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PubMed1999

High-dose natural interferon-alpha therapy for chronic hepatitis C with a high viral load: predictors of efficacy. The Aomori, Akita and Iwate Areas Viral Hepatitis Research Group.

BACKGROUND: The effectiveness of interferon against hepatitis C has been found to be greatly affected by viral factors. However, few controlled interferon trials have involved seemingly intractable cases of chronic hepatitis C. METHODS: In 44 patients with high hepatitis C virus RNA levels (> or = 10(5) copies/mL), we carried out a prospective, controlled study of two natural interferon-alpha regimens, seeking predictors of therapeutic efficacy. Total natural interferon-alpha doses over 6 months in two groups were 780 and 840 million units, respectively. RESULTS: High therapeutic efficacy was achieved with no significant outcome difference between the regimens. The virus eradication rate was 35% and the rate of sustained biochemical response was 45% for both regimens. Multivariate logistic regression analysis identified viral genotype as the only significant predictor of success in viral eradication. CONCLUSIONS: Hepatitis C virus genotype 2 showed high sensitivity to interferon-alpha and this therapy can be recommended even for patients with a high viral load of this genotype. In contrast, with genotype 1b, cure was extremely difficult in cases with 10(7) or more copies/mL with a single 6-month course of interferon-alpha.

Adult↗

PubMed1999

Comparison of viral load and human leukocyte antigen statistical and neural network predictive models for the rate of HIV-1 disease progression across two cohorts of homosexual men.

We compared the performance of HIV-1 RNA and models based on human leukocyte antigen (HLA) in predicting the rate of HIV-1 disease progression using both linear regression and neural network models across two different cohorts of homosexual men. In all, 139 seroconverters from the Multicenter AIDS Cohort Study were used as the training set and 97 seroconverters from the District of Columbia Gay (DCG) cohort were used for validation to assess the generalizability of trained predictive models. Both viral load and HLA markers were strongly predictive of disease progression (p < .0001 and p = .001, respectively), with viral load superior to HLA (change in -2 log likelihood [-2LL] 26.7 and 10.2, respectively, in proportional hazards models). Consideration of both HLA markers and viral load offered no significant predictive advantage over viral load alone in most cases; however, HLA-based predictions obtained from neural networks modeling improved the discrimination among patients with high viral load (p = .02). Viral load, HLA scores, and rapid disease progression were moderately correlated (p < .01 for all three pairs of these variables). The median viral load was 10(3.70) copies/ml among DCG patients who had more favorable than unfavorable HLA markers and 10(4.66) copies/ml among patients with more unfavorable than favorable HLA markers. Viral load is a simpler, stronger predictor of disease progression than early developed HLA models, but neural network methods and further refined HLA models may offer additional prognostic information, especially for rapid progressors. The correlation between viral load and HLA markers suggests a possible HLA effect on setting viral load levels.

Cohort Studies↗

PubMed1999

Viral Load Monitoring in HIV Infection.

Measurement of HIV-1 viral load is now an accepted part of clinical practice for the determination of clinical prognosis and antiretroviral effectiveness in HIV infection. Consensus guidelines have been published on the appropriate use of this testing. Furthermore, recent advances in molecular technology have improved the sensitivity and reproducibility of viral load assays, and these improved assays have provided new insight into the pathogenesis of HIV disease. This article reviews new issues affecting viral load quantification, including viral subtypes, sex, compartmental differences, and other covariables.

Journal Article↗

PubMed2005

Semiquantitative human papillomavirus type 16 viral load and the prospective risk of cervical precancer and cancer.

We examined whether higher human papillomavirus type 16 (HPV16) viral load predicted risk of cervical intraepithelial neoplasia 3 (CIN3) or cancer (together termed > or =CIN3) within a cohort of 20,810 women followed for 10 years with cytologic screening. Semiquantitative viral load for HPV16 was measured on baseline cervicovaginal specimens using a type-specific hybridization probe test with signal amplification. An increased risk of > or =CIN3 associated with higher HPV16 viral load was found only among cytologically negative women in early follow-up, suggesting that these cases were related to the detection of prevalent lesions missed at baseline. Women with higher HPV16 viral load were more likely to undergo ablative treatment during follow-up than those with lower viral load (P(trend) = 0.008), possibly diminishing any additional risk for > or =CIN3 attributable to higher HPV16 viral loads.

