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PubMed1998

[Value of HIV-1 viral load and CD4 lymphocyte count as determinants of progression to AIDS and survival].

BACKGROUND: HIV-1 viral load is regarded as a better surrogate marker for progression and death than CD4+ cell counts. Both markers are analysed in a cohort of patients with unknown seroconversion date and advanced HIV infection. PATIENTS AND METHODS: Retrospective cohort analysis of 421 patients, most on antiretroviral therapy, with a median initial CD4+ cell count of 209 x 10(6)/l and a median initial viral load of 4.7 log copies/ml. One thousand two hundred and eighty-six samples were analysed. Univariate and bivariate analysis were performed with initial and sequential CD4+ cell counts and viral load values to estimate the risk of progression and death by Cox regression models. RESULTS: After a median follow up of 763 days, 124 patients developed AIDS and 117 died. Relative risks of progression related to the group that maintained viral load values always < 35,000 copies/ml were: 5-fold (95% CI: 1.4-17.0; p < 0.05) for patients with any viral load value > 35,000 copies/ml but always < 200,000 copies/ml; and 13.6 fold (95% CI: 5.4-34.2; p < 0.0001) for patients who could not maintain viral load < 200.000 copies/ml. CD4+ counts = 100 x 10(6)/l and viral load = 220,000 copies/ml were the threshold values that best fitted to estimate the probability of survival by a bivariate analysis. CONCLUSIONS: The maintenance of sequential viral load values < 35.000 copies/ml is associated with a lower risk of progression. The maintenance of sequential viral load values < 150,000 copies/ml is associated with higher short-term survival rates.

Acquired Immunodeficiency Syndrome↗

PubMed1999

Dynamics of viral load rebound and immunological changes after stopping effective antiretroviral therapy.

BACKGROUND: This study addresses the dynamic of viral load rebound and immune system changes in a cohort of eight consecutive HIV-1-infected patients in very early stages [all the patients were taking highly active antiretroviral therapy (HAART} and were recruited in the coordinating center from a larger study] who decided to discontinue HAART after 1 year of treatment and effective virologic response. The safety of this procedure and the outcome with reintroduction of the same treatment was also investigated. METHODS: Plasma, cerebrospinal fluid (CSF), and lymphatic tissue viral loads were measured at baseline; lymphocyte immunophenotyping and CD4 lymphocyte proliferative responses to mitogens and specific antigens were assessed. The same antiretroviral therapy was reintroduced as soon as plasma viral load became detectable (above 200 copies/ml). RESULTS: At day 0, plasma viral load was below 20 copies/ml in all eight patients (and below 5 copies/ml in five of eight patients). A rebound in plasma viral load was detected in all patients from day 3 to day 31 with a mean doubling time of 2.01 (SE 0.29) days. Three out of eight patients achieved a peak plasma viral load at least 0.5 log10 above baseline, pretreatment values. Mutations associated with resistance to reverse transcriptase or protease inhibitors were not detected. After 31 days off therapy, CD4 lymphocytes decreased [mean 45% (SE 4) to 37% (SE 3); P = 0.04], CD8+CD28+ lymphocytes decreased [mean 59% (SE 5) to 43% (SE 4); P = 0.03], and CD8+CD38+ lymphocytes increased [mean 55% (SE 3) to 66% (SE 4); P = 0.009]. Mean stimulation indices of lymphocytes treated with phytohemagglutinin (PHA) and CD3 decreased from day 0 to day 31 from 34% (SE 8) to 17% (SE 9) (P = 0.06) and from 24% (SE 8) to 5% (SE 2) (P = 0.02), respectively. These changes were mainly contributed by the group of five patients with plasma viral load below 5 copies/ml at day 0. Viral load dropped below 20 copies/ml in all patients after 1 month of restarting the same antiretroviral regimen. CONCLUSIONS: Discontinuation of HAART after 1 year of successful treatment is followed by a rapid rebound of viral load; this rapidly returns to undetectable levels following reintroduction of the same treatment. In patients with more effective control of virus replication (viremia below 5 copise/ml), discontinuation of treatment was associated with more severe impairment of immunologic parameters.

