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PubMed2005

A study to investigate the impact of the initiation of highly active antiretroviral therapy on the hepatitis C virus viral load in HIV/HCV-coinfected patients.

Changes in the hepatitis C virus (HCV) viral load (VL) were assessed in a retrospective study of 50 HIV/HCV-coinfected patients who initiated highly active antiretroviral therapy (HAART). Most patients responded to HAART [during the first 6 months, plasma HIV VL fell by a mean 1.39 log10, becoming undetectable (<400 copies/ml) in 22% and CD4+ T cells increased by a mean of 100 cells/microl], but surprisingly, 27 (54%) showed some rise and 25 (50%) showed a significant increase in the HCV VL. This figure was considered to be a minimum estimate. A majority of the patients showed an increase of less than 1 log10 that was associated with a rapid decrease in the HIV VL, whereas an increase in the HCV VL of greater than 1 log10, noted in eight patients, was associated with a baseline CD4+ cell count of less than 200 cells/microl. The increase in the HCV VL was not associated with hepatitis as determined by raised alanine transferase.

Adult↗

PubMed2003

Factors associated with the evolution of the viral load in individuals with HIV infection.

The temporal evolution of the viral load (VL) in a group of patients under clinical care and the identification of individual variables that determined this evolution was studied using a retrospective descriptive study of the VL determinations on 1336 patients between September 1996 and June 2000. During follow-up, patients' VLs increasingly fell below the detection threshold. Those patients who had received antiretroviral treatment prior to the monitoring of the viraemia presented lower VLs at the start of their follow-up. Those patients who had been cared for on the same unit throughout their follow-up maintained lower VLs. Female patients uniformly presented lower VL results than the males. The immunological status at the beginning of follow-up and the basal VL determined the initial evolution of the patients' VL, although it did not do so in the final stages of follow-up. The immunological and virological state at the onset of the follow-up determines the evolution of the patients' VL.

Adolescent↗

PubMed2001

Increase in B19 viral load prior to relapse of anaemia in an AIDS patient with persistent B19 infection.

Anaemia caused by persistent parvovirus B19 infection can be remitted by intravenous immunoglobulin (IVIG) treatment. However, maintenance IVIG therapy is required in some AIDS patients as well as patients with combined immuno-deficiency because of relapse of anaemia. We used a simple semi-quantitative polymerase chain reaction (PCR) method to trace plasma B19 viral load after administration of IVIG. We noted that the rebound of B19 viral load occurred 6 weeks prior to detection of anaemia. This method may be helpful in determining the interval of maintenance IVIG therapy.

Acquired Immunodeficiency Syndrome↗

PubMed1998

Effect of antiretroviral therapy and viral load on the perceived risk of HIV transmission and the need for safer sexual practices.

BACKGROUND: Dramatic reductions in plasma HIV RNA levels are possible with current antiretroviral regimens; the effect of potent therapies and "undetectable" viral load on the perceived risk of HIV transmission and need for safer practices remains unknown. METHODS: A questionnaire was developed to examine perceptions of HIV transmission risk and need for safer practices with unprotected anal, vaginal, and oral sex and intravenous drug use with needle sharing for HIV-discordant couples in which the HIV-infected partner was receiving no therapy, was receiving reverse transcriptase inhibitor therapy, and protease inhibitor (PI)-based therapy with viral load "undetectable". This was applied anonymously to 147 unselected HIV-infected individuals attending a university-based HIV clinic. RESULTS: Almost all respondents believed that all sexual activities except oral sex were "very risky" and that safer practices were "extremely important" for those not receiving antiretroviral agents. Significantly fewer considered that anal or vaginal sex was "very risky" for those receiving PI therapy (90.9% and 86.0%, respectively), and fewer thought that safer practices for anal or vaginal sex were "very important" for those receiving PI therapy (93.0% and 91.6%, respectively). In total, 20.4% thought the risk of HIV transmission for at least one activity was reduced for those receiving PI therapy, and 19.0% believed that the need for safer practices was reduced by PI therapy. CONCLUSION: A small but significant proportion of HIV-infected people perceive the need for safer practices to be reduced during antiretroviral therapy, particularly those containing PIs. Even if the risk is truly reduced, the importance of safer practices should be conveyed consistently and terms such as "undetectable" to describe HIV RNA responses should be avoided.

