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PubMed2005

Spontaneous control of viral load and CD4 cell count progression among HIV-1 seroconverters.

OBJECTIVES: To identify factors associated with sustained undetectable viraemia after HIV-1 seroconversion in treatment-naive patients, and to describe concomitant CD4 cell count progression. METHODS: Seroconverters enrolled in CASCADE were assumed to control viraemia if at least two consecutive viral load measurements were < 400/500 copies/ml without treatment. Factors associated with undetectable viraemia were identified through a logistic regression. A joint model was used to describe simultaneously the CD4 cell count progression during and after that period and to identify factors associated with sustained undetectable viraemia. RESULTS: Of 2176 seroconverters, 145 (6.7%) spontaneously controlled viraemia. Women were more likely than men to achieve undetectable viraemia [adjusted odds ratio (OR), 2.12; 95% confidence interval (CI), 1.49-3.12] unlike patients who reported a symptomatic primary infection (adjusted OR, 0.58; 95% CI, 0.36-0.94). AIDS and death rates were significantly lower in patients achieving undetectable viraemia than in the others. The median period of undetectable viraemia was 11.2 months; on average, CD4 cell counts remained stable during that period, and decreased with a mean rate of 5 cells/microl per month thereafter. High CD4 cell count at the beginning of undetectable viraemia and non-symptomatic primary infection favoured the preservation of undetectable viraemia. CONCLUSION: A small proportion of seroconverters appeared to be able to control HIV viraemia spontaneously, mostly those without seroconversion illness and within a few years following seroconversion; this is associated with the benefits of slower CD4 cell count decline and improved long-term prognosis. Such persons should be targeted for in depth investigation.

Acquired Immunodeficiency Syndrome↗

PubMed2003

High levels of plasma dengue viral load during defervescence in patients with dengue hemorrhagic fever: implications for pathogenesis.

Studies of the pathogenesis of dengue hemorrhagic fever (DHF), a potentially life-threatening disease, have revealed the importance of initial high levels of virus replication. However, the possible involvement of virus during the transition from fever to defervescence, a critical stage in determining the severity of disease, has not been appreciated. Using quantitative reverse transcription-polymerase chain reaction, we examined the levels of plasma dengue viral load during both fever and defervescence periods in patients from a DEN-3 outbreak in southern Taiwan in 1998. Higher levels of plasma dengue viral RNA were found in DHF patients than in DF patients. During defervescence, while the level of plasma dengue viral RNA was undetectable in most DF patients, it remains high in all DHF patients. Using a modified immunoprecipitation assay, we demonstrated for the first time that the plasma dengue viruses persisting during defervescence were in the immune complexes for most DHF patients. These findings suggest that continued active viral replication or delay in the clearance of viremia contributes to the pathogenesis of DHF. Moreover, high levels of plasma dengue viral RNA during defervescence may serve as a disease marker for DHF.

Adult↗

PubMed1997

CD8+ T-cell-mediated suppression of HIV replication in the first year of life: association with lower viral load and favorable early survival.

OBJECTIVE AND DESIGN: To study the role and development of non-cytotoxic CD8+ T-cell-mediated suppression of HIV replication in early perinatal HIV infection in a prospective study of vertically infected infants. CD8 T-cell-mediated HIV suppression was measured several times during the first year of life and correlated with viral load, cytotoxic T-cell (CTL) activity, in vitro antibody production (IVAP) and clinical outcome. METHODS: CD8+ T-cell-mediated HIV suppression was measured by comparing the amount of p24 antigen produced by endogenously infected lymphocytes with cultures of the same number of autologous CD4+ T cells from which CD8+ cells were removed immunomagnetically. CD8 viral suppressive activity (VSA) was defined as a > or = 50% reduction in p24 antigen in the cultures containing CD8+ cells. RESULTS: CD8+ T-cell-mediated HIV VSA was detected in 11/16 infants in the first year of life, including six/nine infants studied before 6 months and as early as 3 weeks of age. Infants who demonstrated CD8 VSA had a lower early peak and 6-month 'setpoint' plasma HIV RNA concentration than infants who lacked CD8 VSA [1.51 versus 4.94 and 0.094 versus 0.639 x 10(6) copies/ml, respectively, and higher CD4 percentage at 1 year of age. Survival of infants lacking CD8 VSA (four/six were rapid progressors) was shorter than for infants who demonstrated CD8 VSA (none out of 10 were rapid progressors). CD8 VSA was present before CTL and before or at the same time as IVAP in two of two and 11 of 14 infants studied, respectively. CONCLUSIONS: CD8+ T-cell-mediated VSA can be demonstrated in a large proportion of HIV-infected infants early in the course of infection. This non-cytolytic HIV-suppressive immune response appears to play an important protective role in the early control of perinatal HIV infection at a time when other immune responses are either absent or deficient.