Adult↗

PubMed2000

A prospective study of interferon therapy modified by pre-treatment viral load in cirrhotic patients. Tokyo-Chiba Hepatitis Research Group.

BACKGROUND/AIMS: The relative role of hepatitis C virus (HCV) load and subtype as predictors of the efficacy of interferon therapy has been clarified in patients with chronic hepatitis C, but the effectiveness of interferon therapy in cirrhotic patients is still unclear. METHODS: To resolve this issue, we undertook a multicenter, randomized, and prospective study of 114 cirrhotic patients with hepatitis C virus infection. The patients were selected to undergo two different periods (6 or 12 months) of IFN therapy according to viral load. Patients with "low" viral load (< or = 10(5.8) copies/ml serum) were randomly divided into three groups, receiving 6 or 9 million units (MU) interferon three times a week for 6 months (total dose: 468 or 702 MU), or of a modified regimen using 6MU of IFN over 6 months (total dose 564 MU), while patients with "high" viral load (< or = 10(6.3) copies/ml serum) were also randomly divided into two groups of 6 or 9 MU of IFN three times a week for 12 months (total dose: 936 or 1,404 MU). RESULTS: HCV-RNA negativity rate at the completion of treatment with 6 or 9 MU IFN was 65% in patients with "low" viral load, in contrast to 14% in patients with "high" viral load. Sustained virological response was found in 40% of patients with "low" viral load irrespective of the three different regimens, in contrast to only 1 out of 35 patients (3%) with "high" viral load. Viral eradication was found in approximately 50% of patients having a low virus load (< or = 10(4.3) copies/ml) and with HCV subtype 2a. Univariate and multivariate analysis revealed that pretreatment viral load was a significant factor contributing to efficacy of IFN therapy. CONCLUSIONS: Sustained response was scarcely achieved in cirrhotic patients with high viral loads even after a 12-month course of intensive IFN therapy. This result indicates that there is a certain cut-off level of HCV RNA load which can not be eradicated.

Adult↗

PubMed2003

Results of a physician survey on ordering viral load testing. Opportunity for laboratory consultation.

OBJECTIVE: To profile physicians' practices, utilization, and understanding of human immunodeficiency virus type 1 RNA (viral load) testing and the laboratory's role in this testing. DESIGN: Cross sectional study using a 34-item self-report survey mailed to physicians identified as requesting viral load testing, with follow-up mailings to nonresponders. PARTICIPANTS: A sampling of US physicians specializing in infectious diseases, internal medicine, and family practice associated with high, medium, and low human immunodeficiency virus/acquired immunodeficiency syndrome incidence areas. RESULTS: Most respondents using viral load results were infectious diseases specialists practicing in urban areas. The reasons most frequently given for requesting viral load testing were (1) to assist in patient follow-up or monitoring (75.4%), and (2) to initiate/guide therapy (62.5%). Respondents indicated that the interpretation and use of viral load results presented difficulty in the areas of patient treatment and in determining what change from baseline was clinically significant. Few respondents used the testing laboratory pathologist as a resource for interpreting viral load test results. CONCLUSIONS: Our study indicates that physicians have questions about (1) the meaning of viral load tests, (2) how often to monitor the viral load, and (3) what change from baseline of the viral load is significant. Few physicians avail themselves of the expertise available in the laboratory for testing viral loads and interpreting such results.

Acquired Immunodeficiency Syndrome↗

PubMed2000

Haemophilic patients with hepatitis C have higher viral load compared to other well-defined patient groups.

