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PubMed2000

[Correlation between high plasma viral load and levels of TNF-alpha and cICAM-1 in HIV-1 infected children].

AIM: To assess the relationship among plasma TNF-a and cICAM-1 levels and plasma viral load (VL) in HIV-infected children and to compare these values with those of healthy non-HIV infected children. PATIENTS AND METHODS: We studied 44 HIV-infected children and 38 non-HIV-infected children. The VL was quantified using standard molecular assay. CD4 and CD8 lymphocyte subpopulations were determined by flow cytometry. TNF-a and cICAM-1 were quantified using commercially available specific enzyme-linked immunosorbent assay (ELISA). RESULTS: Levels of TNF-a and cICAM-1 were higher in HIV-infected children than in non-HIV infected children. HIV-infected children with VL > 50000 copies/ml had higher levels of TNF-a (12.83; 95% CI: 24.71 to 0.95 pg/ml) and cICAM-1 (248.94; 95% CI: 419.01 to 78.84 ng/ml) than HIV-infected children with VL < 50000 copies/ml. Interestingly, we found an increase of 6.57 pg/ml of TNF-a and 119.97 ng/ml of cICAM-1 levels for each log10 of VL. CONCLUSIONS: HIV-infected children had higher levels of TNF-a and cICAM-1 than healthy controls. Our data indicate a positive correlation among plasma TNF-a and cICAM-1 and VL levels.

Child, Preschool↗
PubMed2005

High viral loads of human papillomavirus predict risk of invasive cervical carcinoma.

High loads of human papillomavirus (HPV) 16 and HPV 18/45 increase the risk of developing invasive cervical carcinoma, revealing higher risk in percentiles of highest viral loads for HPV 16 (odds ratio (OR) 58.7, 95% confidence interval (CI) 21.9-151.4) compared to HPV 18/45 (OR 3.3, 95% CI 1.5-7.2). Thus, HPV load is a type-dependent risk marker for invasive carcinoma.

Adult↗
PubMed2001

Plasma viral load testing in the management of HIV infection.

The polymerase chain reaction assay, branched DNA assay and nucleic acid sequence-based amplification assay quantitate human immunodeficiency virus (HIV) RNA levels. Plasma viral load (PVL) testing has become a cornerstone of HIV disease management. Initiation of antiretroviral drug therapy is usually recommended when the PVL is 10,000 to 30,000 copies per mL or when CD4+ T-lymphocyte counts are less than 350 to 500 per mm3 (0.35 to 0.50 x 10(9) per L). PVL levels usually show a 1- to 2-log reduction within four to six weeks after therapy is started. The goal is no detectable virus in 16 to 24 weeks. Periodic monitoring of PVL is important to promptly identify treatment failure. When feasible, the same assay should be used for serial PVL testing in the individual patient. At least two PVL measurements usually should be performed before antiretroviral drug therapy is initiated or changed. PVL testing may be helpful in the rare instance of indeterminate HIV antibody testing, especially in a patient with recent infection.

Anti-HIV Agents↗
PubMed2006

Post-weaning breast milk HIV-1 viral load, blood prolactin levels and breast milk volume.

BACKGROUND: The effect of abrupt weaning, advocated as a safe transition from exclusive breastfeeding in HIV-exposed children, on the quantity of HIV viral load in breast milk (BMVL) is not known. OBJECTIVES: To determine the effect of abrupt cessation of breastfeeding on serum prolactin, pumped breast milk volume and BMVL obtained 2 weeks after rapid weaning in HIV-infected women. METHODS: Women enrolled in a prospective study (ZEBS) were randomized to abruptly wean at 20 weeks postpartum or continue exclusive breastfeeding. Breast milk was obtained at 22 weeks by electric breast pump over 10 min from 222 women who had either weaned or continued to breastfeed. Pre- and post-pumping prolactin was measured. BMVL was measured at 20 and 22 weeks in 71 randomly selected women from both groups. RESULTS: Baseline prolactin and breast milk volume was significantly lower among women who had weaned. Detectable (68 versus 42%; P = 0.03) and median BMVL (448 versus < 50 copies/ml; P = 0.005) was significantly higher among those who had weaned in comparison with those who were still breastfeeding and was significantly higher in the same women after weaning compared with 2 weeks earlier (P = 0.001). CONCLUSIONS: BMVL is substantially higher after rapid weaning and this may pose an increased risk of HIV transmission if children resume breastfeeding after a period of cessation. Increases in BMVL with differing degrees of mixed feeding needs to be assessed.

Adult↗
PubMed2006

[The correlation of HIV-1 viral load to expression of CD8+ T lymphocyte activators CD38 and HLA-DR].