Adolescent↗

PubMed2003

Association between virus-specific T-cell responses and plasma viral load in human immunodeficiency virus type 1 subtype C infection.

Virus-specific T-cell immune responses are important in restraint of human immunodeficiency virus type 1 (HIV-1) replication and control of disease. Plasma viral load is a key determinant of disease progression and infectiousness in HIV infection. Although HIV-1 subtype C (HIV-1C) is the predominant virus in the AIDS epidemic worldwide, the relationship between HIV-1C-specific T-cell immune responses and plasma viral load has not been elucidated. In the present study we address (i) the association between the level of plasma viral load and virus-specific immune responses to different HIV-1C proteins and their subregions and (ii) the specifics of correlation between plasma viral load and T-cell responses within the major histocompatibility complex (MHC) class I HLA supertypes. Virus-specific immune responses in the natural course of HIV-1C infection were analyzed in the gamma interferon (IFN-gamma)-enzyme-linked immunospot assay by using synthetic overlapping peptides corresponding to the HIV-1C consensus sequence. For Gag p24, a correlation was seen between better T-cell responses and lower plasma viral load. For Nef, an opposite trend was observed where a higher T-cell response was more likely to be associated with a higher viral load. At the level of the HLA supertypes, a lower viral load was associated with higher T-cell responses to Gag p24 within the HLA A2, A24, B27, and B58 supertypes, in contrast to the absence of such a correlation within the HLA B44 supertype. The present study demonstrated differential correlations (or trends to correlation) in various HIV-1C proteins, suggesting (i) an important role of the HIV-1C Gag p24-specific immune responses in control of viremia and (ii) more rapid viral escape from immune responses to Nef with no restraint of plasma viral load. Correlations between the level of IFN-gamma-secreting T cells and viral load within the MHC class I HLA supertypes should be considered in HIV vaccine design and efficacy trials.

Gene Products, env↗

PubMed2006

Comparison of time to undetectable HIV viral load in the first 16 weeks after the start of three and four antiretroviral regimens.

The aim of this paper is to compare the time to a viral load <50 copies/mL of three or four antiretroviral therapy (ART) regimens among ART naïve patients within the first 16 weeks after the start of treatment. A retrospective study was carried out on ART naïve patients who started HAART between 1 January 1999 and 1 January 2004. ART naïve patients with a viral load >5.3 log10 copies/mL at the time of treatment were routinely started on four ART regimens in one of the HIV centres in Edinburgh. These patients were compared with ART naïve patients with viral load >5.3 log10 copies/mL at the time of start of three ART regimens in the other centre within the study period. During the study period, of 93 ART naïve patients with a viral load >5.3 log10 copies/mL, 56 and 37 commenced four drug and three drug regimens, respectively. Patients in each group were matched for their age, prevalence of HCV, median age, and median viral load at the start of therapy; however, patients on three drug regimens had significantly lower CD4 counts (P<0.01). The median time to undetectable viral load was 13.5 weeks for three and four drug regimens (P>0.05). By the time of undetectable viral load, there was no difference in the CD4 count of patients on three or four drug regimens. Similar proportions of immunosuppressed patients on three and four ART regimens had undetectable viral load within the first 16 weeks of therapy.

Anti-Retroviral Agents↗

PubMed2005

Sexual risk behaviour, viral load, and perceptions of HIV transmission among homosexually active Latino men: an exploratory study.

The objective of the paper was to describe awareness of HIV medications and HIV viral load, and to assess the impact of HIV medications (including highly active antiretroviral therapy) and notions of viral load on sexual risk practices. This was an exploratory cross-sectional study of a non-random sample of 395 homosexually active Latino men in New York City. An anonymous self-administered questionnaire was used focusing on perceptions about HIV/AIDS, HIV treatment medications and viral load, risk perceptions, HIV status, and sexual partners and practices in the past 6 months. HIV-positive participants taking HIV medications, those who knew their viral loads, and those who had undetectable viral loads did not report significantly different frequencies of high-risk (receptive or insertive) unprotected anal intercourse (UAI) in comparison to other HIV-positive individuals in the sample. Perceptions about HIV status (assuming same status) and viral load (penetrating partner or letting partner penetrate one) were related to significantly higher high-risk UAI in the past 6 months. HIV prevention strategies for homosexually active Latino men should not only address the basic issue of assuming similar HIV status but also need to examine misconstructions of the transmissibility of HIV as a result of undetectable viral load.

