Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

Based on a consecutive autopsy series of 184 patients with AIDS, a critical review of the pathology of the central nervous system (CNS) is given. The lesions can be divided into three groups: 1. opportunistic/non-opportunistic infections, 2. changes due to the human immunodeficiency virus (HIV), and 3. neoplasms. The frequency and morphology of CNS lesions in our cohort are compared with those in other series. Marked lesions of the CNS were found in 111 patients (60%), while mild/nonspecific changes were seen in 52 cases (28%). Toxoplasmosis (23%) was the most frequent CNS infection, followed by cytomegalovirus (17%), and papovirus (5%). HIV giant cell encephalitis, HIV leukoencephalopathy, vacuolar myelopathy and leukoencephalopathy were observed in 11%. Primary CNS lymphomas were present in 6%, while secondary involvement of the CNS in systemic lymphomas was seen in only two cases (1%). Lesions due to CNS infections in patients with AIDS often show atypical patterns, and frequently, there are multiple infections with simultaneous involvement of the CNS by lesions of different etiology. The present study confirms the frequent involvement of the CNS in AIDS, although there are differences in the incidence and pattern of lesions related to geographic and/or demographic factors.
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PMID:[Pathology of the central nervous system in AIDS. An overview of 184 patients]. 821 4

Detailed neuropathologic and immunohistologic analysis of a case of serologically and polymerase chain reaction-confirmed human immunodeficiency virus type I (HTLV-I)-associated myelopathy/tropical spastic paraparesis (HAM/TSP) is reported in a 73-year-old North American black woman. In addition to the usual neuropathologic features of HAM/TSP, including tractal degeneration of the spinal cord, leptomeningeal and perivascular fibrosis, perivascular demyelination and chronic inflammation, neuroaxonal spheroids were prominent in the spinal cord. Neuroaxonal dystrophy was characterized by neurofilamentous masses that were immunoreactive for phosphorylated neurofilament epitopes, but not ubiquitin. Neuroimmunologic analysis of the inflammatory reaction revealed a prevalence of CD8+ T cells and class I major histocompatibility molecules (MHC) (HLA-ABC and beta 2-microglobulin), but very few CD4+ T cells. Microglia were highly reactive for class II MHC (HLA-DR alpha) and this was attributed to activation, rather than CD4 interaction, since CD4 presence was minimal. Inflammatory cytokine immunoreactivity was also detected in glia. It is concluded that the cumulative effects of cytotoxic T cell (CD8) infiltration and the possible involvement of cytokines were responsible for the unusual degree of neuroaxonal dystrophy and vascular fibrosis, as well as the observed demyelination in this case.
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PMID:Neuroaxonal dystrophy in HTLV-1-associated myelopathy/tropical spastic paraparesis: neuropathologic and neuroimmunologic correlations. 821 80

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

Microglia are associated with central nervous system (CNS) pathology of both Alzheimer's disease (AD) and the acquired immunodeficiency syndrome (AIDS). In AD, microglia, especially those associated with amyloid deposits, have a phenotype that is consistent with a state of activation, including immunoreactivity with antibodies to class II major histocompatibility antigens and to inflammatory cytokines (interleukin-1-beta and tumor necrosis factor-alpha). Evidence from other studies in rodents indicate that microglia can be activated by neuronal degeneration. These results suggest that microglial activation in AD may be secondary to neurodegeneration and that, once activated, microglia may participate in a local inflammatory cascade that promotes tissue damage and contributes to amyloid formation. In AIDS, microglia are the primary target of retroviral infection. Both ramified and ameboid microglia, in addition to multinucleated giant cells, are infected by the human immunodeficiency virus (HIV-1). The mechanism of microglial infection is not known since microglia lack CD4, the HIV-1 receptor. Microglia display high affinity receptors for immunoglobulins, which makes antibody-mediated viral uptake a possible mechanism of infection. In AIDS, the extent of active viral infection and cytokine production may be critically dependent upon other factors, such as the presence of coinfecting agents. In the latter circumstance, very severe CNS pathology may emerge, including necrotizing lesions. In other circumstances, HIV infection of microglia probably leads to CNS pathology by indirect mechanisms, including release of viral proteins (gp120) and toxic cytokines. Such a mechanism is the best hypothesis for the pathogenesis of vacuolar myelopathy in adults and the diffuse gliosis that characterizes pediatric AIDS, in which very little viral antigen can be detected.
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PMID:Microglia and cytokines in neurological disease, with special reference to AIDS and Alzheimer's disease. 842 65