OBJECTIVE: To investigate the correlation of CD38 and HLA-DR abnormal activating expression on CD8+ T with plasma viral load (VL) and evaluate the possibility of the economical CD38 and HLA-DR test to substitute VL assay in HIV/AIDS patients. METHODS: A multi-point correlation study of the percentage of CD38 and HLA-DR on CD8+ T by flow cytometry with plasma VL by bDNA was performed in 103 HIV/AIDS patients during a 12-month highly active anti-retroviral therapy (HAART). The cutoff values of CD38 and HLA-DR were evaluated with ROC area, sensitivity and specificity for predictive VL < 50 copies/ml, < 500 copies/ml, > 1000 copies/ml and > 10,000 copies/ml respectively. RESULTS: The level of CD38 and HLA-DR on CD8+ T in 103 patients decreased gradually with the reduction of VL during a 12-month HAART. The correlation of CD38 and HLA-DR with VL in the year of HAART was 0.424, 0.376, 0.335, 0.326, 0.297, 0.285 and 0.377, 0.318, 0.333, 0.312, 0.361, 0.358 with significant P value. Moreover, the overall correlation of CD38 and HLA-DR with VL were 0.483 (P < 0.001) and 0.477 (P < 0.001). Depending on optimal ROC, sensitivity and specificity for the substitute method, the cutoffs percentage of CD38 were < 68.5% and < 72.5% for predictive VL < 50 copies/ml and < 500 copies/ml as well as > 39.5% and > 46.5% of HLA-DR cutoff to predict VL > 1000 copies/ml and > 10,000 copies/ml. CONCLUSION: The detection of CD38 and HLA-DR percentage expression on CD8+ T can be available for prediction about HIV VL assay as a substitute method to survey the disease progression and HAART outcome in some resource-limited areas of China.

ADP-ribosyl Cyclase 1↗
PubMed2003

Characterizing the immune system after long-term undetectable viral load in HIV-1-infected children.

Thirty two HIV-infected children, on highly active antiretroviral therapy (HAART) and > 500 CD4+ T cells/mm3, were rated according to the time-course of viral load (VL) during the whole follow-up period (> 18 months) in a longitudinal retrospective study. (a) uVL group: 15 children with VL below 400 copies/mL; (b) dVL group: 17 children with higher VL. The uVL group showed higher memory (CD4+CD45RO+) T cells than did dVL group, and higher number of memory activated CD4+CD45RO+HLA-DR+ than did control group (healthy age-matched uninfected children), whereas CD4+CD45RA(hi)+CD62L+ was similar. However, TCR rearrangement excision circles (TRECs) were higher in uVL group than in dVL group. uVL Group showed CD8+CD45RO+ and CD8+CD45RO+CD38- higher number than the control group, but lower than the dVL group. The percentage of CD8+CD45RA(hi)+CD62L+, CD8+CD45RA+, CD8+CD62L-, and CD8+CD28+ was higher in uVL group than in dVL group, and lower than in control group. The uVL group showed higher number of activated (HLA-DR+CD38+, HLA-DR+, HLA-DR+CD38-) CD4+ T cells and lower percentages of CD4+HLA-DR-CD38+ than dVL group. In activated CD8- T cell, the uVL group had lower CD8+HLA-DR+CD38+, CD8+HLA-DR+, and CD8+CD38+ than the dVL group. Preeffector (CD8+CD57-CD28- and CD8+CD45RA-CD62L-) T cells were lower in the uVL group than in dVL group. In the effector (CD8+CD57+, CD8+CD57+CD28-, and CD8+CD45RA+CD62L-) T cells, HIV-infected-children had higher values than control group. HIV-infected-children who respond to HAART had TRECs reconstitution, decreased immune activation, and lower effector CD8+ T cells. Moreover, successful HAART allow the increment of activated CD4+ T cells.

Anti-HIV Agents↗
PubMed2004

Pathogenic and humoral immune responses to porcine reproductive and respiratory syndrome virus (PRRSV) are related to viral load in acute infection.

Although much research has been performed on porcine reproductive and respiratory syndrome virus (PRRSV), little quantitative information is available on the relationships between virulence and in vivo virus replication, among isolates recovered at different times in the history of PRRS, or the relative levels of virulence associated with individual virus isolates. In this study, the in vivo growth properties of virulent field isolates and attenuated PRRSV isolates were compared. The results show that virulent PRRSV isolates exhibit longer and more elevated levels of viremia, induce faster and more intense humoral immune responses, negatively affect body weight gain, induce higher death rates, and cause more severe clinical signs in a respiratory disease model. We found that the more virulent field isolates grew to significantly higher levels in pigs than did cell-culture adapted isolates. We concluded that the pathogenic consequences and immunological responses of pigs to PRRSV are directly related to viral load in acute infection as reflected in viral titers in blood.