Comparison of hepatitis C viral load between different patient populations has been hampered by the use of different technology in individual studies. We had the impression that haemophilic (HAEM) patients had a higher serum load of hepatitis C virus (HCV) compared to other HCV-infected patients. We therefore studied viral load and genotypes in active illicit drug users (IDU), HAEM patients and patients with post-transfusion hepatitis (PTH). The study comprises 225 HCV-RNA positive patients, 117 IDU, 60 HAEM patients and 48 PTH patients. All patients were anti-HIV negative. HCV-RNA was measured with a quantitative reverse transcription polymerase chain reaction (RT-PCR) method, HCV-genotypes were determined with genotype specific primers in RT-PCR in 221 patients. Four patients could not be genotyped with our assay and were excluded. Overall viral load was higher in genotypes 1 and 2 compared to genotype 3, median values of HCV-RNA were 1,400 x 10(3) geq ml(-1), 2,700 x 10(3) geq ml(-1) and 270 x 10(3) geq ml(-1), respectively. HAEM patients had significantly higher viral load for both genotypes 1 and 3 compared to the IDU and PTH patients. In a multiple linear regression model HCV-RNA viral load was independently associated with HAEM and genotype, but not to age, gender or disease duration. In conclusion, HAEM patients have higher viral load than IDU and PTH patients. The reason for this is unknown, but it may be due to host factors or mode of transmission with multiple inoculations.

Adult↗

PubMed2006

Longitudinal measures of human papillomavirus 6 and 11 viral loads and antibody response in children with recurrent respiratory papillomatosis.

OBJECTIVES: To measure human papillomavirus (HPV) 6 and 11 viral load and antibody response in longitudinal specimens obtained from children with recurrent respiratory papillomatosis and to examine the association of type-specific viral load with clinical severity of disease. DESIGN: Longitudinal pilot study with a median follow-up of 5.4 months. SUBJECTS: The study included 15 children undergoing therapy for recurrent respiratory papillomatosis at the Egleston Children's Hospital, Atlanta, GA, between January 22, 1999, and June 13, 2000. MAIN OUTCOME MEASURES: The kinetics of HPV-6 and HPV-11 viral load and antibody level were examined over time. Longitudinal HPV-6 and HPV-11 viral loads were analyzed for associations with clinical indicators of disease severity. RESULTS: Four children were infected with HPV-11, 4 were infected with HPV-6, and 7 had mixed infections. The HPV-6 and HPV-11 viral loads were stable over time in most of the children. Among children with mixed infections, HPV-6 viral loads were inversely correlated with those of HPV-11 (r = -0.80, P<.001). The HPV-11 infection was significantly associated with more annual surgical procedures (P=.02). Neither HPV-6 nor HPV-11 viral loads were associated with demographic factors or markers of clinical severity. None of the children had detectable antibodies against HPV-6, and only 3 had detectable antibodies against HPV-11 virallike particles. CONCLUSIONS: Our data support the association of HPV-11 infection with clinical severity. Measures of HPV-6 and HPV-11 viral loads are relatively stable over time in most children with recurrent respiratory papillomatosis, suggesting that multiple samples may not be necessary. Cytobrush samples may substitute for tissue biopsy specimens in HPV detection and typing, but not for absolute viral load determination.

Antibodies, Viral↗

PubMed2003

Breastmilk RNA viral load in HIV-infected South African women: effects of subclinical mastitis and infant feeding.

OBJECTIVE: To investigate determinants of breastmilk RNA viral load among HIV-infected South African women, with particular attention to infant feeding mode and subclinical mastitis. DESIGN: Observational, longitudinal study. METHODS: Information on current infant feeding practice and a spot milk sample from each breast were obtained from 145 HIV-infected lactating women at 1, 6 and 14 weeks postpartum. The sodium/potassium (Na+/K+) ratio in milk was taken as an indicator of subclinical mastitis. The association between milk RNA viral load and maternal and infant characteristics was investigated using uni- and multivariate models. RESULTS: Milk viral load was below the limit of detection of the HIV RNA assay (< 200 copies/ml) in 63/185 (34.1%), 73/193 (37.8%) and 68/160 (42.5%) of samples at 1, 6 and 14 weeks, respectively. Multivariate models predicted between 13 and 26% of variability in milk viral load in the first 14 weeks. Low blood CD4 cell count (< 200 x 10(6) cells/l) during pregnancy and raised milk Na+/K+ ratio were significantly associated with raised milk RNA viral load at all times, but there were no consistent associations between infant feeding mode and RNA viral load in milk. There was a non-significant trend for the six infants known to be infected postnatally, compared with the 88 infants who remained uninfected, to have been exposed to breastmilk of higher viral load at each time point. CONCLUSIONS: Breast milk HIV RNA viral load in the first 14 weeks of life varied; high levels were associated with subclinical mastitis and severe maternal immunosuppression. Multivariate models had limited predictive value for milk RNA viral load, illustrating the multiple contributors to viral load.