CD4-Positive T-Lymphocytes↗

PubMedDate not supplied

Psychosocial factors predict CD4 and viral load change in men and women with human immunodeficiency virus in the era of highly active antiretroviral treatment.

OBJECTIVE: Most previous longitudinal studies demonstrating relationships between psychosocial variables and human immunodeficiency virus (HIV) disease progression utilized samples of gay men accrued before the era of highly active antiretroviral treatment (HAART), without including viral load (VL) as an indicator of disease progression or assessing the impact of medication adherence. This study sought to determine whether psychosocial variables would predict both CD4 and VL changes in a diverse sample assessed entirely during the era of HAART and accounting for adherence effects. METHODS: This longitudinal study assessed a multiethnic HIV+ sample (n = 177) of men and women in the midrange of illness (CD4 number between 150 and 500; no previous acquired immunodeficiency syndrome [AIDS]-defining symptom) every 6 months for 2 years. Hierarchical linear modeling was used to model change in CD4 and VL controlling for sociodemographics (age, gender, ethnicity, education) and medical variables (baseline CD4/VL, antiretroviral medications at each time point, adherence). RESULTS: Baseline depression, hopelessness, and education predicted the slope of CD4 and VL. Avoidant coping and life event stress predicted VL change. Cumulative variables produced stronger relationships (depression, avoidant coping, and hopelessness with CD4/VL slope and life events stress with VL slope). High cumulative depression and avoidant coping were associated with approximately twice the rate of decline in CD4 as low scorers and greater relative increases in VL. Social support was not significantly related to CD4 or VL slope. CONCLUSIONS: Psychosocial factors contribute significantly to the variance in HIV disease progression (assessed through CD4 number and VL) in a diverse sample, accounting for adherence and do so in the era of HAART.

Adaptation, Psychological↗

PubMed2002

Significance of immune status, genotype and viral load in the severity of chronic hepatitis C in HIV infected haemophilia patients.

Chronic hepatitis C is associated with more severe liver disease in patients coinfected with HIV, but the pathogenic mechanism of this more aggressive course is still unclear. The aim of this study was to assess the relationship of HCV genotype, viral load and epidemiological factors with the histological severity of chronic hepatitis in haemophilia patients with HCV/HIV coinfection, taking into consideration the immune status of the patients. Twenty-one HIV/HCV coinfected haemophilia patients, with mean age +/- SD 35.7 +/- 8.7 years, underwent transcutaneous liver biopsy 6-15 years (median 12 years) after HIV and 6-32 (median 21.5 years) years after HCV infection. Twelve patients were stage A (CDC), six stage B and three stage C. CD4 cells were < 50 microL(-1) in three patients (14.3%), 50-200 in 11(52.4%) and > 200 in 7(33.3%). Mean +/- SD log(10) HCV-RNA was 6.87 +/- 0.7 copies mL(-1) (range 5.4-7.9), and mean +/- SD log(10) HIV-RNA was 3.75 +/- 0.98 copies mL(-1) (range 2.7-6), at the time of liver biopsy. Minimal hepatitis was diagnosed in five patients (24%), mild in 10 (48%) and moderate in six (28%). Hepatitis stage 0-2 was found in seven cases (33%) and cirrhosis in six (29%). Statistical analysis showed a significant association of CD4 count < 50 with minimal hepatitis and of CD > 200 with mild and moderate hepatitis (P = 0.033). In addition, minimal hepatitis was found only in patients with stage C, while the majority of subjects with HIV stage A showed mild and moderate hepatitis (P = 0.003). Moreover genotype 1 was independently associated with advanced hepatitis stage (P = 0.04). No relationship was found between hepatitis severity, HIV or HCV RNA levels, patient's age and duration of HIV or HCV infection. Our results suggest that HCV/HIV coinfection may aggravate the course of hepatitis in the phase of immunocompetence, most probably through an immune mediated process. Genotype 1 seems to be associated with advanced liver disease.

