Effect of highly active antiretroviral therapy on the serological response to additional measles vaccinations in human immunodeficiency virus-infected children.
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Children infected with human immunodeficiency virus (HIV) often lose their vaccine-induced antibody to measles virus. Before highly active antiretroviral therapy (HAART), an additional immunization against measles infrequently resulted in protective antibodies. The antibody response to an additional measles-mumps-rubella (MMR) vaccination was compared in 28 HIV-infected children who lacked protective antibody to measles virus and were undergoing HAART or non-HAART regimens. Serostatus was measured by automated enzyme-linked immunoassay. Nine (64.3%) of 14 children undergoing HAART, compared with 3 (21.4%) of 14 in the non-HAART group, had antibody to measles virus after the additional vaccination with MMR (P=.027). The groups showed no significant difference in CD4 cell values. Ten of 14 HAART patients had undetectable levels of HIV. The mean HIV load for the HAART group was 27,700 copies/mL (median, <400 copies/mL); for the non-HAART group, it was 86,000 copies/mL (median, 9000 copies/mL). Thus, HAART improves the response to an additional MMR vaccination, which is consistent with immune system reconstitution. (+info)
Concentrations of human immunodeficiency virus type 1 (HIV-1) RNA in cerebrospinal fluid after antiretroviral treatment initiated during primary HIV-1 infection.
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In 6 patients with primary human immunodeficiency virus type 1 (HIV-1) infection, concentrations of HIV-1 RNA and beta(2)-microglobulin were monitored in cerebrospinal fluid (CSF) and in plasma during antiretroviral therapy. Four patients had neurological symptoms. At baseline, the CSF of 5 patients had detectable levels of HIV-1 RNA (median, 3.68 log(10) copies/mL; range, <2.60-5.67 log(10) copies/mL), and the CSF of 3 patients had elevated levels of beta(2)-microglobulin. After 8 weeks of treatment, the median concentrations of HIV-1 RNA in CSF had decreased to <2.60 log(10) copies/mL (range, <1.60-3.00 log(10) copies/mL; P=.04) and in plasma to 3.07 log(10) copies/mL (range, 2.57-3.79 log(10) copies/mL; P=.03). Median concentration of beta(2)-microglobulin in CSF had decreased to 1.2 mg/L (range, 0.9-1.7 mg/L; P=.06) and, in plasma, to 1.7 mg/L (range, 1.1-2.2 mg/L; P=.03). After 48 weeks, HIV-1 RNA concentrations in 1 patient were still 1.97 log(10) copies/mL in CSF and 1.51 log(10) copies/mL in plasma, although beta(2)-microglobulin concentrations in CSF and plasma had normalized after 8 weeks. (+info)
Resolution of chronic parvovirus b19-induced anemia, by use of highly active antiretroviral therapy, in a patient with acquired immunodeficiency syndrome.
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We present what is, to our knowledge, the second case report of a patient with acquired immunodeficiency syndrome and transfusion-dependent anemia caused by persistent infection with parvovirus B19. The patient's anemia was successfully treated, and she demonstrated serologic evidence of eradication of parvovirus after having received effective therapy for human immunodeficiency virus infection. (+info)
Suspension of anticytomegalovirus maintenance therapy following immune recovery due to highly active antiretroviral therapy.
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AIM: To describe the authors' experience with discontinuation of anti-cytomegalovirus (CMV) maintenance therapy in patients showing immune recovery following highly active antiretroviral therapy (HAART). METHODS: Retrospective analysis of the records of 41 patients who presented with CMV retinitis and whose maintenance therapy was discontinued from March 1997 to December 1999. RESULTS: 41 patients had their anti-CMV therapy discontinued. The mean follow up after discontinuation of maintenance therapy in April 2000 was 20.4 months. At the time of discontinuation of maintenance therapy the lowest CD4+ count was 143 cells x 10(6)/l and only three patients had detectable HIV viral load. No reactivation or progression was seen in any of these patients after suspension of maintenance therapy. CONCLUSION: The anti-CMV maintenance therapy could be discontinued safely in patients with CD4+ above 150 cells x 10(6)/l although close follow up remains necessary especially in patients whose CD4+ count drops below this level. (+info)
Restoration of anti-human immunodeficiency virus type 1 (HIV-1) responses in CD8+ T cells from late-stage patients on prolonged antiretroviral therapy by stimulation in vitro with HIV-1 protein-loaded dendritic cells.