Animals↗
PubMed1998

Suppression of plasma viral load below 20 copies/ml is required to achieve a long-term response to therapy.

BACKGROUND: Current guidelines state that the goal of antiretroviral therapy for HIV-infected individuals is to suppress plasma viral load (pVL) to below 400 copies/ml. METHODS: Predictors of achieving and maintaining pVL suppression were examined in a randomized trial of combinations of zidovudine, nevirapine and didanosine in patients with CD4+ T cell counts of between 200 and 600 x 10(6) cells/l who were naive to antiretroviral therapy and AIDS-free at enrolment. RESULTS: One hundred and four patients had pVL > 500 copies/ml at baseline and a pVL nadir below 500 copies/ml. Of these, 77 patients experienced an increase in pVL above 500 copies/ml. The median number of days of pVL suppression to below 500 copies/ml was 285 (42) for patients with pVL nadir < or = (>) 20 copies/ml (P = 00.0001). The relative risk of an increase in pVL above 500 copies/ml associated with a pVL nadir below 20 copies/ml was 0.11 (P = 0.0001). The relative risks of an increase in pVL above 5000 copies/ml associated with a pVL nadir below 20 copies/ml or between 20 and 400 copies/ml were 0.05 [95% confidence interval (CI), 0.02-0.12] and 0.37 (95% CI, 0.23-0.61) respectively, compared with individuals with a pVL nadir > 400 copies/ml. Individuals with a pVL nadir < or = 20 copies/ml were at a significantly lower risk of virologic failure than individuals with a pVL nadir of between 21 and 400 copies/ml (P = 0.0001). CONCLUSIONS: Our results demonstrate that suppression of pVL below 20 copies/ml is necessary to achieve a long-term antiretroviral response. Our data support the need for a revision of current therapeutic guidelines for the management of HIV infection.

Anti-HIV Agents↗
PubMed2000

Effect of antiretroviral therapy on viral load, CD4 cell count, and progression to acquired immunodeficiency syndrome in a community human immunodeficiency virus-infected cohort. Swiss HIV Cohort Study.

OBJECTIVE: To examine the effect of different antiretroviral treatment regimens on viral load, CD4 lymphocyte counts, and rates of progression to clinical acquired immunodeficiency syndrome events among treatment-naive human immunodeficiency virus (HIV)-infected patients enrolled in a large community cohort study. METHODS: Based in 7 outpatient clinics, the Swiss HIV Cohort Study is a cohort with national coverage. Virological, immunologic, and clinical results of 755 treatment-naive patients (median age, 36 years; 28.2% female) who initiated antiretroviral therapy between July 1, 1995, and June 30, 1997, were analyzed. Patients started undergoing monotherapy with 1 reverse transcriptase inhibitor (RTI), combination therapy with at least 2 RTIs, or highly active antiretroviral therapy (HAART) with RTIs and protease inhibitors. RESULTS: Antiretroviral treatment led to a mean reduction of viremia of 1.8 log10 copies per milliliter with HAART, 1.2 log10 copies per milliliter with RTI combination therapy, and 0.4 log10 copies per milliliter with monotherapy. Virological failure, defined as less than 1 log10 reduction per milliliter in viremia, was present in 45 (20%) patients undergoing HAART, 180 (38%) undergoing RTI combination therapy, and 47 (82%) undergoing monotherapy. The proportion of patients reaching undetectable viremia was 12% (n = 7) for monotherapy, 41% (n = 197) for RTI combination therapy, and 63% (n = 137) for HAART. Similar gains of CD4 cells were achieved with RTI combination therapy and HAART. Kaplan-Meier estimates of progression rates to a new acquired immunodeficiency syndrome event at 18 months were 13.6% (monotherapy), 4.7% (RTI combination therapy), and 3.9% (HAART). CONCLUSIONS: The rate of virological failure of antiretroviral treatments was high in this population of treatment-naive patients, even among patients receiving combination regimens. Clinical progression rates were, however, low in patients treated with RTI combination therapy and HAART.

Acquired Immunodeficiency Syndrome↗
PubMed2001

Efavirenz as a substitute for protease inhibitors in HIV-1-infected patients with undetectable plasma viral load on HAART: a median follow-up of 64 weeks.

