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Query: UMLS:C0019693 (HIV)
 170,526 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The AIDS Litigation Project has reviewed nearly 600 reported cases involving individuals with human immunodeficiency virus (HIV) infection and acquired immunodeficiency syndrome (AIDS) in the federal and state courts in the United States between 1991 and 1997. Cases were identified through a federal and 50-state computer and library search. An important subset of litigation relates to HIV/AIDS in the public health and health care systems, since the law affects health care institutions and professionals, patients, and public health policy in America. This subset of HIV/AIDS litigation includes testing and reporting; privacy, the duty to warn, and the right to know; physician standards of care in prevention and treatment; and discrimination and access to health care. In broad terms, the review demonstrates a reliance on voluntary testing and protection of patient privacy through HIV-specific statutes and the common law. Negligence with potential civil and criminal liability has been alleged in cases of erroneous or missed diagnosis of HIV infection. In the first AIDS case to be considered by the Supreme Court, the Court will decide whether patients with asymptomatic HIV infection are protected under the Americans With Disabilities Act. Considerable progress has been made, both socially and legally, during the first 2 decades of the epidemic, but much still needs to be accomplished to protect privacy, prevent discrimination, and promote tolerance.
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PMID:HIV infection and AIDS in the public health and health care systems: the role of law and litigation. 954 71

Lower extremity symptoms are caused by lesions at any level of the neuraxis, from cortex to muscle. HIV affects virtually every level of the nervous system, either directly or indirectly. The presence of pathology at multiple levels and by multiple processes further complicates the bedside diagnosis of a patient with AIDS and neurologic symptoms. Many neuropathies and other conditions that affect the lower extremities can be identified with careful history and physical examination, confirmed with limited testing, and can be treated successfully. Distal symmetric polyneuropathy is the most common lower extremity disorder, but it must be distinguished from similar-appearing neuropathies caused by medications, B12 deficiency, or vasculitis. Diffuse infiltrative lymphocytosis syndrome also causes a painful peripheral neuropathy that must be distinguished from distal symmetric polyneuropathy. Inflammatory demyelinating polyneuropathies are characterized by muscle weakness. They occur in early, asymptomatic HIV infection and respond to plasmapheresis or steroids. Mononeuropathies in patients with CD4 counts more than 200 often resolve on their own. Multiple mononeuropathies, which occur in patients with CD4 counts less than 50, are often associated with cytomegalovirus infection and may follow a rapidly progressive course unless treated promptly and aggressively. Progressive polyradiculopathy occurs late in the course of AIDS, is often caused by cytomegalovirus, is rapidly progressive, and generally is fatal unless recognized and treated promptly. Muscle weakness, myalgia, and fatigue are common in HIV and have multiple causes. Lower extremity spasticity may be caused by treatable etiologies such as spinal cord abscess, tumor, disc compression, B12 deficiency, or ischemia. Gait disturbances are common but nonspecific and may be caused by treatable neurologic disorders at any level of the neuraxis.
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PMID:Neurologic problems of the lower extremity associated with HIV and AIDS. 957 54