Adolescent↗

PubMed2005

The effects of early syphilis on CD4 counts and HIV-1 RNA viral loads in blood and semen.

OBJECTIVE: To examine the effect of early syphilis on blood and semen plasma HIV-1 viral loads and CD4 counts. METHODS: In a retrospective case-control study, blood plasma HIV-1 viral loads and CD4 counts in cases during early syphilis (n = 63, 27 receiving antiretroviral therapy) were compared to those before and after syphilis and with controls with non-systemic acute sexually transmitted infections (STI) (n = 104, 39 receiving antiretroviral therapy). In a prospective substudy in those not receiving antiretroviral therapy, semen plasma viral loads during early syphilis (n = 13) were compared with those 1 month, 3 months, and 6 months after treatment for syphilis and with controls with no STIs (n = 20). RESULTS: Retrospective study: CD4 counts were similar in cases (median 410, n = 139 counts) during early syphilis compared to before (485, n = 80) and after (475, n = 88). In a secondary analysis, a drop in CD4 count (21%) among those with early latent syphilis was observed compared with controls. Blood plasma viral loads did not change significantly overall or in those with primary, secondary, or early latent syphilis. Effects were similar on or off antiretroviral therapy. Prospective study: blood and semen viral loads were slightly higher in cases compared with controls but treatment of early syphilis did not reduce either. CONCLUSIONS: We detected no association between early syphilis and changes in blood or semen viral load or CD4 count. Increased HIV-1 infectivity associated with early syphilis is unlikely to be associated with increased levels of HIV-1 RNA in blood or semen.

CD4 Lymphocyte Count↗

PubMed2003

Viral load and HIV treatment attitudes as correlates of sexual risk behavior among HIV-positive gay men.

OBJECTIVES: People living with HIV who achieve an "undetectable" viral load may assume that they are less infectious, leading to increased sexual risk. We examined the relation between perceiving that one has an undetectable viral load and sexual risk taking among gay men. METHODS: HIV-positive participants (N=60) completed measures assessing HIV serostatus, perceived HIV viral load (detectable vs. undetectable), sexual risk and treatment attitudes. RESULTS: Contrary to hypotheses, HIV-positive men with detectable viral loads were more likely to report unprotected anal sex with a nonprimary partner than were men reporting undetectable viral loads. Although a significant minority endorsed the belief that an HIV-positive partner with an undetectable viral load is less infectious, this belief was unrelated to sexual risk. Multivariate analyses showed that the strongest predictor of sexual risk was a measure assessing participants' reduced concern over HIV stemming from the availability of improved HIV treatments. After controlling for reduced HIV concern, viral load status was no longer a significant predictor of risk. CONCLUSIONS: Results suggest that reduced concern about the consequences of HIV infection may be more important than perceived health status as a determinant of risky sex and highlight the need for continued prevention efforts among people who are HIV-positive.

Adult↗

PubMed1998

Mathematical analysis of antiretroviral therapy aimed at HIV-1 eradication or maintenance of low viral loads.

Motivated by the ability of combinations of antiretroviral agents to sustain viral suppression in HIV-1-infected individuals, we analyse the transient and steady-state behavior of a mathematical model of HIV-1 dynamics in vivo in order to predict whether these drug regimens can eradicate HIV-1 or maintain viral loads at low levels. The model incorporates two cell types (CD4+ T cells and a long-lived pool of cells), two strains of virus (drug-sensitive wild type and drug-resistant mutant) and two types of antiretroviral agents (reverse transcriptase and protease inhibitors). The transient behavior of the cells and virus and the eventual eradication of the virus are determined primarily by the strength of the combination therapy against the mutant strain and the maximum achievable increase in the uninfected CD4+ T cell concentration. We also predict, if the parameters of the model remain constant during therapy, that less intensive maintenance regimens will be unable to maintain low viral loads for extensive periods of time. However, if the reduction in viral load produced by therapy reduces the state of activation of the immune system, the number of cells susceptible for HIV-1 infection may decrease even though total CD4+ T cells increase. Our model predicts that if this occurs strong inductive therapy that reduces viral load followed by weaker maintenance regimes may succeed.