In serum, the enzyme adenosine deaminase (ADA) is known to be divided into two isoenzymes, ADA1 and ADA2, which have different molecular weights and kinetic properties. The present study investigated ADA isoenzyme levels in the sera of patients infected with retroviruses associated with adult T-cell leukemia (ATL), human T-cell lymphotropic virus type 1 (HTLV-1)-associated myelopathy (HAM), and AIDS, ADA isoenzyme activities were found to be significantly (P < 0.001) higher in the sera of patients with ATL, HAM, and AIDS than in the sera of healthy controls. In the case of the ADA subtypes in the sera of patients with ATL, ADA1 activity was significantly (P < 0.001) elevated in patients with the acute and lymphoma types of ATL compared with that in patients with the chronic and smoldering types of ATL. ADA2 activity was significantly elevated in the sera of patients with the acute, lymphoma, and chronic types of ATL (P < 0.001) compared with that in patients with smoldering ATL and HTLV-1 carriers. In the case of patients with human immunodeficiency virus type 1 (HIV-1) infection, ADA1 and ADA2 activities in the sera of patients with AIDS and HIV-1 antibody-positive individuals were significantly (P < 0.001) higher than those in the sera of HIV-1 antibody-negative individuals. A significant elevation in ADA2 activity was also seen in the sera of AIDS patients (P < 0.01) compared with that in the sera of HIV-1 antibody-positive individuals. These results suggest that the magnitude of elevation of ADA isoenzyme levels in serum correlates well with the clinical conditions of the patients with these diseases. Measurement of the activities of ADA isoenzymes may therefore provide an additional parameter for distinguishing the subtypes of ATL and may prove to be useful as prognostic and therapeutic monitors in diseases associated with HTLV-1 and HIV-1 infections.
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PMID:Adenosine deaminase isoenzyme levels in patients with human T-cell lymphotropic virus type 1 and human immunodeficiency virus type 1 infections. 854 45

We report a 29-year-old male hemophiliac with human immunodeficiency virus (HIV)-1-associated dementia complex, who died 2.5 months after the onset of dementia. The patient's cognitive abnormalities including forgetfulness, loss of concentration and slowing of thought appeared about 7 years after HIV infection. His neurological symptoms were characterized as progressive dementia, episodic consciousness loss, transverse myelopathy and peripheral neuropathy. He had generalized slow waves in electroencephalogram (EEG), progressive cerebral atrophy and a diffuse high intensity lesion in the white matter as shown by T2-weighted brain magnetic resonance imaging (MRI). We emphasize the significance of neurological complications, especially acute progressive dementia, in Japanese patients with acquired immunodeficiency syndrome (AIDS).
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PMID:A hemophiliac with human immunodeficiency virus (HIV)-1-associated dementia complex. 856 90

The neurological features of 13 patients with primary hypogammaglobulinaemia are described. Seven patients had X-linked agammaglobulinaemia (XLA) and six had common variable immunodeficiency (CVID). Three clinical pictures emerged: (i) a progressive myelopathy (one case); (ii) a myelopathy progressing to an encephalopathy (four cases); (iii) a pure encephalopathy (eight cases). In four patients the encephalopathy was temporarily reversible; the relationship of this to immunoglobulin therapy is unclear. Additional features occurred in some patients. Three had retinopathy interpreted as retinitis pigmentosa, in one of whom the retinopathy resolved. Two patients had a sensori-neural hearing loss and three had features of dermatomyositis; a variable pleocytosis was found in the CSF of nine patients. Imaging revealed atrophic changes in the cerebral hemispheres in eight cases. Ten patients have died, 1-11 years after the onset of the CNS manifestations, and in four autopsies were obtained. Two patients had encephalopathy, one with XLA had evidence of end-stage encephalitis and the other with CVID had a multi-focal leucoencephalopathy. The other two with XLA had leptomeningitis without evidence of encephalitis. Enteroviral infection is probably an important cause of neurological disease in these patients as CSF from seven patients was either positive by polymerase chain reaction (PCR) or by culture for enteroviruses. Other possible mechanisms are discussed.
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PMID:Encephalomyelitis in primary hypogammaglobulinaemia. 862 73

