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Query: UMLS:C0021051 (immunodeficiency)
71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The autopsied brains of three homosexual men with acquired immune deficiency syndrome (AIDS), progressive encephalopathy and widespread multinucleated giant cell encephalitis were investigated by lectin and immunohistochemical methods to ascertain the cellular distribution of a human immunodeficiency virus (HIV) core protein, p25. Abundant viral antigen was present in all brains, limited to perivascular macrophages, microglial and multinucleated cells, some bearing elongated cytoplasmic processes. The multinucleated cells were consistently labelled by the lectin Ricinus communis agglutinin-1, a marker for microglia, which demonstrated process-bearing variants of these cells. The prominent staining of microglia for viral antigen and the morphological suggestion that they fuse with other microglia and/or macrophages to form the multinucleated cells characteristic of HIV encephalitis indicate that microglia are probably direct targets of HIV infection and serve to propagate and amplify this retroviral encephalitis.
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PMID:Microglia in the giant cell encephalitis of acquired immune deficiency syndrome: proliferation, infection and fusion. 317 3

The value and limitations of CT and MR in human immunodeficiency virus (HIV) infection of the brain was determined by a retrospective analysis of the CT scans (22) and MR images (7) in 22 patients with pathologically proved HIV encephalitis (21) or meningitis (1). Our clinical-radiologic-pathologic correlation suggested that, especially in the early stages of the disease, CT and MR were relatively insensitive in detecting the primary changes of HIV encephalitis. The multiple bilateral diffuse microscopic glial nodules with multinucleated giant cells of HIV found at autopsy in both gray and white matter were usually not directly visualized by either CT or MR. Secondary, nonspecific changes, however, were seen. These included cortical atrophy, found in virtually all patients with HIV encephalitis, and HIV-induced foci of demyelination found in the minority of cases. On CT the latter were seen in the white matter as nonenhancing, nonmass-producing areas of low density; on MR they were seen as frequently progressive high-intensity signal abnormalities on T2-weighted images, usually in the periventricular white matter and centrum semiovale. MR was more sensitive in detecting these demyelinative lesions than was CT. The clinical diagnosis of HIV encephalitis usually antedated the radiographic diagnosis. In HIV meningitis, contrast CT was more definitive than MR, showing striking enhancement of the subarachnoid spaces, although MR was more sensitive in detecting the secondary parenchymal changes.
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PMID:CT, MR, and pathology in HIV encephalitis and meningitis. 326 Jul 30

Aseptic meningitis, subacute encephalitis, and vacuolar myelopathy are the three diseases of the central nervous system that are specifically related to or associated with human immunodeficiency virus (HIV) infection. HIV encephalitis initially is associated with myelin pallor and gliosis of the centrum semiovale, which is found in more than 90% of brains from patients dying with the acquired immunodeficiency syndrome. With increased severity of disease, multiple glial nodules with the multinucleated cells characteristic of HIV encephalitis are present throughout the cerebral white matter, basal ganglia, and cerebral cortex, and also may be found in cerebellum, brainstem, and spinal cord. HIV has been demonstrated in monocytes and multinucleated cells by electron microscopy, immunohistochemical techniques, and in situ hybridization. Vacuolar myelopathy occurs in approximately 30% of patients and is characterized by vacuolation of the white matter of the spinal cord that is most prominent in the posterior and lateral columns at thoracic levels. The severity of the pathological lesions correlates not only with symptoms and signs of spinal cord disease but also with dementia. Although the incidence of vacuolar myelopathy is increased in patients with HIV encephalitis, its etiology is not yet established.
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PMID:Review of central nervous system pathology in human immunodeficiency virus infection. 327 4