Adult↗

PubMed1998

Serial measurement of Epstein-Barr viral load in peripheral blood in pediatric liver transplant recipients during treatment for posttransplant lymphoproliferative disease.

BACKGROUND: Few data are available describing the natural history of the Epstein-Barr virus (EBV) viral load after the diagnosis of EBV-associated posttransplant lymphoproliferative disease (PTLD). Accordingly, we prospectively followed the EBV viral load after the diagnosis of EBV/PTLD in seven pediatric orthotopic liver transplant recipients. METHODS: EBV viral loads were serially measured by quantitative competitive polymerase chain reaction of the peripheral blood from pediatric patients with PTLD and correlated with the clinical course of these children. Viral loads >200 genome copies/10(5) peripheral blood lymphocytes were considered consistent with an increased risk of PTLD. Viral loads <200 obtained during treatment for PTLD were considered evidence of "clearance" of EBV; subsequent loads >200 were considered evidence of virologic "rebound." RESULTS: The mean EBV viral load at the time of diagnosis of PTLD was 1029. All patients "cleared" their EBV viral load during the treatment of PTLD; patient and graft survival in this series was 100%. The mean time to clearance of EBV from the peripheral blood (18.8 days) was similar to the mean time to onset of first rejection (13.8 days). EBV viral load at the time of diagnosis of rejection after PTLD was always <100. A rebound in the EBV viral load to >200 was noted in five of seven patients a median of 3.5 months (range 2.3-13 months) after the diagnosis of EBV/PTLD. However, none of these children has had any evidence of PTLD recurrence. CONCLUSIONS: Clearance of the EBV viral load from the peripheral blood seems to correlate with restoration of the host's immune response as noted both by the regression of the PTLD and the onset of rejection. Late rebound of the EBV viral load is common and does not seem to predict disease recurrence.

Child↗

PubMed2000

Temporal pathogenesis of experimental neonatal woodchuck hepatitis virus infection: increased initial viral load and decreased severity of acute hepatitis during the development of chronic viral infection.

Acute hepatitis B virus (HBV) infections either resolve or progress to chronicity. Identification of early deviations in host-virus responses associated with these outcomes can further differentiate cause-effect mechanisms that initiate and maintain chronicity. Neonatal woodchucks were infected experimentally with the woodchuck hepatitis virus (WHV) at 3 days of age. At 8 or 14 weeks of age (i.e. , the early- or mid-acute stage of infection), whole blood and large surgical biopsies of the liver were obtained from infected animals and uninfected controls. These were stored for later correlating histopathologic responses and viral load with the subsequently determined outcome of infection. As of 1 year postinfection, half of the surgically treated infected woodchucks had developed self-limited infections, while the other half developed chronic infections. The self-limited outcome was characterized by decreased viral load in acute-phase liver and plasma and a generally robust acute hepatic inflammatory response. Comparisons at the same early time points revealed that the chronic outcome was characterized by increasing initial viral load in liver and plasma, and a detectable, but diminished, acute hepatic inflammation. These cotemporal comparisons indicate that there is an early host-response deviation during the acute phase of a developing chronic infection. Continued analysis of the tissues banked from this study will facilitate further temporal characterization of acute-phase mechanisms that determine resolution versus chronicity in WHV infection. Understanding such mechanisms may be useful in the rational design of therapy for established chronic HBV infection.

