southern India. The median baseline plasma viral load was 259,000 copies/ml and at 6 months 95% of patients had plasma viral loads less than 400 copies/ml. The data support the use of generic non-nucleoside reverse transcriptase inhibitor-based regimens in resource-limited settings.

Adult↗

PubMed2002

HIV and cytomegalovirus viral load and clinical outcomes in AIDS and cytomegalovirus retinitis patients: Monoclonal Antibody Cytomegalovirus Retinitis Trial.

OBJECTIVE: To determine the association of cytomegalovirus (CMV) viremia with mortality and CMV retinitis progression in newly diagnosed and relapsed CMV retinitis. DESIGN: Ancillary study of a randomized, placebo-controlled, phase III clinical trial. PATIENTS: A total of 83 patients with AIDS and CMV retinitis, enrolled during the first phase of the Monoclonal Antibody Cytomegalovirus Retinitis Trial, were administered MSL-109 or placebo as adjuvant therapy for CMV retinitis. MAIN OUTCOME MEASURE(S): Mortality and CMV retinitis progression. RESULTS: Treatment with MSL-109 did not predict either progression of CMV retinitis or mortality. Detection in plasma CMV DNA at baseline predicted mortality, but CMV antigenemia did not. CMV DNA was a better predictor of mortality than a high HIV viral load. Neither CMV DNA nor antigenemia predicted the progression of CMV retinitis. Among newly diagnosed patients, there was a decline in the proportion with detectable CMV viral load and CMV antigenemia in response to anti-CMV therapy. However, there was a rebound in CMV viral load to 25% and CMV antigenemia to 54.6% at 6 months. In relapsed patients, anti-CMV therapy was not associated with a change in the percentage with detectable CMV-DNA or CMV antigenemia over time. CONCLUSION: In patients with AIDS and CMV retinitis, the detection of plasma CMV DNA was associated with a higher risk of mortality than was a high HIV viral load. Anti-CMV therapy provided a transient reduction in CMV viremia in newly diagnosed but not relapsed patients with CMV retinitis. Adjuvant therapy with MSL-109 was ineffective in clearing CMV-DNA and CMV antigen from the plasma.

AIDS-Related Opportunistic Infections↗

PubMed2005

Clinical utility of cytomegalovirus viral load in bronchoalveolar lavage in lung transplant recipients.

The utility of cytomegalovirus (CMV) viral load (VL) by quantitative hybrid capture assay (Q-HCA) was investigated in bronchoalveolar lavage (BAL) from lung transplant recipients and compared with BAL cultures and blood VL. Forty-three consecutive BAL samples from 27 lung transplant recipients were analyzed. All samples had shell vial (SV) cultures in addition to Q-HCA. Histopathology was done on all lung tissues, and immunohistochemistry (IHC) in those with positive CMV cultures. Fifteen (56%) lung transplant recipients had both positive BAL SV cultures and BAL VL. Five of 15 had CMV pneumonitis with a VL in BAL >500 000 copies/mL (mean: 1638 450). Ten patients without CMV pneumonitis had VL in BAL <500 000 copies/mL (mean 81 820, p = 0.002). High VL in BAL and blood invariably meant CMV pneumonitis, but 2 patients with CMV pneumonitis had high BAL VL but relatively low blood VL. Initial CMV seronegativity was associated with pneumonitis (4/5 vs. 1/10; p = 0.004) and higher BAL CMV VL (p = 0.03). High CMV BAL or blood VL did not correlate with acute rejection or development of bronchiolitis obliterans syndrome (BOS). High CMV VL in BAL in lung transplant recipients is strongly associated with CMV pneumonitis, and may be more predictive than peripheral blood viral load.

Adult↗

PubMed2002

Viral load of human papillomavirus and risk of CIN3 or cervical cancer.