In this study, we wanted to investigate if there are differences in endogenous interferon (IFN) plasma levels in patients with different stages of HIV infections before and after therapy with zidovudine (ZDV) and determined the influence of ZDV therapy on the hepatic monooxygenase system by measuring the antipyrine pharmacokinetics. Therefore we investigated the endogenous IFN plasma levels in patients with asymptomatic HIV infection (CDC/WHO A1, n = 10) and patients with AIDS (CDC/WHO C3, n = 10). In AIDS plasma IFN-alpha and IFN-gamma levels are elevated (15.6 +/- 5.8 U/ml; 2.1 +/- 0.7 U/ml) compared to patients with an asymptomatic HIV infection (6.1 +/- 3.3 U/ml; 0.6 +/- 0.3 U/ml). The antipyrine clearance was significantly reduced in the group of AIDS patients (43.1 +/- 7.2 ml/min compared to 56.4 +/- 8.7 ml/min). In a second study with 11 patients in stage CDC/WHO A1/2 and CDC/ WHO B/C3 each, we studied the effect of a 14-day administration of ZDV on the endogenous plasma IFN levels and the CYP450 enzyme activity using the antipyrine pharmacokinetics as a parameter. We investigated the antipyrine clearance, clearance to metabolite and half-life by using HPLC. IFNs were measured by RIA or ELISA, respectively. In the first group no significant alterations of antipyrine kinetics or plasma IFN levels were observed after treatment with ZDV. In contrast to these results, we found a significant decrease in IFN-alpha and IFN-gamma (19.8 +/- 3.6 U/ml, 4.6 +/- 1.5 U/ml before; 7.9 +/- 2.6 U/ml, 1.9 +/- 1.3 U/ml after administration of ZDV), a decrease in antipyrine half-life, an elevation of the antipyrine clearance (49.8 +/- 15.7 ml/min, 57.3 +/- 13.7 ml/min) and an elevation of the clearances to metabolite.
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PMID:Effect of zidovudine therapy in patients with HIV infection on endogenous interferon plasma levels and the hepatic cytochrome P450 enzyme system. 961 7

In order to investigate the levels of HHV-6 infection and elevated antibodies to HHV-6 in HIV-1-infected asymptomatic and symptomatic patients, peripheral blood mononuclear cells were (PBMC) cultured. As patients progressed from asymptomatic HIV infection to AIDS, there was a concurrent increase in replicating HHV-6. Plasma obtained from several of these patients showed the presence of IgM antibody and a significantly elevated level of HHV-6 IgG antibody. Serial samples of plasma from 10 AIDS patients collected over a period of 4 years were assayed for the detection of HHV-6 core protein (gp116/64/54) by antigen capture ELISA. The results demonstrated that either a persistent infection or reactivation can occur based on the degree of fluctuation in HHV-6 antigen detected. ELISA to HHV-6 purified viral proteins, i.e., early (p41/38) and late (gp110), demonstrated that IgG antibody to gp110 did not differentiate between HIV-1-infected and healthy donors. IgG and IgM antibody to p41/38, however, showed a significantly higher prevalence in HIV-1-infected individuals (56.7-85.3%) than in normal healthy donors (19.0%), suggesting virus activation. PBMC culture from the AIDS patients expressing significant peaks of HHV-6 core antigen (gp116/64/54) in their plasma showed that in most cases, HHV-6 early and late antigens were detectable; however, those patients with consistently low antigen peaks had no detectable antigens in their PBMC. Only 55% of PBMC cultures established from IgM antibody-positive HIV-1-infected asymptomatic and AIDS patients expressed HHV-6 antigens in the short-term cultures, but HHV-6 antigens could not be demonstrated in PBMC culture from 4 IgM-antibody-positive healthy donors. HHV-6 isolates obtained from the HIV-1-positive patients were predominantly HHV-6 variant A, compared to healthy donors. Based on the data presented here, it is evident that the levels of HHV-6 infection increased in HIV-1-infected asymptomatic individuals as they progressed to AIDS. Our immunovirological data on HHV-6-infected individuals with HIV infection support a role for HHV-6 in the pathogenesis of AIDS. We believe that simultaneous active infection with HIV-1 and HHV-6 may contribute to enhanced immune suppression perhaps leading to disease manifestations.
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PMID:HHV-6 infection in HIV-infected asymptomatic and AIDS patients. 970 59