Adult↗

PubMed2004

Invasive chronic inflammatory monocyte phenotype in subjects with high HIV-1 viral load.

Human immunodeficiency virus type 1 (HIV-1)-infected monocytes trafficking into the central nervous system are a risk factor for HIV-1-associated dementia. We performed global gene expression analysis on CD14+ monocytes isolated from HIV-1-infected individuals and controls to identify HIV-1-related changes in monocyte phenotype. Monocytes from subjects with high viral load (HVL) had a significant increase in monocytes expressing CD16, CCR5, and MCP-1. There was also an increase in sialoadhesin, a macrophage marker of chronic inflammation. Expression of proinflammatory cytokine genes IL-1, IL-6, and TNF-alpha was unchanged in individuals with HIV-1 compared to control CD14+ monocytes. Differential gene expression identified by DNA microarray analysis was confirmed with reverse transcription polymerase chain reaction (RT-PCR), while increased protein expression was characterized by immunofluorescence. We concluded that there is a circulating CD14+ macrophage hybrid phenotype in subjects with HVL.

Adult↗

PubMed2005

Baseline plasma viral load and CD4 cell percentage predict survival in HIV-1- and HIV-2-infected women in a community-based cohort in The Gambia.

OBJECTIVES: To estimate and compare the all-cause mortality rates among HIV-1-infected, HIV-2-infected, and uninfected women and to assess the predictive value of baseline plasma viral load (PVL) and CD4 cell percentage (CD4%) for mortality. DESIGN: Cohort study. METHODS: At presentation to antenatal clinics in The Gambia in 1993-1995, pregnant women were screened for antibodies to HIV-1 and HIV-2. Seropositive subjects and a similar number of seronegative controls were enrolled, and baseline PVL and CD4% were measured. Participants were visited regularly by field-workers until 18 months after delivery and again 4-7 years later. RESULTS: Thirty-two of 101 women infected with HIV-1, 23 of 243 infected with HIV-2, and 9 of 468 seronegative women died during a median follow-up of 6.9 years. The mortality rate was 56 deaths per 1000 person years of observation (pyo) for HIV-1-infected, 16 deaths per 1000 pyo for HIV-2-infected, and 3.1 deaths per 1000 pyo for HIV-uninfected women. After 8 years of follow-up, >50% of HIV-1-infected women were still alive. In multivariate analysis, a 1-log increase of HIV-1 PVL was associated with a 1.8-fold higher rate of mortality (95% confidence interval [CI], 0.9-3.4). In HIV-2 infection, women with a high PVL (>10,000 copies/mL) had an 8.7-fold (95% CI, 2.8-28) higher rate of mortality than did those with a low PVL (<1000 copies/mL). A 10% decrease in CD4% was associated with higher mortality rates among HIV-1-infected (1.6-fold; 95% CI, 1.1-2.3) and HIV-2-infected (1.5-fold; 95% CI, 1.0-2.3) subjects. DISCUSSION: Survival of HIV-1-infected women in The Gambia is similar to that in industrialized countries before the introduction of antiretroviral treatment. Survival of HIV-2-infected women is much better. However, women with high PVLs die as quickly as their HIV-1-infected counterparts.

Adolescent↗

PubMed2006

Efficacy of interventions in improving highly active antiretroviral therapy adherence and HIV-1 RNA viral load. A meta-analytic review of randomized controlled trials.