We investigated, in a prospective cohort follow-up study, whether substituting efavirenz (EFV) for protease inhibitors (PIs) could be safe in HIV-infected patients with optimal viral suppression achieved on PI-containing regimens. In patients with undetectable plasma viral load (pVL) <50 copies/ml who were naive to therapy with nonnucleoside reverse transcriptase inhibitors (NNRTIs), PIs were replaced by EFV whereas associated nucleoside analogs (NAs) were retained. 62 patients were enrolled. Median follow-up on EFV was 64 weeks (2-88 weeks). Side effects due to EFV occurred in 48 patients. Two patients experienced a high level viral rebound due to diminished compliance; 55 (88.7%) maintained a pVL <50 copies/ml; 3 showed one episode of viremia (52-89 copies/ml); 2 stopped EFV before any VL control. Mean CD4 cell count did not change significantly. One AIDS patient experienced a single cutaneous recurrence of Kaposi's sarcoma after 40 weeks on EFV. Replacing PI with EFV in patients with optimal pVL suppression appears to be safe both virologically and immunologically.

Adult↗
PubMed2002

Characterization of nef gene of HIV type 1 in highly active antiretroviral therapy treated AIDS patients with discordance between viral load and CD4+ T cell counts.

The advent of highly active antiretroviral therapy (HAART) has been effective in the treatment of AIDS patients. However, after receiving this treatment for various periods of time, there is in some patients a significant increase in plasma viral load without a decrease in CD4+ T cell count. Our study involved nine such AIDS patients showing this discordance. We characterized changes in the nef gene of plasma HIV-1 isolated from these patients. Viral RNA was extracted from patient plasma, amplified by RT-PCR, cloned, and sequenced. Three sequences from each patient were obtained. The sequences were aligned and compared with other strains of HIV-1. Various substitutions were seen in most patients; however, two patients showed unique insertions of different sizes that are probably due to HAART.

Amino Acid Sequence↗
PubMed1999

Viral load and a locus on chromosome 11 affect the late clinical disease caused by Theiler's virus.

Theiler's virus causes a persistent infection and a demyelinating disease of mice which is a model for multiple sclerosis. Susceptibility to viral persistence maps to several loci, including the interferon gamma locus. Inactivating the gene coding for the interferon gamma receptor makes 129/Sv mice susceptible to persistent infection and clinical disease, whereas inactivating the interferon gamma gene makes C57BL/6 mice susceptible to persistent infection but not to clinical disease. This difference in phenotype is due to the difference in genetic background. Clinical disease depends on high viral load and Tmevd5, a locus on chromosome 11. These results have consequences for the identification of viruses which might be implicated in multiple sclerosis.

Animals↗
PubMed2007

CD8 T-cell subsets and viral load in the cerebrospinal fluid of therapy-naive HIV-infected individuals.

Central nervous system involvement is common in HIV infection. We determined the relationship between T-cell subsets and viral load in the cerebrospinal fluid (CSF) of therapy-naive, asymptomatic HIV-infected individuals. A shift from naive to effector-memory CD8 T cells was observed in the CSF of HIV-infected individuals compared with controls. The HIV load strongly correlated with CD8 T cells in CSF. Effector-memory CD8 T cells were positively and effector CD8 T cells were negatively associated with viral replication in CSF.

CD8-Positive T-Lymphocytes↗
PubMed2006

Asynchronous progression through the lytic cascade and variations in intracellular viral loads revealed by high-throughput single-cell analysis of Kaposi's sarcoma-associated herpesvirus infection.

Kaposi's sarcoma-associated herpesvirus (KSHV or human herpesvirus-8) is frequently tumorigenic in immunocompromised patients. The average intracellular viral copy number within infected cells, however, varies markedly by tumor type. Since the KSHV-encoded latency-associated nuclear antigen (LANA) tethers viral episomes to host heterochromatin and displays a punctate pattern by fluorescence microscopy, we investigated whether accurate quantification of individual LANA dots is predictive of intracellular viral genome load. Using a novel technology that integrates single-cell imaging with flow cytometry, we found that both the number and the summed immunofluorescence of individual LANA dots are directly proportional to the amount of intracellular viral DNA. Moreover, combining viral (immediate early lytic replication and transcription activator [RTA] and late lytic K8.1) and cellular (syndecan-1) staining with image-based flow cytometry, we were also able to rapidly and simultaneously distinguish among cells supporting latent, immediate early lytic, early lytic, late lytic, and a potential fourth "delayed late" category of lytic replication. Applying image-based flow cytometry to KSHV culture models, we found that de novo infection results in highly varied levels of intracellular viral load and that lytic induction of latently infected cells likewise leads to a heterogeneous population at various stages of reactivation. These findings additionally underscore the potential advantages of studying KSHV biology with high-throughput analysis of individual cells.

