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

AIDS, ARC, and other HIV-associated diseases were originally conceptualised exclusively in terms of defects in cell-mediated immunity and its consequences. But it is now becoming clear that HIV disease can also be a primary neuropsychiatric disorder, although the precise mechanism by which the retrovirus causes impairment in brain function and, ultimately, structural brain damage, remains obscure. The work presented here indicates another shift in our thinking concerning HIV infection. Until recently it was believed that neurological and neuropsychiatric phenomena tended to occur in the late stages of HIV disease. While that might be true for the more severe form of symptomatology that has been termed the AIDS dementia complex, we believe there is at least preliminary evidence that cognitive change can occur earlier in the course of illness, perhaps even in some medically asymptomatic HIV+ individuals. Other investigators have also noted increased neuropsychological abnormality in patients before they developed AIDS or ARC. For example, Janssen et al. found that about half their patients with lymphadenopathy syndrome (LAS) had some neuropsychological test deficits. Durara et al. recently reported on cerebral metabolic rates for glucose in seven HIV+ asymptomatic individuals, compared to 10 HIV- controls. Four of the HIV+ individuals had abnormal asymmetry in frontal and temporal regions suggesting focal reduction in cerebral glucose metabolism. Further indirect evidence that virus can enter the central nervous system early in the course of HIV disease comes from the work of McArthur and associates.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Human immunodeficiency virus-associated neurobehavioural disorder. 341 42

In addition to central nervous system (CNS) opportunistic infections and neoplasms, patients with acquired immunodeficiency syndrome (AIDS) develop unexplained dementia and encephalopathy and degeneration of the white matter. We studied autopsied brains from 20 adult patients who expired from AIDS to determine the relationship of human immunodeficiency virus (HIV) infection to white matter lesions and to clinical findings. In four patients with dementia/encephalopathy and abnormalities of the white matter, there was evidence of HIV infection as shown by in situ hybridization. In contrast, the remaining 16 patients who had no evidence of white matter degeneration revealed no hybridization to the HIV probe. The cells infected with HIV included endothelial cells, perivascular macrophages/monocytes, and multinucleated giant cells and were found in or adjacent to white matter degeneration. These results demonstrate a correlation between HIV-infected cells and AIDS leukoencephalopathy and provide further evidence for HIV-related dementia/encephalopathy.
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PMID:Human immunodeficiency virus (HIV) infection in brains with AIDS-related leukoencephalopathy. 344 27

AIDS dementia complex is a major source of disability for many AIDS patients. Less commonly, the spinal cord or peripheral nerves are affected by HIV infection. Physicians working with AIDS patients must differentiate these manifestations from those caused by the infectious, neoplastic and vascular complications.
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PMID:AIDS and the brain. 368 70

AIDS dementia complex is a severe complication related to HIV infection of the central nervous system. It has been estimated to affect about 7% of AIDS patients, with an increased frequency in very young and old patients. In most cases, it appears in severely immuno-deficient patients. Typically, AIDS dementia presents as a subcortical dementia with cognitive, behavioural and motor decline. The mechanism of the dementia remains unclear; the neuronal loss is controversial and a neurotoxicity due to NMDA receptor activation is likely. No treatment proved to be efficient. Beneficial effect of anti-NMDA receptor antagonists are under investigation.
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PMID:[AIDS dementia. Prognosis and therapeutic perspectives]. 747 32

AIDS dementia complex (ADC) is a complex, progressive neuropsychiatric syndrome seen in 60-70% of the patients with AIDS. The structural and functional changes associated with ADC may be the result of a variety of indirect mechanisms mediated via activated brain cells or/and virus that produce neurotoxins including N-methyl-D-aspartate receptor agonist (eg, quinolinic acid, glutamate), cytokines, gp 120 and nitric oxide. The level of the neurotoxin and kynurenine pathway metabolite, quinolinic acid, is increased in the brain and CSF of HIV-1-infected patients, and is correlated with quantitative measures of neurologic impairment. Importantly, increased CSF and brain levels of QUIN also occur in other inflammatory neurologic diseases (bacterial, viral, fungal and parasitic infections, meningitis, autoimmune diseases and septicemia), independent of HIV-1 infection. Therefore, QUIN and other neuroactive kynurenine pathway metabolites may be final common mediators of neurologic dysfunction in a broad spectrum of inflammatory neurologic diseases. Conversion of L-tryptophan to QUIN has also been demonstrated in vitro in both brain tissue following macrophage infiltration, and in macrophages stimulated by interferon-gamma or HIV infection. Macrophages in vitro have a high capacity to synthesize QUIN following exposure to interferon-gamma, tumor necrosis factor-alpha, IL-1 beta and IL-6, compared to cells derived from other tissues. Notably, the concentrations achieved in the macrophage incubates exceeded the levels found in the CNS of HIV-1-infected patients, and exceeded the concentrations shown to be neurotoxic in vitro. We hypothesize that increased kynurenine pathway metabolism following inflammation reflects the presence of macrophages and other reactive cell populations at the site of brain infection. Strategies to attenuate the neurotoxic effects of kynurenines, such as inhibitors of kynurenine pathway metabolism and cytokine antibodies may offer new approaches to therapy.
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PMID:[Biochemical studies on AIDS dementia complex--possible contribution of quinolinic acid during brain damage]. 747 52