Adherence to highly active antiretroviral therapy (HAART) is generally suboptimal, limiting the effectiveness of HAART. This meta-analytic review examined whether behavioral interventions addressing HAART adherence are successful in increasing the likelihood of a patient attaining 95% adherence or an undetectable HIV-1 RNA viral load (VL). We searched electronic databases from January 1996 to September 2005, consulted with experts in the field, and hand searched reference sections from relevant articles. Nineteen studies (with a total of 1839 participants) met the selection criteria of describing a randomized controlled trial among adults evaluating a behavioral intervention with HAART adherence or VL as an outcome. Random-effects models indicated that across studies, participants in the intervention arm were more likely than those in the control arm to achieve 95% adherence (odds ratio [OR] = 1.50, 95% confidence interval [CI]: 1.16 to 1.94); the effect was nearly significant for undetectable VL (OR = 1.25; 95% CI: 0.99 to 1.59). The intervention effect for 95% adherence was significantly stronger in studies that used recall periods of 2 weeks or 1 month (vs. </=7 days). No other stratification variables (ie, study, sample, measurement, methodologic quality, intervention characteristics) moderated the intervention effect, but some potentially important factors were observed. In sum, various HAART adherence intervention strategies were shown to be successful, but more research is needed to identify the most efficacious intervention components and the best methods for implementing them in real-world settings with limited resources.

Antiretroviral Therapy, Highly Active↗

PubMed2004

Strategies to decrease viral load rebound, and prevent loss of CD4 and onset of resistance during structured treatment interruptions.

BACKGROUND: Toxicity and other drug adherence-related factors have contributed to decreased compliance to antiretroviral regimens amongst HIV-infected patients. Irregular therapy disruption causes loss of CD4 T cells, onset of drug resistance and rapid rebound of plasma viral load (VL). However, an appropriate choice of drugs and properly scheduled structured treatment interruptions (STIs) may limit VL rebound, maintain CD4 counts and minimize resistance. METHODS: We conducted a clinical study of STIs, RIGHT 901, involving 60 drug-naive patients with chronic HIV infection (CD4 >300, VL >10,000) randomized to receive didanosine-stavudine-indinavir (IDV group) or didanosine-stavudine-hydroxyurea (HU group), for 12 weeks. Subsequently, all patients were randomized again to start STI (short induction) or to continue the therapy for an additional 24 weeks before starting STI (long induction). Both groups underwent four STI cycles and then stopped therapy as long as viraemia remained below 10,000 copies/ml before reinitiating another four cycles of STI. RESULTS: During continuous therapy VLs were suppressed at similar rates in both the HU and IDV groups, while a blunted CD4 count was documented in the HU group. Following the first stop median VL rebounded close to baseline values in both groups, however, during the following STI median VL rebound decreased in the HU group, while in the IDV group VL continued to rebound to values close to baseline, and the difference between the two groups was statistically significant. Moreover, patients treated with HU had a constant and stable CD4 increase during STI, whereas CD4 counts fluctuated in the IDV group, with sharp falls during treatment interruptions and partial CD4 recovery following treatment restart. Even in the presence of IDV resistance predisposing mutations at baseline, no genotypic change in the protease sequence was observed during STI. A relevant mutation in the reverse transcriptase sequence (K70R) emerged in one patient interrupting treatment after 36 weeks of continuous therapy and in one patient after four STI cycles. Side effects (no major events) were similar among groups. CONCLUSIONS: An appropriate choice of STI schedule and regimens containing drugs less prone to resistance and/or able to prevent CD4 fluctuation may contribute to optimizing STI for chronically infected patients with respect to limiting viral rebound, improving CD4 counts and maintaining a resistance profile comparable to continuous highly active antiretroviral therapy.

Anti-HIV Agents↗

PubMed2002

[Analysis of variables associated to undetectable viral load and therapeutic failure in HIV-infected individuals].

BACKGROUND: To date, antiretroviral therapies have not led to total HIV eradication in infected individuals. The achievement of undetectable viremia levels has been regarded as essential when monitorizing the efficacy of these therapies. The objectives of our study were to assess the time needed to achieve viral load (VL) undetectable levels and subsequent VL risings, as well as to determine the clinical variables associated with both events. PATIENTS AND METHOD: Owing to a follow-up period greater than 1,000 days, 314 patients were retrospectively selected. We determined the percentages of patients with undetectable VL levels and of those with subsequent VL rising. Times needed to reach both events were calculated by Kaplan-Meier analysis. RESULTS: 182 individuals (58%; 95% CI, 52.3-63.5) reached undetectable VL levels with a median follow-up time of 862 days. A more regular VL quantitation was associated with such event. The VL level of 38 out of these individuals (20.9%; 95% CI, 15.2-27.5) increased subsequently (> 30,000 RNA copies/ml) with a mean time of 328 days (after the first undetectable VL determination); this event was associated with changes in the clinical centre where the patient was being cared for. CONCLUSIONS: In our series, the proportion of individuals with undetectable VL levels and therapeutic failure was low. The frequency of VL determination was a determining factor in the evolution of these patients.