Antigens, Viral↗
PubMed2005

Influence of viral load and genotype in the progression of Hepatitis B-associated liver cirrhosis to hepatocellular carcinoma.

AIM/BACKGROUND: Hepatitis B virus (HBV) is an important factor in the development of hepatocellular carcinoma (HCC). We studied the influence of HBV viral load on HCC occurrence in HBV related liver cirrhosis (LC). PATIENTS AND METHODS: Ninety-one LC patients were followed up over a period of 7 years. Twenty three patients received Interferon (IFN) therapy. RESULTS: In 7 years, 23 patients developed HCC. Of them twenty-two (95.6%) were of genotype C. HBV DNA was found to be the only significant variable associated with HCC occurrence on both univariate (P = 0.029) and multivariate analysis (odds ratio 2.33; P < 0.033). The cumulative survival at 5 years was 83% and the annual rate of hepatitis B surface antigen clearance was 0.9 %. All of 17 HCC patients observed over a period of 5 years or more belonged to the continuously high HBV DNA group (annual average >3.7 log copies/ml) and all but one belonged to the continuously high alanine aminotransferase group (annual average >40 IU/l). CONCLUSION: Patients with genotype C and a continuously high HBV DNA for 5 years or more are at a high-risk group for HCC development. Maintaining continuously low HBV DNA for 3 years or more with anti-viral therapy, may be useful in preventing or delaying HCC occurrence.

Adult↗
PubMed2002

Treatment of intestinal worms is associated with decreased HIV plasma viral load.

BACKGROUND: We have previously suggested that helminthic infections make the host more susceptible to HIV infection and enhance its progression due to the chronic immune activation they cause. OBJECTIVE: To study the effect of antihelminthic treatment on HIV plasma viral load (VL) in HIV- and helminth-infected individuals living in Ethiopia. METHODS: Fifty-six clinically asymptomatic HIV-1-infected individuals, 31 (55%) of whom were also infected with helminths, were studied. All participants received antihelminthic treatment at baseline and at 3 and 6 months. Worm egg excretion, HIV plasma VL, and T-cell subsets were determined at baseline and 6 months after treatment. RESULTS: The mean age, number of CD4 T cells, and gender distribution were similar in the helminth-infected and -noninfected groups. At baseline, HIV plasma VL was strongly correlated to the number of eggs excreted (p <.001) and was higher in individuals infected with more than one helminth (5.28 +/- 0.35 versus 4.30 +/- 1.13 log RNA copies/mL, respectively; p =.16). After treatment of helminths, the 6-month change in HIV plasma VL was significantly different between the successfully treated group and the persistently helminth-positive group (p =.04) CONCLUSIONS: Helminth "load" is correlated to HIV plasma VL, and successful deworming is associated with a significant decrease in HIV plasma VL. The results of the current study, if confirmed in a larger study, may have important implications for slowing disease progression and reducing risks of transmission.

Acquired Immunodeficiency Syndrome↗
PubMed2003

Quantitative viral load monitoring and cidofovir therapy for the management of BK virus-associated nephropathy in children and adults.

BACKGROUND: BK virus (BKV)-associated nephropathy (BKVAN) has been increasingly recognized as an important cause of renal transplant dysfunction. We report the role of quantitative viral load monitoring in the management of BKVAN. METHODS: We developed a real-time quantitative polymerase chain reaction (PCR) assay for BKV detection in urine and plasma. Four renal allograft recipients, including two children, with BKVAN were treated with low-dose cidofovir and followed prospectively. RESULTS: The PCR assay showed a detection limit of 10 viral copies with an intra-assay coefficient of variation of 19%. All four patients with BKVAN demonstrated intranuclear inclusions on allograft biopsy and a progressive rise in serum creatinine; three patients underwent multiple biopsies before the diagnosis of BKVAN was made. Three of the patients experienced a "viral syndrome" before the onset of renal dysfunction. One child also demonstrated an echogenic renal mass. All of the patients demonstrated strongly positive urinary PCR values (>100,000 copies/microL). BKV DNA was also detected in the plasma of three patients. All the patients were treated with intravenous low-dose cidofovir (0.25-1 mg/kg per dose, every 2-3 weeks, without probenecid). BK viruria resolved within 4 to 12 weeks (after 1-4 doses) of the cidofovir therapy, and all patients remain with stable renal function 6 to 26 months posttherapy. CONCLUSIONS: Quantitative PCR for BKV is a sensitive and reliable method for following the course of the infection in renal transplant patients. In addition, cidofovir therapy may be useful in the treatment of some of these patients, and its role needs to be investigated further.

Adult↗