Antiviral Agents↗

PubMed2003

High-density lipoprotein concentrations relate to the clinical course of HIV viral load in patients undergoing antiretroviral therapy.

OBJECTIVE: To determine whether levels of HDL are associated with viral load response in HIV-treated patients, and to seek an explanation based on amino acid sequence similarity between the key apolipoprotein A1 and HIV proteins concerned in viral replication. DESIGN: The major HDL lipoprotein is apolipoprotein A1, which is able to inhibit HIV-induced syncytium formation. This retrospective clinical study assessed the relationship between the response to antiretroviral treatment (time of undetectable viral load/duration of viral suppression below the limit of detection) and HDL-cholesterol levels on commencing antiretroviral treatment. PATIENTS AND METHODS: HIV-treated patients with undetectable HIV viral loads were followed every 3 months for 36 months. We measured total cholesterol, HDL-cholesterol, triglycerides, previous responses to antiretroviral treatment, opportunistic infections, sex and age. These variables were assessed in relation to the time of undetectable viral load until viral rebound. Amino acid sequence alignment was performed with HIV proteins and apolipoprotein A1 to detect shared similarity. RESULTS: The Cox proportional hazards model showed a significant association between HDL-cholesterol and the time of undetectable viral load. The other variables studied were not associated. There was 30% sequence similarity in an area of 50 amino acids shared between apolipoprotein A1 and p17 Gag-HIV protein. CONCLUSION: High levels of HDL-cholesterol are associated with a better viral response in treated HIV patients. This association could be related to the sequence similarity and structure homology between apolipoprotein A1 and p17 Gag-HIV protein, which raises the intriguing clinical possibility that inducing an increase in HDL could assist HIV therapy.

Adult↗

PubMed2005

HPV16 semiquantitative viral load and serologic biomarkers in oral and oropharyngeal squamous cell carcinomas.

A considerable subset of oropharyngeal squamous cell carcinomas (SCCs) are positive for human papillomavirus (HPV); however, delineating etiologically-associated HPV infections from SCCs with concurrent HPV infection unrelated to tumorigenesis is challenging. Viral load assessment in biopsy specimens may help facilitate such differentiation. HPV16 viral load and serologic markers were assessed among oral and oropharyngeal cases from a multinational study conducted by the International Agency for Research on Cancer (IARC). HPV16 viral load, measured semiquantitatively by PCR-enzyme immunoassay, was dichotomized as high or low based on the median optical density value. Serologic antibodies to HPV16 virus-like particles (VLPs) and to HPV16 E6 and E7 proteins were measured by ELISA. Compared to HPV DNA-negative cases (n = 852), HPV16 DNA-positive cases with high viral load (n = 26) were significantly more likely to originate in the oropharynx (odds ratio [OR], 12.0; 95% confidence interval [CI], 5.2-27.5) and, after adjustment for tumor site (AdjOR), have antibodies against HPV16 VLPs (AdjOR, 14.6; 95% CI, 6.0-35.6), E6 (AdjOR, 57.6; 95% CI, 21.4-155.3) and E7 (AdjOR, 25.6; 95% CI, 9.3-70.8). HPV16 DNA-positive cases with low viral load (n = 27) were more commonly oropharyngeal (OR, 2.7; 95% CI, 1.1-6.2) and seropositive for HPV16 VLPs (AdjOR, 2.7; 95% CI, 1.1-6.9), E6 (AdjOR, 3.0; 95% CI, 0.7-14.0) and E7 (AdjOR, 3.5; 95% CI, 0.7-16.3), compared to HPV DNA-negative cases; the associations, however, were neither as strong nor as significant as the associations for high viral load. As there appears to be a strong association between HPV16 serologic markers and viral load, in the absence of data on serologic markers, HPV16 viral load may be used to help delineate the subset of HPV16 DNA-positive oral and oropharyngeal cancers that may be the consequence of HPV infection.