Carcinogenic human papillomaviruses (HPV) are thought to be necessary for development of cervical cancer. We assessed whether higher viral loads of such viruses predicted future risk of CIN3 or cancer (CIN3+) in a cohort of 20810 women followed up for 10 years with cytological screening. We measured the viral load for 13 types of carcinogenic HPV (relative light units normalised to 1 pg/mL HPV 16 positive controls [RLU/PC]) using Hybrid Capture 2 testing of cervicovaginal lavages obtained at enrolment. Results were stratified into four groups (RLU/PC 1 to <10, 10 to <100, 100 to <1000, > or = 1000). Although presence of HPV strongly increased risk of CIN3+, high viral load did not further predict risk of CIN3+.

Adolescent↗

PubMed2002

Prevalence of oral lesions in Mexican children with perinatally acquired HIV: association with immunologic status, viral load, and gender.

It has been proposed that HIV-related oral lesions (HIV-ROL) have a significant diagnostic and prognostic value for human immunodeficiency virus (HIV) infection in adult patients. However, in HIV-infected children, the relation between HIV-ROL and immune and virologic status is not well established. The principal objective of this paper is to assess the prevalence of HIV-related oral lesions (HIV-ROL) in Mexican HIV-infected children in relation to their immunologic status, viral load, and gender. Forty-eight HIV-infected children from Immunodeficiency Clinic, Child's Hospital of México, México City, were examined for oral pathology. The data obtained from medical records were: name, gender, age, route of infection, CD4 lymphocytes cells count/mL, HIV-1-RNA level of copies/mL (viral load), and type and time of treatment. The prevalence of HIV-ROL was 29.2%. Oral candidosis was the most prevalent oral lesion (20.8%) followed by periodontal and gingival disease (4.2%), herpes simplex (2.1%), and parotid enlargement (2.1%). There was no association between the prevalence of HIV-ROL and gender, immunological status, or viral load. The most frequent clinical form of oral candidosis was erythematous candidosis (12.5%, N = 6). Our results do not suggest a direct relationship between prevalence of HIV-ROL, severe immunodepression, and/or viral load > 100000 copies in this population.

AIDS-Related Opportunistic Infections↗

PubMed2000

Genotype and viral load as prognostic indicators in the treatment of hepatitis C.

Interferon-alpha (IFN-alpha), either alone or in combination with ribavirin, is the standard treatment for patients with hepatitis C. However, most patients do not achieve a sustained remission with this treatment regimen. A number of studies have demonstrated that genotype, baseline viral load and/or a decrease in viral load early after treatment induction are the major predictive factors for response to treatment with IFN. Patients with hepatitis C virus (HCV) genotype 1 are more resistant to treatment with IFN, whereas low viral load at baseline and a marked decline in the HCV RNA level during the first 2-12 weeks of IFN therapy are associated with enhanced treatment efficacy. These variables could potentially be used to develop treatment algorithms that tailor therapies for specific clinical situations. Continued development and refinement of such algorithms would facilitate both the selection of patients who are most likely to benefit from therapy and the development of optimal treatment regimens for different patient groups. Predictive factors will also enable clinicians to identify subsets of patients who are not expected to respond well to current treatment. The development of new delivery methods for IFN that produce sustained antiviral pressure may provide a means of treating these previously difficult-to-treat patient groups.

Algorithms↗

PubMed2001

A patient with chronic hepatitis C who obtained sustained response by retreatment of interferon after decrease of viral load and mutation in interferon sensitivity determining region.

A 44-year-old man with chronic hepatitis C received three courses of interferon (IFN) therapy. HCV genotype was 1b, viral load was 1,200 kcopies/ml and interferon sensitivity determining region (ISDR) was the intermediate type before the 1st IFN therapy. The 1st and 2nd IFN therapies resulted in failure to yield a sustained response. Seven years after from the 1st therapy, viral load had decreased to 15 kcopies/ml and ISDR had changed to mutant type. The 3rd IFN therapy yielded sustained response. Thus, we should consider retreatment with IFN when a decrease of the viral load and change of ISDR to mutant type are observed.