A 40-year-old HIV-positive right handed homosexual man was admitted for progressive mental deterioration coexisting with permanent segmental middle-amplitude arrhythmic, asynchronous and asymmetrical myoclonic jerks. EEG showed fronto-central bursts of rhythmic triphasic 1.5-2 Hz sharp waves similar to the characteristic periodic pattern of Jakob-Creutzfeldt disease. Biological procedures were negative, thus eliminating a metabolic encephalopathy. Dramatic neurological improvement occurred shortly after initiation of i.v. and then oral zidovudine which produced perfect EEG normalisation. This unusual electroclinical presentation of the AIDS-dementia complex underlines the fact that this affection may present a diagnostic challenge, particularly in individuals in whom HIV infection is unknown.
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PMID:Reversible myoclonic encephalopathy revealing the AIDS-dementia complex. 751 Jun 31

We have demonstrated that human brain capillary endothelial (HBCE) cells, unlike umbilical or aortic endothelial cells are permissively infected by HIV. HIV infection of HBCE cells is noncytolytic and is mediated by a CD4- and GalCer-independent mechanism, implying that HBCE cell tropic strains utilize a unique receptor. The V3 loop of gp120 appears to be important in this reaction. T-cell tropic but not brain-derived macrophage tropic HIV strains selectively infect brain endothelium suggesting that T-cell tropism is important for HIV entry through the blood-brain barrier (BBB). The ability of HIV to infect cells that compose the BBB implies that the virus may be directly involved in the BBB dysfunction observed in AIDS patients. HIV infection of HBCE cells may allow the flow of cytokines or toxic metabolites from the circulating blood into the brain parenchyma either by disrupting tight junctions or by altering the ability of the cells to regulate transport of substances across the BBB by transcytosis. HIV infection may also result in endothelial cell-induced astrocytosis by release of cytotoxic substances or modulation of abluminal surface antigens which contact astrocytic foot processes. Finally, HIV infection of the brain endothelium could facilitate virus entry to the CNS either by infection of HBCE cells or via entry of HIV-infected leucocytes. The establishment of our in vitro HIV-HBCE cell system will allow us to explore the potential mechanisms which mediate AIDS dementia.
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PMID:HIV infection of human brain capillary endothelial cells--implications for AIDS dementia. 753 40

Mice infected with the LP-BM5 murine leukemia virus mixture develop severe immunosuppression and an encephalopathy characterized by spatial learning deficits. Twelve weeks after infection of C57BL/6J mice with LP-BM5, significant (50-60%) reductions in Met-enkephalin and substance P levels were observed in the striatum, whereas somatostatin levels were unchanged. In addition, a 39% decrease in hypothalamic substance P concentrations was observed, with no alteration in Metenkephalin levels. The apparent selectivity of the decrease in neuropeptide concentrations indicates that a functional alteration of the primary striatal efferent neurons occurs in this infection, which may contribute to the impairment of spatial learning observed in these mice. Moreover, this decrease in striatal neuropeptide levels is similar to the neuropathological changes in basal ganglia observed in HIV-infected individuals and is consistent with previous studies suggesting that the LP-BM5-infected mouse may serve as a useful model of AIDS dementia.
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PMID:Striatal met-enkephalin and substance P levels are decreased in mice infected with the LP-BM5 murine leukemia virus. 753 38

Degradation of purified myelin basic protein (MBP) was studied by SDS gel electrophoresis after addition of CSF samples obtained from HIV-1-infected patients. An increase in MBP degradation was detected in patients with neurological complications, such as AIDS dementia complex (ADC) or progressive multifocal leukoencephalopathy (PML), when compared with patients with no neurological symptoms (NA) or with other neurological opportunistic infections (OI). In the ADC and PML patients, in addition to CSF proteolytic activity, an increase in CSF-MBP levels and presence of white matter lesions were also observed by neuroimaging (MRI). In other opportunistic infections of the brain, MBP levels but not anti-MBP proteolytic activity increased. Results suggest the involvement of proteases in the virus-induced demyelination.
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PMID:Myelin degrading activity in the CSF of HIV-1-infected patients with neurological diseases. 753 76

The aim of the present study is to evaluate the relationship between the alpha tumor necrosis factor (TNF-alpha), interleukin 1 beta (IL-1 beta) and the neurological disease associated to the HIV-1 infection and different neurological manifestations (15 infections of the CNS and 11 AIDS-dementia complexes) and 14 from a control group. The mean value of TNF-alpha in CSF of patients with HIV-1 infection and AIDS-dementia complex was 19.8 +/- 30.6 pg/ml, superior to that of the control group (p < 0.05). The group of patients with HIV-1 and opportunistic CNS infection has a TNF-alpha value of 28.5 +/- 37.8 pg/ml, that is superior to that of the patients with the AIDS-dementia complex (TNF-alpha = 7.9 +/- 9.4 pg ml; p < 0.05). Within the group of patients with a CNS infection, the value of TNF-alpha was greater in those in the acute phase (44.2 +/- 42.4 pg/ml) than in those in the chronic phase (6.8 +/- 7.6 pg/ml; p < 0.05). The TNF-alpha in the CSF is a good marker of infection of the CNS in the HIV-1 infection.
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PMID:[Alpha tumor necrosis factor in central nervous system disease associated with HIV infection]. 754 40


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