Anti-HIV Agents↗

PubMed2002

Effects of changing immunosuppressive regimen on the incidence, duration, and viral load of cytomegalovirus infection in renal transplantation: a single center report.

Background. In this retrospective single center study we have evaluated the relation between the immunosuppressive regimen and the incidence and characteristics of cytomegalovirus (CMV) infection in the setting without CMV prophylaxis from 1989 through 1998. Methods. All (470) first cadaveric renal transplantations in nonsensitized (PRA < 60%) patients were analyzed. Immunosuppression consisted of cyclosporine A (Sandimmune) and prednisolone from 1989 through 2-1993 (S; 189 patients), of cyclosporine microemulsion (Neoral) and prednisolone from 3-1993 through 5-1997 (N; 200 patients) and of mycophenolate mofetil, Neoral and prednisolone from 5-1997 until 1998 (M; 81 patients). The CMV pp65-antigenemia was measured routinely at least once weekly from day 10 till 12 weeks after transplantation or until pp65-antigenemia became negative. No CMV-prophylaxis was given. Results. By changing from Sandimmune to Neoral and by adding mycophenolate mofetil, respectively, we observed a higher frequency of especially secondary CMV infections (S vs. N vs. M, respectively, 28 vs. 50 vs. 63%, P = 0.026; S vs. N, P = 0.027; S vs. M, P = 0.015; and N vs. M, n.s). The CMV infections lasted longer (median duration antigenemia S vs. N vs. M, respectively, 3 vs. 5 vs. 7 weeks, P = 0.0003; S vs. N, P < 0.002; S vs. M, P < 0.001; and N vs. M, P < 0.05). Viral load was higher in M (median maximal pp65-antigenemia S vs. N vs. M, respectively, 19 vs. 14.5 vs. 73, P < 0.01; S vs. N, n.s.; S vs. M, P < 0.001 and N vs. M, P < 0.01). Conclusions. The use of Neoral and the addition of mycophenolate mofetil caused significant changes in the incidence, duration and viral load of CMV infections.

Cyclosporine↗

PubMed2006

Performance of immunologic responses in predicting viral load suppression: implications for monitoring patients in resource-limited settings.

BACKGROUND: World Health Organization (WHO) guidelines for the use of antiretroviral therapy (ART) in resource-limited settings state that CD4 cell counts may be used to indicate when ART regimens should be changed because of treatment failure. The performance of immunologic monitoring for this purpose has not been evaluated, however. METHODS: Participants aged > or =18 years from the British Columbia HIV/AIDS Drug Treatment Program who had CD4 cell counts < or =200 cells/microL or an AIDS diagnosis at baseline had CD4 cell counts measured at 6 and 12 months after treatment initiation. Logistic regression analysis was used to calculate sensitivity, specificity, and positive and negative predictive values for immunologic responses in terms of predicting failure to achieve 2 viral load measurements < 500 copies/mL within 1 year. RESULTS: Viral load suppression occurred in 674 (60%) of 1125 subjects. Using no increase in CD4 cell counts at 6 months as a definition of treatment failure had a sensitivity of 34%, specificity of 94%, positive predictive value of 75%, and negative predictive value of 71% for predicting failure to achieve virologic suppression. Using 12-month CD4 cell count values, the measurements were 35%, 95%, 79%, and 73%, respectively. CONCLUSION: Immunologic criteria to predict which patients have not achieved virologic suppression results in significant misclassification of therapeutic responses.

Anti-HIV Agents↗

PubMedDate not supplied

Psychological distress is associated with decreased memory helper T-cell and B-cell counts in pre-AIDS HIV seropositive men and women but only in those with low viral load.