In HIV-1 infection, circulating HIV-1-specific cytotoxic T lymphocytes (CTL) exist in different states of activation, including activated cytotoxic cells and memory cells. We report that a subpopulation of HIV-1-specific CTL is capable of clonal expansion upon culture with IL-2 without exogenous antigen. The IL-2-expandable HIV-1-specific CTL precursor frequency was reduced in patients with advancing infection, although HIV-1-specific memory CTL could still be detected by stimulation in vitro with allele-specific HIV-1 peptide. Longitudinal analysis during advancing infection showed a progressive decline in the IL-2-expandable HIV-1-specific CTL precursor (CTLp) frequency without a decline in Epstein-Barr virus (EBV)-specific or allo-specific CTLp frequencies. To address mechanisms that may contribute to the decline in the IL-2-expandable HIV-specific CTL response, the requirements for in vitro generation of HIV-1-specific and EBV-specific effector CTL were examined. In the absence of exogenous IL-2 in limiting dilution, generation of EBV-specific CD8+ effector CTL was dependent upon help from CD4+ cells. CD4+ help for EBV-specific CD8+ CTL was observed in asymptomatic HIV infection but not in advanced infection. In the presence of exogenous IL-2, CD4+ cells could also provide help for the optimal generation of HIV-1 peptide-specific CD8+ CTL, because in vitro depletion of CD4+ cells prior to culture using stimulation with an MHC class I-restricted HIV-1 peptide reduced the peptide-specific CD8+ CTL response. We conclude that there is a decline in the IL-2-expandable HIV-1-specific CTL response during advancing infection. There are a number of possible mechanisms for this decline, including a reduction in CD4+ T cell help for in vivo antigen-activated CD8+ T cells.
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PMID:Progressive loss of IL-2-expandable HIV-1-specific cytotoxic T lymphocytes during asymptomatic HIV infection. 984 99

Concorde was a randomized trial to compare immediate and deferred zidovudine (AZT) treatment for persons with asymptomatic HIV infection. Alpha was a randomized trial to compare the efficacy of two doses of didanosine (ddI), in persons with symptomatic HIV disease who were intolerant of zidovudine. The two trials overlapped in time, and a single Data and Safety Monitoring Committee (DSMC) monitored accumulating data from both trials. This paper describes the deliberations of the DSMC and its recommendations to the parent steering committee during the course of each trial. In the discussion on Concorde, I draw attention to the problems of interpreting early survival data and trends in surrogate markers. With Alpha, interest focusses on the conflicting considerations that arose in discussions about possible termination at an interim stage.
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PMID:Data and safety monitoring in the Concorde and Alpha trials. 1035 95

Qualitative and quantitative virological parameters were investigated in 68 long-term nonprogressor (LTNP) HIV-1-infected patients and 9 slow-progressor controls. LTNP status was defined as an asymptomatic HIV infection for at least 8 years, a stability of CD4+ cell counts > or =600 cells/mm3 and no antiretroviral therapy. LTNP subjects exhibited a lower median plasma RNA load than controls (6,000 vs. 40,000 RNA copies/ ml) despite a wide range of values in both groups. When compared to the control group, LTNP subjects also exhibited a lower virus isolation rate (65% vs. 100%) and cell-associated viremia (0.75 vs. 56.8 number of infectious unit/ million cells) when CD8-depleted CD4+ cells were tested. By contrast, no major differences in virus replication properties or cell tropism were observed. After 1 year of follow-up, no major overall changes in the virological parameters was observed in the 50 LTNP subjects evaluated at this time. However, nine patients had started antiretroviral therapy, and six others had increased viral loads. Despite the progression observed during the first year of follow-up, the hypothesis that there is a specific subgroup of LTNP patients who will not develop disease cannot be ruled out as yet.
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PMID:Status of long-term asymptomatic HIV-1 infection correlates with viral load but not with virus replication properties and cell tropism. French ALT Study Group. 1044 21