Adult↗

PubMed2004

Comparison of three current viral load assays for the quantitation of human immunodeficiency virus type 1 RNA in plasma.

The LCx HIV RNA quantitative assay (Abbott Laboratories, Delkenheim, Germany) was compared with the Versant HIV-1 RNA 3.0 (bDNA) assay (Bayer, Tarrytown, NY) and the COBAS Amplicor HIV-1 Monitor v1.5 test (Roche Diagnostics, Branchburg, NJ), using plasma samples of various viral load levels from HIV-1-infected patients. Considering the lower limit of the linear range of 50 copies/ml of both assays, the detection range of the LCx was 127/151 (84.1%) versus the 131/151 (86.8%) of the bDNA 3.0 assay, while overall agreement between the two assays was 93.4% (141/151). LCx and bDNA 3.0 results were found to be strongly correlated (r = 0.96). The fitted regression line was described by the equation log10(LCx copies/ml) = 0.05 + 1.06 x log10(bDNA 3.0 copies/ml) with 95% CI for the estimated slope and intercept at 1.01, 1.12 and -0.16, 0.26, respectively. Similarly, the detection range of the LCx was 115/148 (77.7%) versus the 128/148 (86.5%) of the Monitor v1.5 test. A 91.2% concordance (135/148) was observed between these two assays at a cut-off of 50 copies/ml. LCx and Monitor v1.5 results were highly correlated (r = 0.96). The fitted regression line was described by the equation log10(LCx copies/ml) = 0.06 + 1.03 x log(10)(Monitor v1.5 copies/ml) with 95% CI for the estimated slope and intercept at 0.97, 1.09 and -0.16, 0.28, respectively.

HIV-1↗

PubMed2003

Discrepancies between protease inhibitor concentrations and viral load in reservoirs and sanctuary sites in human immunodeficiency virus-infected patients.

The variable penetration of antiretroviral drugs into sanctuary sites may contribute to the differential evolution of human immunodeficiency virus (HIV) and the emergence of drug resistance. We evaluated the penetration of indinavir, nelfinavir, and lopinavir-ritonavir (lopinavir/r) in the central nervous system, genital tract, and lymphoid tissue and assessed the correlation with residual viral replication. Plasma, cerebrospinal fluid (CSF), semen, and lymph node biopsy samples were collected from 41 HIV-infected patients on stable highly active antiretroviral therapy regimens to determine drug concentrations and HIV RNA levels. When HIV RNA was detectable, sequencing of the reverse transcriptase and protease genes was performed. Ratios of the concentration in semen/concentration in plasma were 1.9 for indinavir, 0.08 for nelfinavir, and 0.07 for lopinavir. Only indinavir was detectable in CSF, with a concentration in CSF/concentration in plasma ratio of 0.17. Differential penetration into lymphoid tissue was observed, with concentration in lymph node tissue/concentration in plasma ratios of 2.07, 0.58, and 0.21 for indinavir, nelfinavir, and lopinavir, respectively. HIV RNA levels were <50 copies/ml in all CSF samples of patients in whom HIV RNA was not detectable in plasma. HIV RNA was detectable in the semen of three patients (two patients receiving nelfinavir and one patient receiving lopinavir/r), and its detection was associated with multiple resistance mutations, while the viral load in plasma was undetectable. HIV RNA was detectable in all lymph node tissue samples. Differential drug penetration was observed among the three protease inhibitors in the sanctuary sites, but there was no correlation between drug levels and HIV RNA levels, suggesting that multiple factors are involved in the persistence of viral reservoirs. Further studies are required to clarify the role and clinical relevance of drug penetration in sanctuaries in terms of long-term efficacy and drug resistance.