Adult↗

PubMed2003

Hepatitis C virus-associated hypobetalipoproteinemia is correlated with plasma viral load, steatosis, and liver fibrosis.

OBJECTIVES: A relationship between chronic hepatitis C virus (HCV) infection and lipid metabolism has recently been suggested. The aim of this study was to determine the correlation between lipid profile and virology, histologic lesions, and response to alpha interferon therapy in noncirrhotic, nondiabetic patients with hepatitis C. METHODS: A total of 109 consecutive untreated chronic hepatitis C patients were studied to assess the following: 1) the effects of HCV genotype, viral load, steatosis, hepatic fibrosis, and body mass index (BMI) on lipid profile; and 2) whether lipid parameters could predict response to antiviral therapy. RESULTS: The control group showed a significantly higher apolipoprotein B (apoB) concentration compared with patients with chronic hepatitis C. Hypobetalipoproteinemia (apo B <0.7 g/L) was found in 27 (24.7%) chronic HCV patients and in five (5.3%) control subjects (p = 0.0002). Levels of apo B were negatively correlated with steatosis and HCV viral load (r = -0.22; p = 0.03). This last correlation was strong for non-1 genotype and genotype 3 (r = -0.48; p = 0.0005, and r = -0.47; p = 0.007, respectively) but was not found in genotype 1. In multivariate analysis, low apo B concentration was significantly associated with fibrosis grade 2 or 3 versus grade 0 or 1 (p < 0.001), steatosis >5% (p < 0.001), low body mass index (p < 0.001), and high HCV viral load (p < 0.014). No correlation was found in the 76 treated patients between apo B and response to interferon therapy. CONCLUSIONS: In chronic HCV patients, hypobetalipoproteinemia occurs already in the early stages of HCV infection before the development of liver cirrhosis. The correlation between apo B levels and HCV viral load seems to confirm the interaction between hepatitis C infection and beta-lipoprotein metabolism.

Adult↗

PubMed2004

High viral load is a risk factor for hepatocellular carcinoma in patients with chronic hepatitis B virus infection.

BACKGROUND AND AIMS: Hepatitis B virus (HBV) is considered a major risk factor for the progression to liver cirrhosis and hepatocellular carcinoma (HCC). The serum level of HBV-DNA is correlated with progression of the disease. The aim of the present study was to determine the relationship between the level of HBV-DNA and hepatocarcinogenesis in patients with chronic HBV infection. METHODS: The authors studied 73 patients who were diagnosed with chronic HBV infection at Nagasaki University Hospital (Nagasaki, Japan) between January 1980 and December 1999. The significance of age, sex, habitual drinking, serum alanine aminotransferase level, HBV viral load, interferon treatment, hepatic fibrosis and hepatic inflammation on the development of HCC were examined using univariate and multivariate analyses. RESULTS: The cumulative incidence rates of HCC were 14%, 29% and 48% at 5, 10 and 15 years after liver biopsy, respectively. Multivariate analysis identified high viral load, together with age and severe fibrosis, as independent and significant risk factors (P = 0.045, 0.047 and 0.013, respectively) for HCC. CONCLUSIONS: The present findings indicate that high viral load is a risk factor for HCC in patients with chronic HBV infection. Patients with a high HBV viral load should be carefully monitored for HCC.

Adolescent↗

PubMed2004

Quantification of infectious HIV-1 plasma viral load using a boosted in vitro infection protocol.

