Disease relevance of Antiretroviral Therapy, Highly Active

• Restoration of cytomegalovirus-specific CD4+ T-lymphocyte responses after ganciclovir and highly active antiretroviral therapy in individuals infected with HIV-1 [1].
• UNAIDS and the London School of Hygiene and Tropical Medicine recently estimated that at least US $9.2 billion annually is required to mount an appropriate response to the HIV pandemic, including substantial funding for HAART [2].
• INTERPRETATION: These findings suggest that the early immunological effects of HAART may not provide sufficient protection to prevent CMV retinitis in patients who have very low CD4 counts when therapy is started [3].
• In two of 15 patients coinfected with HIV and hepatitis C virus who received interferon-alpha plus ribavirin in addition to HAART, we observed multiorgan dysfunction and lactic acidaemia [4].
• Parvovirus B19-related anemia in an HIV-infected patient: rapid control after production of neutralizing antibodies during highly active antiretroviral therapy [5].

Psychiatry related information on Antiretroviral Therapy, Highly Active

• RESULTS: Despite significant improvement in CD4 counts, and suppression of plasma and cerebrospinal fluid (CSF) viral loads, elevated brain metabolites (choline compounds and myoinositol in the frontal lobes) and neuropsychological tests abnormalities (including the computerized tests [CalCAP]) persisted after 3 months of HAART [6].
• Injection drug abuse impairs short and long-term CD4 cell recovery in HIV-positive patients initiating successful highly active antiretroviral therapy [7].
• OBJECTIVE: To determine changes in CD14/CD69 cells of HIV seropositive patients with HIV-1 associated dementia (HAD) on highly active antiretroviral therapy (HAART) and to determine the effect of soluble factors from cultured monocyte/macrophage (M/M phi) on neural cell functional proteins [8].
• RESULTS: No significant differences in CD4 cell count or HIV RNA level were found across the categories of alcohol consumption for patients who were not receiving HAART [9].
• We describe a young man who had AIDS complicated by parvovirus B19 infection and RBC aplasia and who developed a painless, progressive dyspraxia of the left arm and an expressive dysphasia 4 weeks after commencing effective HAART [10].

High impact information on Antiretroviral Therapy, Highly Active

• Virus could not be isolated from the peripheral blood CD4+ T cells in three patients receiving IL-2 plus HAART, despite the fact that large numbers of resting CD4+ T cells were cultured [11].
• Adult HIV-infected patients treated with highly active antiretroviral therapy (HAART) show a progressive increase in their number of naive CD4-positive T cells [12].
• In 74 individuals receiving highly active antiretroviral therapy, we found no appreciable effect on alpha1 circle numbers in those whose baseline values were already within the normal range, but significant increases were observed in those with a preexisting impairment [13].
• IL-7 also showed a positive trend for inducing proviral reactivation from resting CD4(+) T lymphocytes from HIV-1-infected patients on suppressive HAART [14].
• Skeletal muscle glucose uptake was reduced by 66% in treated patients and explained 46% and 43% of whole-body glucose disposal in patients on HAART and therapy-naive patients, respectively [15].

Chemical compound and disease context of Antiretroviral Therapy, Highly Active

• OBJECTIVE: Neutropenia is the most frequent side effect of cotrimoxazole in sub-Saharan Africa. We estimated the incidence of haematological disorders during the first 6 months of a zidovudine-containing highly active antiretroviral therapy (HAART) regimen in sub-Saharan African adults receiving cotrimoxazole [16].
• MATERIALS AND METHODS: A HIV-1 patient database was scanned in March 1998, and 750 patients were identified who had received HAART including indinavir [17].
• STUDY DESIGN AND METHODS: The database of the Swiss HIV Cohort Study was screened for all subjects naive to protease inhibitor (PI) treatment who started HAART with nelfinavir or indinavir, responded initially (HIV-RNA <400 copies/ml) and received >24 weeks of treatment [18].
• METHODS: A 48-week prospective evaluation of 28 HIV-infected children, with stable undetectable HIV-1 loads, who were taking highly active antiretroviral therapy (HAART) containing lamivudine, stavudine and a PI [19].
• We report on medium-term lipid profiles (up to 5 years) for antiretroviral-naive patients starting NNRTI- and PI-based HAART in the Swiss HIV Cohort Study. METHODS: Since April 2000, blood samples taken at visits scheduled every 6 months have been analysed for cholesterol and triglyceride concentrations [20].