Antibodies, Viral↗

PubMed2001

Viral load test reports: a description of content from a sample of US laboratories.

CONTEXT: Human immunodeficiency virus (HIV) RNA testing (viral load testing) is increasingly important in the care of patients infected with HIV-1 to determine when to initiate, monitor, and change antiretroviral therapy. Patient viral load testing information is communicated to the clinician through the laboratory test report. OBJECTIVES: To examine the format and information used in reporting viral load testing results and determine the clarity of the information provided in these reports. DESIGN: Patient test reports with all personal identifiers removed were requested of viral load testing laboratories participating in a telephone survey of laboratory practices. Hospital, independent, health department, and "other type" laboratories identified as university-associated laboratories participated in the telephone survey. RESULTS: Thirty-seven unique test reports were collected. All laboratories reported results in copies/mL, while 14% also reported results as "log(10) copies/mL." The test kit was identified by only 24% of the laboratories. Reportable ranges were specified by 70% of the laboratories, but there was considerable variation in terminology. One laboratory reported a viral load copy number below the manufacturer's test kit lower limit of sensitivity. The layout and format differed among reports. Some results were expressed in log(10), others contained nonsignificant integers, while others contained exponential numbers. Supplemental information in some reports included previous patient test results and significance of changes from baseline. The format of some reports made it difficult to read the report information and interpret the testing results. CONCLUSION: This study emphasizes the importance of standardizing the reporting of HIV-1 viral load test results to minimize result misinterpretation and incorrect treatment.

Data Collection↗

PubMed2001

Clinical and immunological benefits from highly active antiretroviral therapy in spite of limited viral load reduction in HIV type 1 infection.

Both naive and memory T lymphocyte responses are lost during advanced HIV infection. Treatment with highly active antiretroviral therapy (HAART) is associated with an increase in T lymphocytes and a reduction in viral load. However, the viral response to HAART in patients with low levels of helper T lymphocytes and a high viral load is often not satisfactory. We investigated the capacity of long-term HAART to reconstitute the immune system in severely ill patients. A nonselected longitudinal patient population with high baseline viral levels and CD4(+) cells below 100 x 10(6)/liter were monitored for 2 years during HAART. Markers to estimate the therapeutic effects included viral levels and cell surface markers representing naive and memory T lymphocytes as well as activation markers, B cells, NK cells, and clinical events. After 2 years of treatment, viral load was reduced to undetectable levels in 55% (viral responders, vRs) and less than 1 log (median value) from baseline in 45% (viral low responders, vLRs). Elevated numbers of memory and naive CD4(+) and CD8(+) cells as well as a decrease in activation markers were seen in both vRs and vLRs. However, the magnitude was greater in vRs. No differences in the clinical outcome were observed between vRs and vLRs. We conclude that most patients, even in advanced stages of HIV disease, benefited from HAART. The magnitude of the response was related to good viral reduction, but even patients with poor viral reduction had a recovery of naive and memory CD4(+) and CD8(+) cells. Even a small reduction in viral load is thus of importance for health and potentially also for years of survival.

Adult↗

PubMed2002

Viral load in Epstein-Barr virus-associated hemophagocytic syndrome.

The viral load in peripheral blood from patients with Epstein-Barr virus (EBV)-associated hemophagocytic syndrome was measured by real-time quantitative PCR and compared with that in infectious mononucleosis. Patients with EBV-associated hemophagocytic syndrome generally had larger viral burdens, although it was difficult to differentiate EBV-associated hemophagocytic syndrome from infectious mononucleosis simply by viral load. The difference in viral load seemed to be clearer in peripheral blood mononuclear cells than in plasma.

Adult↗

PubMed2006

Attempted therapeutic immunization in a chimpanzee chronic HBV carrier with a high viral load.