Combined medical, neurological, and serological investigations were carried out in 59 patients infected with human immunodeficiency virus (HIV). In stage I clinical and neuropsychiatric testing did not reveal evidence for HIV encephalitis as diagnosed by local antibody production in CSF. Neuropsychiatric abnormalities, brain atrophy, memory and cognitive impairment reliably indicated HIV encephalitis in later stages. The commonest symptoms were cerebellar and brainstem signs, followed by dementia. Epileptic fits and hemiparesis always were associated with cerebral toxoplasmosis. A polyneuropathy was frequently found but other causes have to be considered.
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PMID:Chronic HIV encephalitis--II. Clinical aspects. 334 5

Histopathologic findings in the central nervous system in 100 autopsy cases of the acquired immunodeficiency syndrome (AIDS) gave evidence of a variety of opportunistic infections and probably of infection by human immunodeficiency virus (HIV). Gliomesenchymal cell nodules (47 per cent of cases) and spongiform alterations with demyelination were common. Vasculitides (8 per cent) and lesions such as acute hemorrhagic leukoencephalitis may be attributable partly to hypersensitivity reactions. Multinucleated cells, including giant cells that could be a hallmark of HIV encephalitis, were common in normal neuropil, in gliomesenchymal cell nodules, near blood vessels, and in cavitating lesions. Degeneration in long tracts (13 per cent) included posterior column demyelination and spongiform change with or without corticospinal tract degeneration. Some long tract degeneration appeared to originate from bilateral degeneration of the internal capsule, and this may be part of the origin of subacute combined degeneration-like changes in AIDS vacuolar myelopathy. Prominent brainstem inflammatory infiltration suggests that the brainstem is a relatively prominent site of infection or immunopathologic activity. Early ependymal lesions in infants and frequent healed ependymal lesions in adults (16 per cent) could be related to the origin and pathogenesis of HIV lesions in the brain. Some characteristic lesions in AIDS encephalitis may result from immune-mediated responses to HIV antigens on neural cell receptors or from cross-reactivity occurring against epitopes common to neural constituents and to hematopoietic cells, with the latter being under direct antiviral attack.
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PMID:Histopathology of the central nervous system in the acquired immunodeficiency syndrome. 359 83

Mononuclear phagocytes (monocytes, macrophages, and dendritic cells) play major roles in human immunodeficiency virus (HIV) persistence and disease pathogenesis. Macrophage antigen presentation and effector cell functions are impaired by HIV-1 infection. Abnormalities of macrophage effector cell function in bone marrow, lung, and brain likely result as a direct consequence of cellular activation and HIV replication. To further elucidate the extent of macrophage dysfunction in HIV-1 disease, a critical activation-specific regulatory molecule, nitric oxide (NO.), which may contribute to diverse pathology, was studied. Little, if any, NO. is produced by uninfected human monocytes. In contrast, infection with HIV-1 increases NO. production to modest, but significant levels (2-5 microM). Monocyte activation (with lipopolysaccharide, tumor necrosis factor alpha, or through interactions with astroglial cells) further enhances NO. production in HIV-infected cells, whereas its levels are diminished by interleukin 4. These results suggest a possible role for NO. in HIV-associated pathology where virus-infected macrophages are found. In support of this hypothesis, RNA encoding the inducible NO synthase (iNOS) was detected in postmortem brain tissue from one pediatric AIDS patient with advanced HIV encephalitis. Corresponding iNOS mRNA was not detected in brain tissue from five AIDS patients who died with less significant brain disease. These results demonstrate that HIV-1 can influence the expression of NOS in both cultured human monocytes and brain tissue. This newly described feature of HIV-macrophage interactions suggests previously unappreciated mechanisms of tissue pathology that result from productive viral replication.
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PMID:Regulation of nitric oxide synthase activity in human immunodeficiency virus type 1 (HIV-1)-infected monocytes: implications for HIV-associated neurological disease. 753 Jul 62