Acute Disease↗

PubMed2005

Human leukocyte antigen phenotypes and hepatitis C viral load.

BACKGROUND: After hepatitis C virus (HCV) infection, 55% to 85% of patients become chronic carriers. HCV-RNA could be detected in the sera of these patients though the viral load varies. Various factors may be involved in determining the viral load. OBJECTIVES: In this study, we want to investigate the relationship between human leukocyte antigen phenotypes and hepatitis C viral load. STUDY DESIGN: One hundred and sixty HCV-RNA positive subjects were investigated in this study. RESULTS: We have analyzed 160 HCV-RNA positive subjects and found that lower HCV viral load is significantly associated with HBsAg-positivity (P = 0.017) but not age, gender, or mixed infection (infection with different HCV genotypes). One hundred and fifty-four HBsAg-negative subjects were further analyzed to explore the relationship between human leukocyte antigen (HLA) phenotypes and HCV viral load. Subjects with certain HLA alleles (A*34, B*56, DRB1*1502) have significantly lower viral load than those without these alleles (P = 0.0074, 0.0039 and 0.016, respectively) while those with HLA-B*4001 have significantly higher viral load (P = 0.0026). Furthermore, lower viral load was significantly associated with HLA-DRB1 heterozygosity in subjects with HLA-B heterozygosity (P = 0.048). CONCLUSIONS: Our data suggests a role for host immunogenetic factors in determining viral load during HCV infection.

Aged↗

PubMed1999

[Virologic evolution in HIV-infected subjects with an undetectable viral load in the first trimester of 1997].

OBJECTIVES: Assess the evolution of viral load in HIV-infected patients whose viral load was < 500 copies/ml during the first three months of 1997. PATIENTS AND METHODS: The viral load during the first three months of 1998 was recorded for comparison. Data were collected from the DM12 database implanted in the CISIH and concerned 2113 patients. RESULTS: Virological failure was observed in one-third of the patients in the study cohort whose viral load was undetectable in 1997 (< 500 copies/ml) as their load was > 500 copies/ml one year later in 1998. The percentage of patients in a situation of virological failure in 1998 who were taking tritherapy in 1997 (38%) was lower than that in those who were not (47%). The clinical and immunological characteristics were however similar. The difference in the therapeutic regimen would probably explain the difference. CONCLUSION: These findings demonstrate that virological failure is an important problem. Other analyses should be conducted in other cohorts to determine the influence of non compliance or resistance to antiretroviral treatments. Future therapeutic strategies should take into account the results of such studies.

Anti-HIV Agents↗

PubMedDate not supplied

[Detection of the viral load and its use as a virological marker in the follow-up of HIV-1-positive patients].

The evaluation of viral load as virological marker and its clinical and immunological correlation are presented. The first viral load studies were performed during 1996 at the National Reference Center for AIDS in Argentina in HIV-1 positive patients derived from different Hospitals in Buenos Aires. The study included 216 HIV-1 positive patients, 49 females and 167 males. Plasma was used for evaluating viral load and a second sample was obtained in 25 of the 216 patients for their monitoring. Viral load was performed using bDNA technique (Quantiplex HIV RNA assay 2.0, Chiron Corporation, USA). Other parameters such as CD4 count determined by flow cytometry and clinical stages according to CDC classification were obtained in order to correlate clinical and immunological status of the patients. When CD4 count was compared with viral load, the results showed a trend of viral RNA increase in plasma along with a decrease in CD4+ lymphocytes. This trend was also observed to correlate with the progression to AIDS disease. In all groups of patients, considering either CD4 counts or clinical status, ranges of viral load values were broad. Thus, as shown by percentiles 25 and 75, patients with CD4 counts < 200/ml, presented viral load values between 18,395 c/ml to 215,425 c/ml and patients with > 200/ml viral RNA showed values from < 10,000 to 35,180 c/ml. Patients with CDC's A and B stages presented values from < 10,000 to 45,160 c/ml and 87,000 c/ml respectively, while patients classified as C had 10,582 to 215,000 c/ml. Results of two consecutive samples in the 25 patients showed the usefulness of this technique for monitoring antiretroviral therapy. Nevertheless, despite the tendency of viral load to increase along with the progression of the disease, the broad range of values suggested the importance of using both virological and immunological parameters for the management of HIV infected patients.