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We demonstrate that dendritic cells loaded in vitro with human immunodeficiency virus type 1 (HIV-1) protein-liposome complexes activate HLA class I-restricted anti-HIV-1 cytotoxic T-lymphocyte and gamma interferon (IFN-gamma) responses in autologous CD8+ T cells from late-stage HIV-1-infected patients on prolonged combination drug therapy. Interleukin-12 enhanced this effect through an interleukin-2- and IFN-gamma-mediated pathway. This suggests that dendritic cells from HIV-1-infected persons can be engineered to evoke stronger anti-HIV-1 CD8+ T-cell reactivity as a strategy to augment antiretroviral therapy. (+info)
HIV associated nephropathy: a treatable condition.
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OBJECTIVES: To describe current knowledge on the aetiology, pathology, diagnosis, and treatment of HIV associated nephropathy. METHODS: A Medline search was performed using the key words "HIV," "nephropathy," "renal," and "kidney." A further search was performed for each of the currently licensed antiretroviral agents linked to key words "renal" or "kidney" and also using the MeSH heading "pharmacokinetics." RESULTS: HIV associated nephropathy is a common complication of HIV in black African and Afro-Caribbean patients and presents with progressive renal failure and heavy proteinuria. As other causes of renal failure are likely to fall in incidence among patients successfully treated with highly active antiretroviral therapy (HAART), HIV associated nephropathy will become increasingly prominent as a cause of renal impairment in HIV infected patients. Recent evidence suggests that HIV associated nephropathy will respond to HAART with a dramatic improvement in renal function. CONCLUSION: HIV associated nephropathy is a treatable condition. This condition should be actively sought in HIV infected patients if they are to receive the benefits of therapy. (+info)
Long-term clinical outcome of human immunodeficiency virus-infected patients with discordant immunologic and virologic responses to a protease inhibitor-containing regimen.
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Within a prospective cohort of 150 human immunodeficiency virus (HIV)-infected patients who began first-line protease inhibitor therapy in 1996, the outcome of 42 patients with discrepant virologic and immunologic responses to antiretroviral treatment at 12 months was analyzed at 30 months of treatment. The incidence of AIDS-defining events and deaths (14%) in the group of patients with immunologic responses in the absence of a virologic response was higher than that in full-responder patients (2%); yet, the incidence in this group was lower than that in patients with no immunologic response, despite a virologic response (21%), and was lower than that in patients without an immunologic or virologic response (67%; P<.0001, log-rank test). Differences in outcome were significant (relative risk, 6.9; 95% confidence interval, 1.9-39.3) when factors for progression were compared with those of responder patients. The results support the relevance of the CD4 cell marker over plasma HIV load for predicting clinical outcome in patients who do not achieve full immunologic and virologic responses. (+info)
Cytomegalovirus (CMV)-specific CD4+ T lymphocyte immune function in long-term survivors of AIDS-related CMV end-organ disease who are receiving potent antiretroviral therapy.
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To better understand the relation of cytomegalovirus (CMV)-specific CD4+ T lymphocyte immunity and clinical outcome in AIDS-related CMV end-organ disease, 2 patient groups were prospectively studied: patients recently diagnosed with active CMV end-organ disease and survivors of CMV retinitis who had responded to highly active antiretroviral therapy and had quiescent retinitis when anti-CMV therapy was discontinued. Most patients with active CMV disease had negative CMV-specific CD4+ T lymphocyte responses at diagnosis, as measured by lymphoproliferation (7/7) or cytokine flow cytometry (3/5) assays. In contrast, all 10 subjects with quiescent retinitis and >150 absolute CD4+ T lymphocytes/microL whose anti-CMV therapy was discontinued during 6 months of follow-up had positive CMV-specific immune responses at least once by each assay. However, 6 of these 10 subjects also had negative CMV-specific immune responses > or =1 time. Such patients may be at risk for future CMV disease progression and should be closely monitored. (+info)