Adult↗

PubMed2003

Ethnicity and discordance in plasma HIV-1 RNA viral load and CD4+ lymphocyte count in a cohort of HIV-1-infected individuals.

BACKGROUND: Guidelines for commencing therapy for HIV infection have been based upon HIV-1 RNA and CD4 lymphocyte thresholds. The influence of confounding factors such as gender, ethnicity and co-infections is unproven. OBJECTIVES: To analyse ethnic discordance in plasma HIV-1 viral load (VL) and CD4+ count and its potential clinical significance in Black and Caucasian groups. STUDY DESIGN: Retrospective, cross-sectional, observational study of 537 antiretroviral nai;ve HIV-1-positive individuals attending two East London clinics. Baseline data were obtained from individuals who registered at the clinic from November 1996 to August 1999. An analysis was performed comparing ethnic differences in plasma HIV-1 VL, CD4+ count, CD8+ count, co-infections, CDC disease category, AIDS-defining illnesses and mode of transmission. RESULTS: Plasma HIV-1 VL was significantly lower in Blacks (4.5 copies/ml versus 4.7 copies/ml; P<0.05) despite lower baseline CD4+ counts and similar rates of disease progression to Caucasian groups. This association remained for patients with less advanced disease after stratification for CD4+ count (CD4+ 200-500, VL 4.5 copies/ml versus 4.7 copies/ml, P<0.01; CD4+ >500, VL 3.4 copies/ml versus 4.3 copies/ml, P<0.001) and disease category (non-AIDS, 4.4 copies/ml versus 4.7 copies/ml; P<0.005). On multivariate analysis, the association persisted following adjustment for gender, age, co-infections, CD4+ count and mode of transmission. CONCLUSIONS: These results suggest that plasma HIV-1 VL is discordantly low in Black compared with Caucasian groups stratified for CD4+ count, in this cohort of antiretroviral nai;ve HIV-1-positive individuals living in London. Although there are a number of possible explanations for this finding, it has considerable clinical relevance for the management of Black HIV-1-infected patients within UK, with significant implications for the decision about when to commence antiretroviral or immune-based therapies.

Adult↗

PubMed2006

Effect of a liquid nutritional supplement on viral load and haematological parameters in HIV-positive/AIDS patients.

The effect of a nutritional supplement on the immune status and haematological parameters of HIV-positive/AIDS patients is tested using standard procedures. This clinical trial of 35 patients consists of a baseline visit and three months of supplementation from April to September 2003. Results showed that viral load decreased significantly (P<0.002) with time following supplementation. Mean cell volume (MCV) and mean cell haemoglobin concentration (MCHC) increased significantly (P<0.002 and P<0.0002, respectively), reflecting the positive effect of the supplement on these haematological parameters. Supplementation had no effect on CD4+ T-cell count, which decreased significantly with disease progression. Owing to certain limitations of the study (small sample size, short duration and the late stage of HIV infection), further studies are needed to confirm the effect attributed to the supplement.

Acquired Immunodeficiency Syndrome↗

PubMed1999

Strong correlation between the complement-mediated antibody-dependent enhancement of HIV-1 infection and plasma viral load.