Adolescent↗

PubMed2006

Multilaboratory comparison of hepatitis C virus viral load assays.

We report a multilaboratory evaluation of hepatitis C virus (HCV) viral load assays to determine their linear range, reproducibility, subtype detection, and agreement. A panel of HCV RNA samples ranging in nominal concentration from 1.0 to 7.0 log10 IU/ml was constructed by diluting a clinical specimen (genotype 1b). Replicates of the panel were tested in multiple laboratories using the Abbott TaqMan analyte-specific reagent (Abbott reverse transcription-PCR [RT-PCR]), Roche TaqMan RUO (Roche RT-PCR), Roche Amplicor Monitor HCV 2.0 (Roche Monitor), and Bayer VERSANT HCV RNA 3.0 (Bayer bDNA) assays. Bayer bDNA-negative specimens were tested reflexively using the Bayer VERSANT HCV RNA qualitative assay (Bayer TMA). Abbott RT-PCR and Roche RT-PCR detected all 28 replicates with a concentration of 1.0 log10 IU/ml and were linear to 7.0 log10 IU/ml. Roche Monitor and Bayer bDNA detected 27 out of 28 and 13 out of 28 replicates, respectively, of 3.0 log10 IU/ml. Bayer TMA detected all seven replicates with 1.0 log10 IU/ml. Bayer bDNA was the most reproducible of the four assays. The mean viral load values for panel members in the linear ranges of the assays were within 0.5 log10 for the different tests. Eighty-nine clinical specimens of various genotypes (1 through 4) were tested in the Bayer bDNA, Abbott RT-PCR, and Roche RT-PCR assays. For Abbott RT-PCR, mean viral load values were 0.61 to 0.96 log10 greater than the values for Bayer bDNA assay for samples with genotype 1, 2, or 3 samples and 0.08 log10 greater for genotype 4 specimens. The Roche RT-PCR assay gave mean viral load values that were 0.28 to 0.82 log10 greater than those obtained with the Bayer bDNA assay for genotype 1, 2, and 3 samples. However, for genotype 4 samples the mean viral load value obtained with the Roche RT-PCR assay was, on average, 0.15 log10 lower than that of the Bayer bDNA. Based on these data, we conclude that the sensitivity and linear range of the Abbott and Roche RT-PCR assays enable them to be used for HCV diagnostics and therapeutic monitoring. However, the differences in the viral load values obtained with the different assays underscore the importance of using one assay when monitoring response to therapy.

Genotype↗

PubMed2003

Changes in viral load in people with virological failure who remain on the same HAART regimen.

OBJECTIVES: To assess the rate of change in viral load and CD4 count over time in HIV-infected patients experiencing virological failure on a HAART regimen. DESIGN: Study population included patients from EuroSIDA, a large, multicentre, observational study enrolling HIV-infected patients across Europe. METHODS: Median change in viral load and CD4 count per month were estimated using the viral load and CD4 measurements obtained over a 12-month period after confirmed virological failure between 3 and 4 log10 copies/ml in a population of 488 HIV-infected patients who were left on a failing HAART regimen. RESULTS: The estimated median viral load change in our study population was 0.024 log10 copies/ml per month, statistically different from 0 (P=0.0001). In 20.9% of the patients studied viral load showed a tendency to decrease, in 47.8% showed a tendency to increase by a positive rate no higher than 0.04 log10 copies/ml per month and in the remaining 31.3% showed a tendency to increase by a rate greater than 0.04 log10 copies/ml per month. On average, CD4 counts were estimated to remain stable (decrease at a slow rate of about -0.53 cells/microl per month). CONCLUSIONS: In patients that remained on a stable, but virologically failing HAART regimen (with viral load ranging 1000-10000 copies/ml), the viral load over the ensuing 12-month period increased at a relatively slow rate. In contrast, the CD4 count remained stable, possibly because of partial but sustained viral suppression below the viral load natural set-point. The time-course of selecting more replication-competent virus in patients with virological failure remains to be fully clarified.

