Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Bartonella henselae can cause cat scratch disease and bacillary angiomatosis, a multisystem disorder seen primarily in patients with the acquired immunodeficiency syndrome. Both of these diseases are associated with neurologic complications, particularly encephalopathy. B. henselae may also cause bacteremia and endocarditis, and has been associated with aseptic meningitis and with dementia in patients also infected with the human immunodeficiency virus. Recent advances in identification of this difficult-to-culture organism will lead to recognition of more neurologic complications.
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PMID:Neurologic complications of Bartonella henselae infection. 755 Nov 13

We have observed an unusual low amplitude, slow and featureless electroencephalogram (EEG) pattern in some human immunodeficiency virus (HIV) infected patients without focal lesions on computerized tomography (CT scan) of the head. Out of 17 cases, 13 with AIDS and 4 with HIV positive status, 6 had low amplitude EEGs with slowing, all in the AIDS group. Nine of the 13 AIDS patients were demented, and 4 of these demented patients had slow verbal responses and mutism, indicating advanced HIV-related dementia. All 4 had low amplitude, slow EEGs. The patients with low amplitude, slow EEGs also had atrophy on CT scan by visual assessment and by measurement of ventricular indices. Of 17 age-matched controls referred for non-specific complaints such as headache and dizziness or for psychiatric disorders, 3 had EEGs read as low amplitude with slowing; two had normal mental status and one was psychotic. Although this EEG pattern is not etiologically specific, it may correlate with advanced dementia and atrophy on CT scan in AIDS patients.
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PMID:Low amplitude EEGs in demented AIDS patients. 768 54

The cause of acquired immunodeficiency syndrome (AIDS) dementia, which is a frequent late manifestation of human immunodeficiency virus (HIV) infection, is unknown but radiological and pathological studies have implicated alterations in subcortical white matter. To investigate the pathological basis of these white matter abnormalities, we performed an immunocytochemical and histological analysis of subcortical white matter from AIDS patients with and without dementia, from pre-AIDS patients (asymptomatic HIV-seropositive patients), and from HIV-seronegative control subjects. Reduced intensity of Luxol fast blue staining, designated "diffuse myelin pallor," was detected in 8 of 15 AIDS dementia patients, 3 of 13 AIDS nondemented patients, and none of the pre-AIDS patients (n = 2) or control subjects (n = 9). In contrast to Luxol fast blue staining, sections stained immunocytochemically for myelin proteins did not show decreased staining intensities in regions of diffuse myelin pallor. In addition, neither demyelinated axons nor active demyelination were detected in light and electron micrographs of subcortical white matter from brains of patients with AIDS dementia. An increase in the number of perivascular macrophages and hypertrophy of astrocytes and microglia occurred in brain sections from HIV-infected patients. These changes were not specific to dementia or regions of diffuse myelin pallor and they occurred in both gray and white matter. In contrast to the lack of myelin pathology in AIDS dementia brains, significant accumulations of serum proteins in white matter glia were detected in the brains of 12 of 12 patients with AIDS dementia and 6 of 12 AIDS patients without dementia. Serum protein-immunopositive cortical neurons were detected in the frontal cortex of 11 of 12 patients with AIDS dementia and 3 of 12 nondemented AIDS patients. Seronegative control subjects showed minimal serum protein immunoreactivity in both cortex and white matter. We conclude therefore that alterations in the blood-brain barrier and not demyelination contribute to the development of AIDS dementia.
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PMID:Cerebral white matter changes in acquired immunodeficiency syndrome dementia: alterations of the blood-brain barrier. 768 19

The central nervous system (CNS) is a target for human immunodeficiency virus infection, and, in individuals with acquired immune deficiency syndrome, this can lead to a devastating dementia. Only certain viral variants appear capable of invading the CNS and infecting microglia and brain macrophages. To determine whether the virus entering the brain may be particularly pathogenic to the CNS, we isolated microglia from the brains of simian immunodeficiency virus-infected rhesus monkeys. Serial transfer of these cells into naive animals indicated that productive simian immunodeficiency virus infection could indeed be transferred. Furthermore, CNS infection occurred within a relatively short time span and was associated with viral gene expression in the brain and pathology characteristic of human immunodeficiency virus encephalitis. While demonstrating that neuropathogenic variants partition into the CNS, our approach will allow the dissection of functional neuropathogenic elements present in these viruses.
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PMID:Transfer of neuropathogenic simian immunodeficiency virus with naturally infected microglia. 771 58

Human immunodeficiency virus (HIV) infection leads within about 10 years to the progressive collapse of the 2 most complex regulatory networks of the human body: the immune system, and the central nervous system. AIDS results from the loss, in each organ, of a selective cell population: CD4 + T cells in the immune system, leading to immune in competence; neurons in the brain, leading to dementia. Research on AIDS pathogenesis has mainly focused on 2 different approaches: 1. the cytopathic effect of HIV is the main driving force in the collapse of the immune system; 2. the immune system is a major participant in its own destruction, and HIV is the trigger of the immunopathological disturbances that results in disease. These virological and immunological views of AIDS pathogenesis are not mutually exclusive. An integrated approach is required in order to fully understand AIDS, and to design the optimal therapeutic strategies aimed at preventing the development of disease.
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PMID:[Mechanisms of immunodeficiency in human immunodeficiency virus infection]. 775 8