The mechanism of cell death in the brains of patients with acquired immune deficiency syndrome was examined in 15 cases, 8 of whom had human immunodeficiency virus (HIV) encephalitis, and in 8 control cases. Postmortem formalin-fixed, paraffin-embedded sections were prepared for routine histology and immunohistochemistry to detect cell-specific antigens. Apoptosis was detected by its morphology and by in situ end labeling of its characteristic oligonucleosomal fragments. Combined in situ end labeling and immunohistochemistry identified specific cell types. Six acquired immune deficiency syndrome brains, 5 of which had HIV encephalitis, contained positive nuclei by in situ end labeling. Co-labeling studies identified the cells as neurons, reactive astrocytes, and, rarely, the multinucleated giant cells of HIV encephalitis. The only control with nuclei positive by in situ end labeling had hepatic encephalopathy and Alzheimer type II astrocytes; the location and absence of cell-specific markers suggested a glial origin for the labeled cells. These results demonstrate that at least some neuronal and astrocytic death in HIV infection occurs by apoptosis. Its stimuli are unknown, but likely candidates include tumor necrosis factor or HIV viral products. Additionally, we hypothesize that apoptotic death of reactive astrocytes may be a normal mechanism whereby the brain removes an excess number of astrocytes that have proliferated after certain types of brain injury.
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PMID:Evidence of apoptotic cell death in HIV encephalitis. 774 97

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

The nervous system is frequently involved in patients with AIDS. The lesions can be due to the human immunodeficiency virus (HIV), to opportunistic agents, to the development of tumours, and to occasional nonspecific factors, such as circulatory, metabolic and degenerative changes. The changes directly related to the presence of the HIV include the HIV encephalitis and leucoencephalopathy, the diffuse polydystrophy and the vacuolar myelopathy. The pathogenesis of these lesions is not yet completely clear. Macrophages are the main cells infected by the HIV, and it seems that the cytotoxic effects on the nervous tissue are indirect, may be due to the release of substances by infected macrophages. Among the opportunistic infections, the most frequent is toxoplasmosis followed by cryptococcosis and cytomegalovirus infection, with some differences in series from various countries. Many other agents have been observed in the brain of patients with AIDS. B-cell lymphoma is the most frequent tumour found in the brain and it is not uncommon the association of infections and/or tumours.
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PMID:[The neuropathology of the acquired immunodeficiency syndrome (AIDS)]. 812 70

True demyelination, or at least a leukoencephalopathy with predominant involvement of myelin, may occur in many neurological complications of human immunodeficiency virus (HIV)-infection, resulting from various mechanisms which are not all well understood. These include lesions directly related to infection of the nervous tissue by HIV, opportunistic infections and lymphomas secondary to the cell-mediated immunodeficiency, and changes due to other general or systemic complications of acquired immunodeficiency syndrome (AIDS). HIV-induced pathology of the nervous system includes HIV-specific disease, due to direct infection of the nervous system by the virus. This is characterized by the presence of distinctive multinucleated giant cells and white matter changes, HIV encephalitis and HIV leukoencephalopathy, which may overlap in one third of cases. The pathogenesis of myelin destruction is unclear. Direct infection of neurons or glial cells has never been demonstrated. Indirect immunopathologic, toxic, metabolic, or vascular mechanisms secondary to infection of monocytes/macrophages are more likely. Less specific HIV-associated central nervous system (CNS) pathology including vacuolar myelopathy, and vacuolar leukoencephalopathy are characterized by numerous vacuolar myelin swellings in spinal or cerebral white matter. The exact aetiopathological relationship of these changes to HIV infection is uncertain. It seems likely that factors other than, or additional to, HIV infection play a role in their causation. Apart from these changes which usually occur at the late stages of the disease, acute perivenous inflammatory leukoencephalopathy, presenting either as acute haemorrhagic leukoencephalopathy, acute demyelinating perivenous encephalitis, or acute multiple sclerosis-like leukoencephalopathy revealing HIV-infection occur in rare cases.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:HIV-related demyelinating disease. 825 24


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