OBJECTIVE: Although some studies have demonstrated the association of psychological distress and diminished immune system function in HIV spectrum disease, other studies have yielded apparently conflicting findings; the lack of consideration of the role of HIV viral burden may be central to this controversy. This study examined whether HIV viral burden moderated the relationship between psychological distress and enumerative and functional immune measures in pre-AIDS HIV spectrum disease. METHODS: This cross-sectional study used factor analysis to derive a composite measure of psychological distress incorporating measures of dysphoria, anxiety, and perceived stress. Multiple regression analyses used distress as the predictor, immune measures as the outcome variables, with viral load as the moderator variable, while controlling for age, medication use, and HIV symptomatology. Subjects were 148 pre-AIDS, HIV seropositive men and women (89 asymptomatic, 59 symptomatic), aged 18 to 45 years. The main outcome measures were enumerative and functional immune measures. RESULTS: A model of psychological distress was derived using each of the proposed measures. Findings indicated that high distress was associated with decreased numbers of helper T (memory) cells and B cells, but only at low levels of viral burden after controlling for age, medication use, and HIV-related symptoms. CONCLUSIONS: These findings highlight the importance of assessing the role of HIV viral burden when examining distress-immunity relationships in HIV-infected individuals. The lack of association in those persons with high viral load suggests that, even before AIDS onset, disease-related processes are disrupting CNS and immune system communication.

Adolescent↗

PubMed2006

Mucosal innate immune factors in the female genital tract are associated with vaginal HIV-1 shedding independent of plasma viral load.

Recent studies indicate that mucosal innate immune factors modulate HIV-1 infection in vitro. Our interest was to examine the levels of innate mucosal factors for their potential association with HIV-1 shedding in the female genital tract. Vaginal lavages were collected from HIV-1-infected women who had vaginal viral loads (VVL) that were below, within, or above the 90% confidence interval (CI) predicted by their matched plasma viral loads. Innate immune factors [cathepsin D, lactoferrin (Lf), myeloid related protein (MRP)-8, MRP-8/14, secretory leukocyte protease inhibitor, and gp340], cytokines (IL-1beta and TNF-alpha), and chemokines (MIP-1alpha, MIP-1beta, RANTES, and SDF-1alpha) were quantified by ELISA. Leukocyte levels were determined using a leukocyte reagent strip for urinalysis. Lf, MRP-8/14, gp340, and IL-1beta levels were significantly higher in vaginal lavages above the 90% CI and generally correlated with each other and with VVL. Leukocyte levels were significantly higher in the lavages that had virus shedding above the 90% CI and correlated strongly with Lf levels and VVL. In this group of women, these results suggest that the levels of certain innate immune factors are more closely associated with HIV-1 shedding in the genital mucosa than plasma virus concentrations.

Adolescent↗

PubMed2026

Hepatitis B virus genome mutations in precore and basal core promoter regions among HBeAg-negative chronic hepatitis B patients with high viral load in Indonesia.