Adult↗

PubMed2004

Modelling HIV-RNA viral load in vertically infected children.

Human immunodeficiency virus (HIV) ribo-nucleic acid (RNA) viral load is a measure of actively replicating virus and is used as a marker of disease progression. For a thorough understanding of the dynamics of the evolution of the virus in the early life of HIV-1 vertically infected children, it is important to elucidate the pattern of HIV-RNA viral load over age. An aspect of assay systems used in the quantification of RNA viral load is that they measure values above particular cut-off values for detection, below which the assays used are not sufficiently sensitive. In this way, measurements are potentially left-censored. Recent adult studies suggest that to adequately model RNA pattern over age, it is necessary to account for within-subject correlation, due to repeated measures, and censoring. The aim of this study, therefore, was to establish whether it is necessary to use complex methods to allow for repeated measures within individuals and censoring of the HIV-RNA viral load in children enrolled in a cohort study. The approach involved the identification of an appropriate model for the basic pattern of RNA viral load by age and subsequent assessment of various estimation procedures accounting for repeated measures and censoring in different ways. Methods developed by Hughes involving the expectation-maximization (EM) algorithm and the Gibbs sampler were taken as the benchmark for comparison of simpler alternatives. Other approaches considered involve linear mixed-effects and ordinary least squares in which censoring is dealt with informally by taking the cut-off value as absolute or taking the mid-point between cut-off and zero. Fractional polynomials provided a substantially superior approach for modelling the dynamics of viral load over age compared to conventional polynomials or change-point models. Allowing for repeated measures was necessary to improve the power of the likelihood ratio tests required to establish the final model, but methods beyond taking the mid-point for censored values did not further improve the fit. Although Hughes' methodology is the best approach, its implementation is not necessary for the identification of the optimal model.

Algorithms↗

PubMed2003

Comparison of the effects of acute influenza infection and Influenza vaccination on HIV viral load and CD4 cell counts.

PURPOSE: Influenza vaccination is recommended for HIV-infected patients, although the efficacy is not clear. Prior studies have yielded differing results with regard to the effects of influenza vaccination on HIV viral load and CD4 cell counts. The effects of acute influenza on HIV viral replication and CD4 cell counts have not been well described. We sought to assess the effect of influenza infection and vaccination on HIV viral load and CD4 cell counts. SUBJECTS AND METHODS: All cases of influenza occurring in HIV-infected individuals over 3 years at a large county hospital were reviewed. For the year 1997-1998, data on all HIV clinic patients who were vaccinated for influenza were recorded prospectively. In order to assess the effects of influenza infection (Group I) and vaccination (Group II) on HIV viral load and CD4 cell counts, values from before and after influenza infection or vaccination were compared to each other and to a matched control group not vaccinated and without influenza infection (Group III). RESULTS: Forty-three cases of influenza were diagnosed. Pre- and post-influenza viral load in Group I was not significantly different: 3.34 versus 3.49 log copies/ml (P=0.36). Viral load was unchanged in 22 of 37 patients, increased in ten patients and decreased in five patients. Similarly, pre- and post-vaccination viral load in Group II was not significantly different: 3.52 versus 3.66 log copies/ml (P=0.12). Thirty-four of 47 patients who received influenza vaccine had no significant change in viral load-viral load increased in ten patients and decreased in three patients. No significant CD4 cell count changes were noted following influenza infection or vaccination. In contrast, Group III patients experienced a small decline in viral load from 4.23 to 3.39 log copies/ml, P<0.05, while there was a trend towards an increase in CD4 cell counts (P=0.06). CONCLUSIONS: Following influenza infection or vaccination, most patients did not have a significant increase in HIV viral load or decrease in CD4 cell count.