Signaling lymphocytic activation molecule (SLAM) is a transmembrane lymphocytic receptor which gets rapidly upregulated following cell activation. SLAM engagement augments T cell expansion and interferon-gamma (IFN-gamma) production independently of CD28. SLAM signaling is regulated by the SLAM-associated protein. We evaluated the expression and function of SLAM on CD4(+) and CD8(+) lymphocytes in HIV-infected individuals with either recently acquired infection (Group A) or asymptomatic HIV infection (Group B) and in healthy controls (HC). Soluble antigen (HIV env peptides and tetanus toxoid)- and mitogen-stimulated proliferation and IFN-gamma and IL-10 production upon SLAM costimulation were also measured. Results showed that: (1) SLAM-expressing CD4(+) and CD8(+) lymphocytes diminish in group A patients compared to both group B patients and HC; (2) SLAM expression on CD4(+) lymphocytes is preferentially associated with the lack of CD7 on cell surface (CD4(+)CD7(-) produce IL-10 but not IFN-gamma); (3) SLAM engagement increases HIV env peptide-stimulated, but neither tetanus toxoid- nor PHA-stimulated proliferation of peripheral blood mononuclear cells (PBMC) in patients but not in HC; and (4) SLAM engagement augments IFN-gamma and reduces IL-10 production by env peptide-stimulated PBMC of HIV-infected individuals. These results demonstrate that early HIV infection results in an altered SLAM expression which correlates with a time-limited impairment of cell-mediated immunity. Furthermore, they show that triggering via SLAM potentiates HIV-specific proliferative responses with simultaneous downregulation of IL-10 and redirection of the response to TH0/TH1.
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PMID:Altered signaling lymphocytic activation molecule (SLAM) expression in HIV infection and redirection of HIV-specific responses via SLAM triggering. 1047 32

HHV-6A in vitro augments expression of CD4 molecules on the surface of immune cells, facilitates HIV replication and cell death in dual infections. It is hardly known whether these processes take place in vivo; does HHV-6A enhance HIV infection and AIDS progression? To study HHV-6A fresh infections and reactivation, IgM, IgG and low avidity IgG were quantitated in the serum samples of patients with asymptomatic HIV infection, early and terminal AIDS, that of their HIV seronegative homo- or bisexual partners and healthy adults (altogether 65 persons). Indirect immunofluorescent assay on JJHAN cells infected with HHV-6A U1102 was used. It was found that as compared to controls, the mean level of IgM in the sexual partners of HIV infected subjects raised 30-fold, that of IgG increased 10-fold, and 80% of persons had low avidity IgG indicating fresh HHV-6A infection. These suggest that they are frequently infected through sexual intercourse. As compared to healthy adults, mean titre of IgM to HHV-6A remained 10-fold increased in each group of patients with HIV infection. The IgG level was 6-fold increased in asymptomatic HIV infected subjects, 4-fold in early and 5-fold in terminal AIDS patients. More than one quarter of AIDS patients had low avidity IgG to HHV-6A. As compared to slow progressors of AIDS, the IgG level continuously increased in progressor persons. These suggest that HHV-6A maintains a chronic persistent infection in a significant number of HIV infected subjects.
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PMID:[Level of HHV-6A antibodies in symptomless HIV infection as well as in the course of AIDS]. 1050 70

We report detailed quantitative analysis of human immunodeficiency virus-1 (HIV-1) p24 and HIV-1 RNA in tonsil biopsies from 13 patients with early, asymptomatic HIV infection before and during combination antiretroviral therapy. Using fluorescent microscopy in conjunction with reverse transcriptase-polymerase chain reaction of frozen tissue sections, we show that plasma and tissue viral loads decreased by approximately 3 logs during the 1-year treatment period, with good correlation between the HIV-1 p24 and HIV-1 RNA response in tissue. The decrease of tissue viral load was delayed compared to plasma viral load, possibly explained by the observation that the amount of follicular dendritic cell-associated virus correlated best with the area under the curve of plasma HIV-1 RNA throughout the last 12 weeks. Before and during treatment, the relative proportions of HIV-1 on follicular dendritic cells and within mononuclear cells remained constant, suggesting similar decay characteristics in these two lymphoid tissue compartments. However, viral p24 or RNA remained almost always detectable in tissue despite full suppression of HIV-1 RNA in plasma, and increased even after short-term rebounds in plasma viral load. Thus, full and sustained suppression of viral replication was required to efficiently decrease viral load in lymphoid tissue, but complete abolition of residual viral replication was not achieved.
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PMID:Treatment-induced decline of human immunodeficiency virus-1 p24 and HIV-1 RNA in lymphoid tissue of patients with early human immunodeficiency virus-1 infection. 1085 20


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