Hepatitis B e antigen (HBeAg) is widely used as a marker for active HBV replication and serves as a surrogate for HBV DNA > 200,000 IU/mL to determine eligibility for tenofovir disoproxil fumarate (TDF) prophylaxis to prevent vertical transmission, according to WHO guidelines. However, some HBeAg-negative patients still harbor high viral loads. Mutations in the precore (PC) and basal core promoter (BCP) regions may reduce or abolish HBeAg expression without necessarily suppressing viral replication. Next-generation sequencing (NGS)-based characterization of these mutations remains limited in Indonesia. This study aimed to analyze the mutation prevalence in the BCP and PC regions associated with HBeAg negativity in Indonesian patients. We conducted a cross-sectional study of 32 chronic HBV treatment-naïve, unvaccinated patients with HBV DNA > 200,000 IU/mL (16 HBeAg-negative, 16 HBeAg-positive) at Cipto Mangunkusumo General Hospital. BCP and PC mutations were analyzed using NGS, classifying mutations as major (mutation frequency index [MFI] ≥20%) or minor (MFI 1- < 20%). Associations were analyzed using the Chi-square or Fisher's exact test and p-values were adjusted using the Benjamini-Hochberg procedure. Among 29 major mutation sites, PC mutations A1846T/C and G1896A were more frequent in HBeAg-negative than HBeAg-positive patients (81.3% vs 6.3% and 75.0% vs 12.5%, respectively; all adjusted p = 0.019). Combined analysis showed higher mutation frequencies in HBeAg-negative patients (93.8%, 81.3%, and 62.5% for A1846T/C, G1896A, and G1899A, respectively; all adjusted p = 0.015). In conclusion, HBeAg-negative patients with high viral loads are strongly associated with PC mutations, particularly G1896A, A1846T/C, and G1899A. These exploratory findings provide regional NGS-based molecular evidence that established PC mutations may contribute to the coexistence of HBeAg negativity and continued high-level HBV replication in Indonesian patients. Larger studies incorporating broader virological and clinical comparison groups are required to determine the clinical significance of these findings.

Humans↗

PubMed2004

Epstein-Barr virus viral load in Crohn's disease: effect of immunosuppressive therapy.

BACKGROUND: More than 80% of non-Hodgkin lymphomas (NHLs) occurring in transplant recipients on immunosuppressive therapy are associated with Epstein-Barr virus (EBV) infection. EBV viral load (EBV-VL) is predictive of NHL occurrence in this setting. The aim of this work was to determine EBV-VL in patients with Crohn's disease (CD), both according to disease activity and use of immunosuppressive therapy, including infliximab. METHODS: Between December 1999 and July 2001, EBV-VL was determined 212 times by quantitative polymerase chain reaction (PCR) assay in 138 patients with CD and in 24 EBV-seropositive controls free of CD. RESULTS: EBV-VL did not differ significantly between the controls and the patients with CD and was not influenced by CD activity or by immunosuppressive therapy, including recent infliximab infusion. High EBV-VL values were observed in two patients with severe uncontrolled CD, but returned to normal once the flare-up had been controlled (by immunosuppressive drugs in one case and by surgery in the other case). CONCLUSIONS: EBV viral load is on the whole similar in patients with Crohn's disease and in EBV-seropositive controls. Infliximab infusion does not seem to increase significantly EBV-VL in the short-term. However, some patients with Crohn's disease have transient, very high EBV-VL values that are compatible with an increased risk of NHL in the transplant setting. The long-term clinical outcome of these patients must be determined.

Adolescent↗

PubMed2006

Changes in viral loads of lamivudine-resistant mutants and evolution of HBV sequences during adefovir dipivoxil therapy.

The addition of adefovir dipivoxil (ADV) to ongoing lamivudine therapy is effective against lamivudine-resistant virus in patients with hepatitis B virus (HBV) infection. We studied 39 patients who received ADV added to lamivudine for breakthrough hepatitis. We determined early viral changes (12 weeks) in YMDD mutants (rtM204I [YIDD sequence], rtM204V [YVDD]) and rtL180M in all 39 patients as well as amino acid changes in the polymerase reverse transcriptase (rt) region and precore/core promoter mutations in 15 patients who received long-term treatment (more than 1 year). Changes in rtM204I and rtL180M viral loads were greater than that of the rtM204V, albeit statistically insignificant. Moreover, the greatest change in viral load was seen for rtM204I without hepatitis B e antigen (HBeAg). The precore mutant was replaced with wild-type virus in three of eight patients after 1 year of added ADV therapy. Compared to baseline with lamivudine therapy only, new amino acid mutations were seen in the rt region at baseline with ADV in seven patients. At 1 year after ADV coadministration, the YMDD motif was replaced with wild-type (rt204M) in two patients, in whom mutations were fewer and of a different type. We conclude that the rtM204I may be more sensitive to ADV in vivo. ADV tended to select wild-type virus from precore mutants. Moreover, viruses that were wild-type in the rt region reappeared after 1 year of ADV coadministration in some patients.