Human immunodeficiency virus (HIV)-1-associated dementia is a frequent consequence of HIV infection and is associated with neuronal deficits. Increased concentrations of the kynurenine pathway metabolites 3-hydroxykynurenine (3-HK) and quinolinic acid (QA) may contribute to this neuronal damage. We measured 3-HK concentrations and the activity of its catabolising enzyme, 3-hydroxykynureninase, in postmortem brain tissue from eight controls and 32 HIV-positive patients, including a group that exhibited dementia. 3-HK concentrations were significantly increased (over threefold) in the HIV-positive group when compared with controls. This increase was greater in those patients with dementia, but it was still apparent in the nondemented cases. 3-Hydroxykynureninase activity was significantly increased in the HIV-infected group compared with the control values. The effect was apparent in both nondementia and dementia cases, although the latter showed a slightly greater increase. The 3-HK content increase is thus unrelated to a reduction in activity of this enzyme and is likely to reflect an overall increase in the kynurenic metabolic pathway. Elevated levels of the neurotoxin 3-HK may contribute to the neuronal deficits underlying HIV-associated dementia.
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PMID:Increased concentrations of the neurotoxin 3-hydroxykynurenine in the frontal cortex of HIV-1-positive patients. 783 88

Complications of human immunodeficiency virus type 1 infection and acquired immunodeficiency syndrome may involve any level of the central or peripheral nervous system. Acute encephalitis, aseptic meningitis and acute demyelinating polyneuropathy may occur early in the course of HIV infection, while dementia, central nervous system-related cancer, opportunistic infections and autonomic neuropathy typically present later. Headache and mental status changes are common early manifestations of central nervous system involvement. Most severe headaches are related to an identifiable cause, including a mass lesion, opportunistic cerebral infection and medication side effect. Memory deficits, concentration difficulties and abnormalities on mental status testing may represent early AIDS dementia complex (HIV encephalopathy), the most common neurologic complication. In patients with AIDs, the differential diagnosis of cerebral mass lesions on computed tomography or magnetic resonance imaging includes cerebral toxoplasmosis, tuberculous or fungal abscess, focal viral encephalitis, metastatic resonance imaging includes cerebral toxoplasmosis, tuberculous or fungal abscess, focal viral encephalitis, metastatic Kaposi's sarcoma and primary CNS lymphoma. Peripheral neuromuscular disease, including distal symmetric polyneuropathy, autonomic neuropathy, and HIV and chronic zidovudine myopathy, affects 15 to 40 percent of all persons with HIV infection or AIDS.
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PMID:Common neurologic complications of HIV-1 infection and AIDS. 784 35

Dementia is a common process in which there is gradual decrease in mental function due to disease of either cortical or subcortical structures. The numerous causes of dementia can be divided into those in which dementia is the primary manifestation, as in Alzheimer's disease, or secondary to chronic disease, neoplasms, endocrine and metabolic disorders and chronic infections. The dementia in AIDS is usually part of the syndrome of acquired immunodeficiency and may be its first manifestation.
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PMID:[AIDS-related dementia]. 784 51

The dementia associated with human immunodeficiency virus (HIV) is poorly understood. Dementia is accompanied by infection and activation of macrophage lineage cells in the brain and production of toxic products by these cells has been postulated to play a role in the pathogenesis of dementia. Eicosanoids are potential products of activated macrophages that can mediate cell injury. We measured the levels of prostaglandin E2 in the cerebrospinal fluid of HIV-positive individuals with dementia and/or myelopathy and compared these levels with those of HIV-negative patients with other neurological diseases and HIV-positive patients without dementia. Cerebrospinal fluid prostaglandin E2 levels were increased in dementia. This increase was associated with severity of dementia and correlated with cerebrospinal fluid levels of neopterin and beta 2-microglobulin. Prostaglandins F2 alpha and thromboxane B2, additional products of the cyclooxygenase pathway of arachidonic acid metabolism, were also elevated in dementia, but leukotriene C4, a product of the lipoxygenase pathway was not. Since synthesis of prostaglandins is regulated in part by the levels of inducible forms of cyclooxygenase, we measured the levels of cyclooxygenase-1 and 2 mRNAs in the brains of HIV-positive individuals with and without dementia by reverse transcriptase polymerase chain reaction. Levels of intact cyclooxygenase-1 mRNA were higher in the brains of demented individuals, but this did not reach statistical significance. These data demonstrate that prostaglandins are increased in the central nervous system in HIV-associated dementia and may play a role in the development of neurological dysfunction.
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PMID:Elevated central nervous system prostaglandins in human immunodeficiency virus-associated dementia. 791 4

While dementia has been observed in approximately one-fourth of terminally ill patients with acquired immunodeficiency syndrome, it has been difficult to attribute this clinical disorder to a single neuropathological substrate. We used a simple and readily reproducible scale for estimating the burden of human immunodeficiency virus (HIV) in the central nervous system (i.e., severity of HIV encephalitis) and compared this to autopsy neurological summaries of dementia. Like others, we found that multinucleated giant cells were present in only half of the dementia patients. However, all of the dementia patients had severe HIV encephalitis as assessed by measurements of intra-central nervous system viral burden. Additional patients had severe HIV encephalitis without clinical histories of dementia. We interpret these latter findings as evidence that HIV encephalitis exists for a period of time before the clinical symptomatology develops. Comparison of presence or absence of concurrent cytomegalovirus encephalitis showed no association with dementia.
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PMID:Human immunodeficiency virus encephalitis is the pathological correlate of dementia in acquired immunodeficiency syndrome. 794 4


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