Methods currently used for HIV-1 viral load measurements are very sensitive, but cannot distinguish between infectious and noninfectious particles. Here we describe the development of a novel, sensitive, and highly reproducible method that allows rapid isolation and quantification of infectious particles from patient plasma. By immobilizing HIV-1 particles in human plasma to platelets using polybrene, we observed a 10- to 1000-fold increase in infectivity over infection protocols using free virus particles. Using this method, we evaluated infectivity in plasma from 52 patients at various disease stages. At plasma viral loads of 1000-10000 HIV-1 RNA copies/ml 18%, at 10,000-50,000 copies/ml 73%, at 50,000-100,000 copies/ml 90%, and above 100,000 copies 96% of cultures were positive. We found that infectious titers among patients vary distinctively but are characteristic for a patient over extended time periods. Furthermore, we demonstrate that by evaluating infectious titers in conjunction with total HIV RNA loads, subtle effects of treatment intervention on viremia levels can be detected. The immobilization procedure does not interfere with viral entry and does not restore the infectivity of neutralized virus. Therefore, this assay system can be utilized to investigate the influence of substances that specifically affect virion infectivity such as neutralizing antibodies, soluble CD4, or protease inhibitors. Measuring viral infectivity may thereby function as an additional, useful marker in monitoring disease progression and evaluating efficacy of antivirals in vivo.

Adult↗

PubMed1997

Plasma viral load and CD4+ lymphocytes as prognostic markers of HIV-1 infection.

BACKGROUND: The rate of disease progression among persons infected with human immunodeficiency virus type 1 (HIV-1) varies widely, and the relative prognostic value of markers of disease activity has not been defined. OBJECTIVE: To compare clinical, serologic, cellular, and virologic markers for their ability to predict progression to the acquired immunodeficiency syndrome (AIDS) and death during a 10-year period. DESIGN: Prospective, multicenter cohort study. SETTING: Four university-based clinical centers participating in the Multicenter AIDS Cohort Study. PATIENTS: 1604 men infected with HIV-1. MEASUREMENTS: The markers compared were oral candidiasis (thrush) or fever; serum neopterin levels; serum beta 2-microglobulin levels; number and percentage of CD3+, CD4+, and CD8+ lymphocytes; and plasma viral load, which was measured as the concentration of HIV-1 RNA found using a sensitive branched-DNA signal-amplification assay. RESULTS: Plasma viral load was the single best predictor of progression to AIDS and death, followed (in order of predictive strength) by CD4+ lymphocyte count and serum neopterin levels, serum beta 2-microglobulin levels, and thrush or fever. Plasma viral load discriminated risk at all levels of CD4+ lymphocyte counts and predicted their subsequent rate of decline. Five risk categories were defined by plasma HIV-1 RNA concentrations: 500 copies/mL or less, 501 to 3000 copies/mL, 3001 to 10000 copies/mL, 10001 to 30000 copies/mL, and more than 30000 copies/mL. Highly significant (P < 0.001) differences in the percentages of participants who progressed to AIDS within 6 years were seen in the five risk categories: 5.4%, 16.6%, 31.7%, 55.2%, and 80.0%, respectively. Highly significant (P < 0.001) differences in the percentages of participants who died of AIDS within 6 years were also seen in the five risk categories: 0.9%, 6.3%, 18.1%, 34.9%, and 69.5%, respectively. A regression tree incorporating both HIV-1 RNA measurements and CD4+ lymphocyte counts provided better discrimination of outcome than did either marker alone; use of both variables defined categories of risk for AIDS within 6 years that ranged from less than 2% to 98%. CONCLUSIONS: Plasma viral load strongly predicts the rate of decrease in CD4+ lymphocyte count and progression to AIDS and death, but the prognosis of HIV-infected persons is more accurately defined by combined measurement of plasma HIV-1 RNA and CD4+ lymphocytes.

Acquired Immunodeficiency Syndrome↗

PubMed1994

Viral load as a determinant for transmission of human papillomavirus type 16 from mother to child.