Acute Disease↗

PubMed2006

Determination of viral load thresholds in cervical scrapings to rule out CIN 3 in HPV 16, 18, 31 and 33-positive women with normal cytology.

An increased high-risk human papillomavirus (hrHPV) viral load in cervical scrapings has been proposed as a determinant for high-grade cervical intraepithelial neoplasia (CIN) and cervical cancer (> or =CIN 2), but data so far for HPV types different from HPV 16 are limited and inconsistent. In addition, a viral load threshold to distinguish hrHPV positive women without > or =CIN 2 still has not been defined. Here, we used baseline cervical scrapings of women with normal cytology participating in a large population-based cervical screening trial (i.e. POBASCAM) who were GP5+/6+-PCR positive for 4 common hrHPV types, i.e. HPV 16, 18, 31 or 33, as a reference to arbitrarily define various viral load thresholds (i.e. 25th, 33rd, 50th, 67th and 75th percentiles of the lowest viral load values) for distinguishing women having single infections with these types without high-grade CIN. Viral load assessment was performed by real time type-specific PCR. The viral load threshold values were subsequently validated on abnormal cervical scrapes of 162 women with underlying, histologically confirmed CIN lesions containing 1 of these 4 hrHPV types. All 59 women with CIN 3 had viral load levels that were higher than those of 33% of the women with normal cytology containing the respective hrHPV type detectable by GP5+/6+-PCR (i.e. higher than the 33rd percentile of viral load). By using this 33rd percentile viral load cut-off, sensitivity for CIN 3 of 100% (95% CI 93.9-100) was obtained. Hence, application of this viral load threshold would increase the specificity of HPV testing for HPV 16, 18, 31 and 33-associated prevalent CIN 3 without the cost of a marked reduction in sensitivity. In practice, on the basis of viral load analysis, a less aggressive management can be foreseen for 33% of the women with normal cytology participating in a population-based screening program who are GP5+/6+-PCR positive for HPV 16, 18, 31 or 33.

Adult↗

PubMed2003

Spontaneous viral clearance in patients with acute hepatitis C can be predicted by repeated measurements of serum viral load.

Early interferon (IFN) therapy prevents viral persistence in acute hepatitis C, but in view of the resulting costs and morbidity patients who really need therapy have to be identified. Twelve consecutive patients with acute hepatitis C (9 women, 3 men, mean age: 39.5 +/- 18.8 y, genotype 1: 7, genotype 3a: 3, 2 could not be genotyped) were studied. The sources of infection were medical procedures in 6, sexual transmission in 3, and intravenous drug abuse in 3 patients. Viral load was measured by Cobas Amplicor HCV Monitor v2.0 (Roche Diagnostic Systems, Branchburg, NY). The time from infection to clinical symptoms was 43.3 +/- 8.6 (mean +/- SD) days. Eight patients cleared hepatitis C virus (HCV) spontaneously and remained HCV-RNA negative with a follow-up of 9.0 +/- 3.9 months. In these patients viral load declined fast and continuously. The time from exposure to HCV-RNA negativity was 77.4 +/- 25.3 and from the first symptoms was 34.7 +/- 22.1 days. In 4 patients HCV-RNA levels remained high or even increased. Two of them became sustained responders to treatment initiated after a 6-week observation period. The 2 remaining patients were not treated (one because of contraindications for IFN, the other declined therapy) and are still HCV-RNA positive. In conclusion, patients with acute icteric hepatitis C have a high rate of spontaneous viral clearance within the first month after the onset of symptoms. IFN therapy appears only needed in patients who fail to clear the virus within 35 days after onset of symptoms. By this approach, IFN therapy was not necessary in two thirds of patients with acute hepatitis C.

Acute Disease↗