OBJECTIVE: We have previously demonstrated that complement-mediated antibody-dependent enhancement (C-ADE) of HIV-1 infection correlates with accelerated immunosuppression and disease progression in HIV-1-infected individuals. In the present work the relationship between C-ADE and plasma HIV-1 RNA concentrations was studied to determine the effect of C-ADE on viral replication. METHODS: Three studies were performed: (a) C-ADE and HIV-1 RNA concentrations were determined in the serum and plasma aliquots taken at the same time from 98 HIV patients, mostly in the advanced stage of the disease; (b) the above two parameters as well as HIV enzyme-linked immunosorbent assay (ELISA)-reactive antibodies (Abbott HIV 1/2 test), and p24 antigen levels (Abbott antigen test; Abbott, Delkenheim, Germany) were determined in four seroconversion panels purchased from the Boston Biomedica firm; (c) changes of HIV-1 RNA concentration and C-ADE during a 17 month follow-up period were determined in 18 HIV-infected patients. C-ADE was measured by the method previously established in our laboratories. The results were expressed by an enhancement/neutralization index (E/NI). HIV-1 RNA levels were determined with the Amplicor monitor kit (Roche, Basel, Switzerland), and in some experiments with the nucleic acid sequence based amplification (Organon Teknika, Turnhout, Belgium) kits. RESULTS: (a) We found a highly significant (P<0.0001) positive correlation between E/NI values reflecting the extent of HIV-1 infection enhancement and plasma HIV-1 RNA levels. Both E/NI and HIV-1 RNA levels negatively correlated to the CD4 cell counts. (b) C-ADE was first detected just before, or concomitantly with, seroconversion in 4/4 seroconversion panels. (c) Both E/NI values and HIV-1 RNA levels significantly (P<0.001) increased during a 17 month observation period in 18 HIV-infected patients. CONCLUSION: We found strong association between the extent of the complement-mediated antibody-dependent enhancement of HIV-1 infection and the plasma viral load in HIV patients. On the basis of these findings, C-ADE correlates with HIV replication in vivo, and potentially contributes to the progression of HIV disease.

Adolescent↗

PubMed2006

Viral load in 1-day-old and 6-week-old chickens infected with chicken anaemia virus by the intraocular route.

Although the effects of chicken anaemia virus (CAV) infection have frequently been investigated in young chickens, there have been few studies of the pathogenesis of CAV infection in older birds. The aim of the work reported here was to study viral loads in 6-week-old chickens and to compare these with those seen in younger birds. Specific pathogen free chickens were inoculated at 1 day or at 6 weeks of age with 10(4) median tissue culture infective doses of CAV by the intraocular route. Chicks infected when 1 day old were euthanized at day 14, 18 or 22 post inoculation (p.i.), and those infected when 6 weeks old at day 16, 18 or 20 p.i. Their body and thymus weights were determined and samples were collected from their spleen, liver and thymus. A quantitative polymerase chain reaction assay was developed and used to determine the number of viral genome copies in the tissue samples. In both age groups, viral genome concentrations increased in all organs up to day 18 p.i. and reached a peak in the spleen and liver at day 18 p.i. The peak viral concentrations in the thymus were detected at day 18 in the younger birds and at day 20 p.i. in older chickens. These studies have shown that exposure to CAV in older birds leads to similar levels of active viral replication to those seen in younger birds, and may result in subclinical infections in older birds with the potential to increase susceptibility to other infectious agents.

Aging↗

PubMed2002

[Helper cells, viral load, genetic factors, co-infections. Prognostic factors in HIV-1 infection].

The ideal time to initiate antiretroviral therapy in asymptomatic patients with chronic HIV infection remains to be defined. The most relevant laboratory parameter is the CD4 cell count. Therapy should be started before the CD4 cells drop below 200/microliter and the immune system becomes compromised. In contrast to past recommendations, viral load should not be used as a single laboratory parameter for initiation of antiretroviral therapy in asymptomatic untreated patients. The determination of genetic factors to assess the prognosis of HIV patients has not yet been incorporated into daily clinical practice. While co-infection with GBV-C is a prognostically favorable factor for the course of the HIV infection, replicative hepatitis C is associated with increased mortality.

AIDS-Related Opportunistic Infections↗

PubMedDate not supplied

Improved liver function and decreased hepatitis C viral load after tacrolimus was replaced by cyclosporine.

Potential antiviral properties of cyclosporine against hepatitis C virus have been highlighted in several publications. Therefore, we investigated the effect of a switch from tacrolimus to cyclosporine in a liver transplant recipient with recurrent hepatitis C who did not respond to antiviral therapy. The patient received a liver transplant for hepatitis C cirrhosis. Initial immunosuppressive treatment was based on tacrolimus. Because of viral activity, a combined therapy was initiated 20 months later including interferon and ribavirine. Then, due to a lack of virological and biochemical response, tacrolimus was replaced by cyclosporine (Neoral), while maintaining the same antiviral therapy. Decreases in the viral load and transaminases levels were observed.

Adolescent↗