Adenine↗

PubMedDate not supplied

The significance of HIV viral load assay precision: a review of the package insert specifications of two commercial kits.

Quantification of HIV-1 RNA levels is a vital tool in the medical management of individuals infected with HIV. The commercially available US Federal Drug Administration (FDA)-approved assays vary in their ability to accurately measure and detect significant changes in plasma viral load. A more precise assay can accurately distinguish true clinically significant biologic changes in viral plasma load from background noise, or systematic variation. These differences in precision between assays are profound at low, near-cutoff levels, but also occur throughout the dynamic range of the assays. This review examines the precision specifications, expressed as fold changes in test and retesting, across the dynamic ranges of the Bayer Versant bDNA assay, and the two available versions of the Roche Amplicor Monitor PCR assays. Highly validated data from their respective package inserts are analyzed to confirm each assay's performance throughout its dynamic range. The precision of a viral load assay is critical to patient management, and gives the clinician a clearer picture of the patient's true virologic status that is attributable to infection or treatment as opposed to systematic variation in assays.

Branched DNA Signal Amplification Assay↗

PubMed2006

Viral load and outcome in SARS infection: the role of personal protective equipment in the emergency department.

This study was conducted to evaluate the effectiveness of personal protective equipment (PPE) against severe acute respiratory syndrome (SARS). Sixteen patients in a SARS cluster, including 4 health care workers (HCWs) and 12 non-HCWs were studied. We compared the initial viral load by nasopharyngeal swabs, clinical progression, and outcome of this cluster. The HCWs had a lower viral load. The non-HCWs had a higher mean C-reactive protein, lower oxygen saturation, and a higher incidence of intubation and death. Secondary household transmission developed in three of the non-HCWs' families. One month after discharge, non-HCWs had more signs of fibrosis on high resolution computed tomography (HRCT) scan and an impaired pulmonary function test. Although most of the PPE do not confer absolute protection against SARS, it seems that they may lower exposure to the virus, leading to a lower risk of secondary transmission, and be associated with relatively mild disease and a better early outcome.

Adolescent↗

PubMed1999

Lower human immunodeficiency virus (HIV) type 2 viral load reflects the difference in pathogenicity of HIV-1 and HIV-2.

Human immunodeficiency virus type 2 (HIV-2) is less pathogenic than HIV type 1 (HIV-1), but the mechanisms underlying this difference have not been defined. We developed an internally controlled quantitative reverse transcriptase-polymerase chain reaction to measure HIV-2 viral load and determined levels of plasma virus in a cohort of registered commercial sex workers in Dakar, Senegal. The assay has a lower limit of detection of 100 copies/mL and is linear over 4 logs. HIV-2 viral RNA was detectable in 56% of all samples tested; the median load was 141 copies/mL. Levels of viral RNA in the plasma were inversely related to CD4+ cell counts. HIV-2 and HIV-1 viral loads were compared among the seroincident women in the cohort; the median viral load was 30x lower in the HIV-2-infected women (P<.001, Wilcoxon rank sum test), irrespective of the length of time infected. This suggests that plasma viremia is linked to the differences in the pathogenicity of the 2 viruses.

Adult↗

PubMed2004

Estimates of intracellular delay and average drug efficacy from viral load data of HIV-infected individuals under antiretroviral therapy.

We analyse viral load data of five patients under ritonavir monotherapy using a model of HIV dynamics under antiretroviral therapy that includes both drug pharmacokinetics and the intracellular delay from the time of cell infection to viral production. Using this approach we separate pharamacokinetic from intracellular delays, and obtain new estimates of intracellular delay and the antiviral efficacy of ritonavir. We find the average intracellular delay to be 1 day, in agreement with experiments. The average viral generation time is now estimated at 2 days, resulting in approximately 180 replication cycles per year. The model also reveals that ritonavir monotherapy is approximately 65% as efficacious as a recently used potent four-drug therapy, suggesting that selection for drug resistance may be facilitated by the relatively low efficacy of individual drugs, contributing in part to the inherent limitations of current therapies in combating HIV-1 infection.