Biological context of Antiretroviral Therapy, Highly Active

• Drug resistance mutations in HIV-1-infected subjects during protease inhibitor-containing highly active antiretroviral therapy with nelfinavir or indinavir [18].
• Conversely, after 3 months of HAART, the glial component (from PCA) correlated positively with CSF MCP-1 levels (r=0.70, P=0.0002; ANCOVA interaction for treatment status, P=0.003) [21].
• Increased UCP1 mRNA, a marker of brown adipose tissue phenotype, was associated with non-stavudine, PI-containing HAART, and may represent an adaptive response to the increased fatty acid flux associated with PI therapy, and may contribute to the increased resting energy expenditure reported in such patients [22].
• Expression of CD10 was associated with a preserved immunocompetence, whereas CD20 was less frequent in patients developing ARL while on highly active antiretroviral therapy (P = .04) [23].
• A serious metabolic syndrome combining insulin-resistance, dyslipidemia, central adiposity, and peripheral lipoatrophy has arisen in HIV-infected patients receiving highly active antiretroviral therapy [24].

Anatomical context of Antiretroviral Therapy, Highly Active

• Ex vivo labeling with BrdUrd showed that CD4 and CD8 cell turnover increased after withdrawal of HAART and correlated with viral load whereas lymphocyte turnover decreased after reinitiation of drug treatment [25].
• We have evaluated mitochondrial (mt) DNA content in CD4 and CD8 peripheral blood lymphocytes (PBLs) from HIV-infected patients taking highly active antiretroviral therapy (HAART) who display different types of adipose tissue alterations [26].
• BACKGROUND: Damage to mitochondria (mt) is a major side effect of highly active antiretroviral therapy (HAART) that includes a nucleoside reverse transcriptase inhibitor (NRTI) [27].
• Treatment of HIV-1-infected thymus with highly active antiretroviral therapy normalizes MHC I expression and surface CD8 expression on such CD4(-)CD8(+) thymocytes [28].
• Defective dendritic cell function in HIV-infected patients receiving effective highly active antiretroviral therapy: neutralization of IL-10 production and depletion of CD4+CD25+ T cells restore high levels of HIV-specific CD4+ T cell responses induced by dendritic cells generated in the presence of IFN-alpha [29].

Associations of Antiretroviral Therapy, Highly Active with chemical compounds

• Indinavir concentrations in hair from patients receiving highly active antiretroviral therapy [30].
• PATIENTS: One-hundred-and-fifty HIV-infected patients on long-term first highly active antiretroviral therapy including stavudine (n=75) or zidovudine (n=75) [31].
• A once-daily HAART regimen containing indinavir + ritonavir plus one or two nucleoside reverse transcriptase inhibitors (PIPO study) [32].
• RESULTS: Among patients currently undergoing 3TC-containing HAART, the prevalence of M184V/I was 82.5% (78.3/4.2%, respectively) and significantly associated to current 3TC use at GRT [33].
• Gynaecomastia in HIV-infected men on highly active antiretroviral therapy: association with efavirenz and didanosine treatment [34].

Gene context of Antiretroviral Therapy, Highly Active

• Zidovudine-based HAART recipients (n=7) also displayed significant mtDNA depletion (34.45% of control, P=0.031), increased mitochondrial protein mass (5.7-fold of control, P=0.009), and markedly increased UCP1 (18-fold of control, P=0.009) mRNA [22].
• Involvement of Bcl-2 and IL-2R in HIV-positive patients whose CD4 cell counts fail to increase rapidly with highly active antiretroviral therapy [35].
• This analysis was repeated after one cycle of HAART + IL-2, after virus rebound [36].
• Increased CCR-3 expression and spontaneous IFN-gamma as well as mitogenic induced IL-13 were observed at baseline and decreased slightly under HAART [37].
• Decreased CD14/CD69 levels may reflect changes in some aspects of the pathophysiology of brain injury in the era of HAART [8].

Analytical, diagnostic and therapeutic context of Antiretroviral Therapy, Highly Active

• High levels of Fas-susceptibility found in peripheral CD4 T lymphocytes before HAART were significantly reduced after HAART, coinciding with decreases in viral load (P = 0.018) and increases in peripheral CD4 T lymphocyte counts (P < 0.01) [38].
• PATIENTS AND METHODS: Seventy patients with CD4<200 cells/mm3 and CV<1000 copies/ml were enrolled in a 6-month randomized controlled study to evaluate the subcutaneous injection of IL-2 in addition to HAART versus HAART alone [39].
• The average regeneration rate of naive CD4 T cells during HAART, i.e., 0.34 x 10(6) cells/l per day, is not lower than regeneration rates in HIV-negative adults following cytotoxic chemotherapy or CD4 monoclonal antibody therapy [40].
• DESIGN: Cross-sectional study of spontaneous, CD3- and CD95-mediated apoptosis in lymphocytes from 53 HIV-infected individuals taking HAART [41].
• Eleven patients of the HAART group and eight patients of the control group received intravenous arabinoside cytosine cycles [42].

References