BACKGROUND: We previously reported successful therapeutic immunization in a chimpanzee having a relatively low viral load, which was immunized with recombinant plasmid hepatitis B surface antigen (HBsAg) DNA and boosted with recombinant HBsAg encoding canarypox virus. In the present study, we attempted to confirm these findings in an animal with a high virus load. METHODS AND RESULTS: We tested three immunization strategies successively over a 3-year period. In the first of these, we administered four monthly injections of DNA encoding HBsAg + PreS2 + hepatitis B core antigen (HBcAg) + DNA encoding interleukin (IL)-12, (given 3 days later), and boosted with canarypox expressing all of the above HBV genes 6 months after initial immunization. No reduction in viral load was observed. In the second trial, we administered lamivudine for 8 weeks, and then began monthly DNA-based immunization with plasmids expressing the above viral genes; however, viral loads rebounded 1 week after termination of lamivudine therapy. In a third trial, we continued lamivudine therapy for 30 weeks and immunized with vaccinia virus expressing the above viral genes 18 and 23 weeks after the start of lamivudine therapy. Again viral loads rebounded shortly after cessation of lamivudine treatment. Analysis of cell-mediated immune responses, and their avidity, revealed that DNA-based immunization produced the strongest enhancement of high avidity T-cell responses, while recombinant vaccinia immunization during lamivudine therapy enhanced low avidity responses only. The strongest low and high avidity responses were directed to the middle surface antigen. CONCLUSIONS: Three strategies for therapeutic immunization failed to control HBV viremia in a chronically infected chimpanzee with a high viral load.

Animals↗

PubMed2000

Correlation of baseline quantitative plasma human immunodeficiency (HIV) type 1 RNA viral load with clinical status and CD4+ T-cell counts in treatment-naïve HIV-positive patients in Singapore.

INTRODUCTION: Quantitative measurement of plasma HIV-1 RNA viral load has been available in Singapore since 30 November 1996. This study investigates the relationship, in antiretroviral-naïve, HIV-positive Singapore residents, between the baseline HIV-1 RNA viral load and clinical status at the time of quantification. The association of HIV-1 RNA viral load with CD4+ T-cell counts was also studied. MATERIALS AND METHODS: HIV-1 RNA viral load was determined using Amplicor HIV-1 Monitor Test. One hundred and eighty subjects had baseline plasma HIV-1 RNA levels quantified during the period 30 November 1996 to 27 July 1998. They were classified into three clinical groups: A for asymptomatic infection (n = 110), B for symptomatic infection (n = 29) and C for AIDS (n = 41). RESULTS: The differences between mean HIV-1 RNA levels were statistically significant (P < 0.001) for groups A and B (mean difference = -0.61 log10), and for groups A and C (mean difference = -0.75 log10). However, there was no statistically significant difference (P = 0.68) between groups B and C (mean difference = -0.13 log10). Of those subjects with CD4+ T-cell counts measured within 30 days of viral load quantification, there were statistically significant negative correlations between HIV-1 viral load and CD4+ T-cell counts for groups A (n = 91, r = -0.536, P < 0.01) and C (n = 34, r = -0.446, P < 0.01) but not group B (n = 26, r = -0.297, P > 0.05). CONCLUSION: This suggest that the more advanced the phase of HIV infection, the higher the baseline plasma viral load and the lower the CD4+ T-lymphocyte counts.

Adult↗

PubMed1999

Viral loads in dual infection with HIV-1 and cytomegalovirus.

OBJECTIVE: A one year study of the relation between cytomegalovirus (CMV) and human immunodeficiency virus (HIV) viral loads in a cohort of children with vertically acquired HIV-1 infection. DESIGN: Comparative analysis of viral load measurements for CMV and HIV-1 in peripheral blood leucocytes (PBLs) of individual children in relation to age and clinical staging. METHODS: Nested polymerase chain reaction (PCR) was used to measure HIV-1 proviral DNA and CMV genomic DNA in PBLs of 56 children. RESULTS: The CMV load was highest in 0-2 year old HIV positive children with stage C disease (range, 1-7143 copies/100 ng DNA; median, 125) and was significantly lower in older children. Although higher in young children, HIV-1 viral load did not show the same marked reduction with age that is seen with CMV. Over a one year period, testing of serial samples for both viruses in a subgroup of children revealed a discordant relation between viral loads for CMV and HIV-1. CONCLUSIONS: CMV viral load falls much faster than HIV viral load in dually infected children. Screening for clinical CMV disease is most likely to be of benefit in children under 2 years of age with stage C disease. In the few children studied, levels of CMV and HIV replication appear to be independent.

Adolescent↗