Whilst genital papillomaviruses are commonly believed to be sexually transmitted, transmission of human papillomavirus type 16 (HPV-16) from mother to child at delivery has been described previously [Pakarian et al. (in press) British Journal of Obstetrics and Gynaecology]. In order to determine whether viral load in cervical/vaginal cells was an important determinant of transmission 15 pregnant women with HPV-16 infections were studied. Eight of these women had infants who were positive for HPV-16 DNA at genital and/or buccal sites. Viral load was estimated by laser densitometry of polymerase chain reaction (PCR) products. The eight mothers--four with a previous history of abnormal smears and two with previous genital warts--who transmitted infection to their infants had significantly higher viral loads (P < 0.05) than those who did not. It is concluded that viral load is an important, but not the sole, determinant for the transmission of HPV-16 from mother to infant.

Adolescent↗

PubMed2000

Assessment of viral loads in patients with chronic hepatitis C with AMPLICOR HCV MONITOR version 1.0, COBAS HCV MONITOR version 2.0, and QUANTIPLEX HCV RNA version 2.0 assays.

The correlation between response to antiviral therapy and pretreatment viral load in patients with chronic hepatitis C has prompted the development of quantitative assays to measure viral load. The aim of our study was to assess the clinical relevance of the newly developed semiautomated PCR system COBAS HCV MONITOR version 2.0 in comparison with (i) the AMPLICOR HCV MONITOR version 1.0 assay, which underestimates RNA concentration of hepatitis C virus (HCV) genotypes 2 to 6, and (ii) the QUANTIPLEX HCV RNA version 2.0 assay, which achieves equivalent quantification for each HCV genotype, with samples from 174 patients diagnosed with chronic hepatitis C before therapy. The level and range of quantification measured with AMPLICOR HCV MONITOR version 1.0 were 1 log lower than when measured with the COBAS HCV MONITOR version 2.0, at 0.261 x 10(6) RNA copies/ml (range, 0.001 x 10(6) to 2.50 x 10(6) RNA copies/ml) and 4.032 x 10(6) RNA copies/ml (range, 0.026 x 10(6) to 72.6 x 10(6) RNA copies/ml), respectively. The two assays showed a poor correlation (r(2) = 0.175). The level and range of quantification were similar when measured with the COBAS HCV MONITOR version 2.0 and QUANTIPLEX HCV RNA version 2.0 assays, at 3.03 x 10(6) RNA copies/ml (range, 0.023 x 10(6) to 72.6 x 10(6) RNA copies/ml) and 4.91 Meq/ml (range, 0.200 to 49.5 Meq/ml), respectively. The two assays showed a strong correlation (r(2) = 0. 686) for each HCV genotype. The duration of treatment (6 or 12 months) is modulated according to HCV genotype and viral load. Our results indicate that COBAS HCV MONITOR version 2.0 and QUANTIPLEX HCV RNA version 2.0 assays showing an equal dynamic range for each HCV genotype are suitable tools to assess patients before therapy.

Evaluation Studies as Topic↗

PubMed2002

Lack of correlation between seminal and plasma HIV-1 viral loads is associated with CD4 T cell depletion in therapy-naïve HIV-1+ patients.

The present study was conducted to investigate a possible correlation between plasma (PVL) and seminal viral load (SVL) on treatment-naïve HIV-1-infected patients in Vitória, ES, Brazil. We also evaluated whether the progressive immunosuppression associated with HIV disease (as evidenced by declining CD4 T cell counts) has any impact on the correlation between PVL and SVL HIV-1. Viral load on paired blood and semen samples from 56 consecutive treatment-naïve patients were evaluated and compared to CD4 cell counts. Viral load and T cell counts (cells/microl) were determined by NASBA and by flow cytometry, respectively. Overall, a strong positive correlation between PVL and SVL (rho = 0.438, p = 0.001) was observed. However, when patients were grouped according to their CD4 counts, this correlation was only significant among patients with CD4 counts > 200 cells/microl. Results presented here demonstrate the existence of a strong correlation between PVL and SVL on patients with CD4 cell counts > 200 cells/microl, suggesting that this association may correlate with disease progression.

CD4 Lymphocyte Count↗