Vacuolar myelopathy is a common neurological complication in AIDS patients. The pathogenesis of this spinal cord white matter disease remains unclear and it is still debated whether infection of spinal cord with the human immunodeficiency virus type 1 (HIV-1) is causing the disease. We have generated transgenic mice expressing the entire HIV-1 genome under the regulation of an oligodendrocyte-specific promoter. These mice develop spinal cord vacuolar lesions similar to those found in AIDS patients. This animal model provides in vivo evidence linking the expression of HIV-1 proteins in oligodendrocytes to the spinal cord damage found in vacuolar myelopathy.
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PMID:Vacuolar myelopathy in transgenic mice expressing human immunodeficiency virus type 1 proteins under the regulation of the myelin basic protein gene promoter. 864 May 56

Human T-lymphotropic virus type I (HTLV-1) is associated with tropical spastic paraparesis (TSP) and adult T-cell leukemia/lymphoma. HTLV-I infection is endemic in certain parts of the Natal/KwaZulu region of South Africa. No studies on the seroprevalence of HTLV-I infection in the Free State (FS) have been published. This study was designed to determine the prevalence of HTLV-I antibodies among different patient groups in the FS. Sera from 863 patients were analyzed. There were: 178 asymptomatic rural Blacks, 200 asymptomatic urban Blacks, 50 asymptomatic Whites, 60 patients with spastic myelopathy, 70 patients with other neurologic disorders, 12 patients with T-cell haematologic malignancies and 293 human immunodeficiency virus (HIV) seropositive patients. Sera were tested for the presence of HTLV-I/II antibodies using an enzyme linked immunosorbent assay (ELISA). Positive results were confirmed using a modified Western blot assay. None of the asymptomatic Whites were HTLV-I antibody positive (95 pc confidence interval (CI): 0 to 7 pc), while 2 pc (95 CI: 0.5 to 5 pc) of asymptomatic urban Blacks and 1.1 pc (95 pc CI: 0.14 to 4 pc) of asymptomatic rural Blacks had HTLV-I antibodies. Of the group of patients with spastic myelopathy 33.3 pc (95 pc CI: 21.7 to 46.7 pc had HTLV-I antibodies, while none of the patients with T-cell haematologic malignancies (95 pc CI: 0 to 26.5 pc) or other neurologic disorders (95 pc CI: 0 to 5 pc) had HTLV-I antibodies. Of the HIV seropositive patients 6.1 (95 pc CI: 4 to 9.5) were co-infected with HTLV-I. HTLV-I infection is present in the Free State. It is strongly associated with spastic myelopathy in this region. HIV seropositive patients have a high rate of HTLV-I co-infection.
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PMID:HTLV-I infection in the Free State region of South Africa: a sero-epidemiologic study. 865 70

The spreading of human immunodeficiency virus (HIV) infection and its increasing scientific knowledge keep the medical staff involved with these patients in permanent need of updating themselves. The different neurologic manifestations caused by HIV are related to a variety of pathogenic mechanisms, as follows: immunodeficiency, autoimmunity, direct effects of the virus on the nervous system, and toxic and metabolic effects. The opportunistic infections are caused by the immunodeficiency due to the action of the virus on CD4+ T cells and on cells of the monocytic-macrophage lineage. Demyelinating polyradiculoneuropathy and polymyositis-like syndromes are related to autoimmune mechanisms involving, probably, the non-specific stimulation of T cells by viral proteins. The primary action of the virus on the nervous system brings out aseptic meningitis, cognitive dysfunction, dementia, vacuolar myelopathy and sensory polyneuropathy probably through liberation of neurotoxic products by the infected macrophages. Antiretroviral drugs and others used to treat patients with AIDS may also have neurotoxic effects. The better understanding of the neuropathogenesis of HIV infection will permit the use of new, and more specific, therapeutical options in the future as well as a more precocious control of its neurologic complications.
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PMID:[Neuropathogenesis of HIV infection]. 898 98


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