HIV Infections↗

PubMed2005

Modelling the association between adherence and viral load in HIV-infected patients.

The primary objective of this paper is to investigate the effect of adherence to prescribed antiretroviral therapy on virologic response measured repeatedly over time in HIV-infected patients. To this end observations on plasma viral load (HIV RNA) assessed in copies/ml are categorized into four clinically meaningful states, [0--50[, [50--400[, [400--2000[, [2000 and up. A time-dependent continuation ratio model is used to analyse longitudinal ordinal responses. The main challenge lies in modelling dependencies over time and using information contained in the data efficiently to establish a dynamic relation between observed patient adherence and viral load. Among the several measures of adherence investigated, two specifically account for long periods of time without intake. One is derived from the third moment of the inter-dose interval distribution, while the second reflects internal drug exposure using pharmacokinetic parameters. The approach is applied to a clinical trial involving 35 patients who were followed over 12 months. Results demonstrate a significant relation between patient adherence and virologic response.

Female↗

PubMed2006

Predicting cirrhosis risk based on the level of circulating hepatitis B viral load.

BACKGROUND & AIMS: Cirrhosis develops as a result of hepatic inflammation and subsequent fibrosis in chronic hepatitis B infection. We report on the relationship between hepatitis B viremia and progression to cirrhosis in chronic hepatitis B infection. METHODS: This was a population-based prospective cohort study of 3582 untreated hepatitis B-infected patients established in Taiwan from 1991 to 1992. Serum samples were tested for HBV DNA on cohort entry serum samples and the diagnosis of cirrhosis was by ultrasound. RESULTS: During a mean follow-up time of 11 years, the 3582 patients contributed 40,038 person-years of follow-up evaluation and 365 patients were newly diagnosed with cirrhosis. The cumulative incidence of cirrhosis increased with the HBV-DNA level and ranged from 4.5% to 36.2% for patients with a hepatitis B viral load of less than 300 copies/mL and 10(6) copies/mL or more, respectively (P < .001). In a Cox proportional hazards model adjusting for hepatitis B e-antigen status and serum alanine transaminase level among other variables, hepatitis B viral load was the strongest predictor of progression to cirrhosis relative risk [95% confidence interval] was 2.5 [1.6-3.8]; 5.6 [3.7-8.5]; and 6.5 [4.1-10.2] for HBV-DNA levels >/=10(4) - <10(5); >/=10(5) - <10(6); >/=10(6) copies/mL, respectively. CONCLUSIONS: These data show that progression to cirrhosis in hepatitis B-infected persons is correlated strongly with the level of circulating virus. The risk for cirrhosis increases significantly with increasing HBV-DNA levels and is independent of hepatitis B e-antigen status and serum alanine transaminase level.

Adult↗

PubMed2004

Complex patterns of viral load decay under antiretroviral therapy: influence of pharmacokinetics and intracellular delay.

We present a model of HIV dynamics under antiretroviral therapy that combines drug pharmacokinetics and intracellular delay. A two compartment pharmacokinetic model is employed to determine the time evolution of the intracellular concentrations of the active forms of drugs, and thereby drug efficacy. The viral replication period is divided into pre- and post-drug action parts, allowing for the introduction of an intracellular delay in drug action. The standard model of viral dynamics is modified to account for the drug dependence of intracellular delay and continuously varying drug efficacy. Model calculations reveal that viral load decay in HIV infected patients under monotherapy can exhibit remarkably complex patterns depending on the relative magnitudes of the pharmacokinetic, intracellular, and intrinsic viral dynamic time-scales. The commonly assumed exponential decay is only a special case. However, uncertainties in measurement and the low sampling frequencies employed in present clinical studies preclude the identification of these patterns from existing clinical viral load data.

Adenine↗