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)

HIV-induced neurological disease is postulated to be caused by indirect mechanisms. Tumor necrosis factor (TNF)alpha is increased in the brains in human immunodeficiency virus (HIV)-associated dementia and in the spinal cord in vacuolar myelopathy and may play a pathogenetic role in these diseases. Microglia, astrocytes and infiltrating macrophages can be induced to produce TNF alpha and each has been identified as a source of TNF alpha in neurological disease. Reverse transcriptase synthesis of cDNA and polymerase chain reaction amplification of the cDNA was combined with immunocytochemistry to identify the cellular source of TNF alpha in HIV-induced neurological disease. Cells positive for TNF alpha mRNA were more abundant in white matter than gray matter of the brain from demented individuals. TNF alpha mRNA-positive cells in brains and spinal cords were almost exclusively macrophage-lineage cells. Only rare TNF alpha mRNA-positive cells were astrocytes. We conclude that macrophage-lineage cells are the primary source of elevated central nervous system TNF alpha mRNA in providing further evidence that macrophage activation is an important element in the pathogenesis of HIV-associated neurological disease.
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PMID:Cellular localization of tumor necrosis factor mRNA in neurological tissue from HIV-infected patients by combined reverse transcriptase/polymerase chain reaction in situ hybridization and immunohistochemistry. 911 60

A 35-year-old man infected with human immunodeficiency virus presented with cervical myelopathy of 2 months duration. Clinical and radiographic evaluation revealed a discrete, subdural mass at C-6. At surgery, the mass proved to have a dural attachment and thus clinically, radiographically, and grossly, it resembled meningioma. Histopathological analysis revealed a leiomyosarcoma that stained diffusely for muscle-specific actin. Electron microscopy revealed basal lamina surrounding the tumor cells and intracytoplasmic bundles of myofilaments. Epstein-Barr virus (EBV) was demonstrated within tumor cell nuclei by in situ hybridization for EBER1 messenger RNA and immunohistochemical staining for EBNA2 protein. Epstein-Barr virus latent membrane protein (LMP1) was not detected. This is the first documentation of an EBV-associated smooth-muscle tumor of the dura, and the first demonstration that tumors in this location contain EBV in an unusual form of latency not seen in lymphoid cell lines. With increasing numbers of individuals being afflicted with long-term immunosuppression, EBV-associated dural leiomyoma and leiomyosarcoma may be encountered more frequently in the future.
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PMID:Epstein-Barr virus-associated dural leiomyosarcoma in a man infected with human immunodeficiency virus. Case report. 912 7

Fas/APO-1 mediates apoptosis via Fas and Fas ligand transduction. Recently, a soluble form of Fas (sFas) was described which seems to be functionally implicated in the Fas signal system, suggesting a relationship between some disorders and sFas function. We measured sFas-levels in sera from normal controls and patients with disorders linked to human retroviral infection of human immunodeficiency virus (HIV) and human T-cell leukemia virus type-1 (HTLV-1). The sFas level of normal controls. HTLV-1 carriers seronegative for HIV, and patients with HTLV-1 associated myelopathy/tropical paraparesis (HAM/TSP), adult T-cell leukemia (ATL), and AIDS was 1.62 +/- 0.49, 1.90 +/- 0.49, 2.00 +/- 0.59, 3.32 +/- 2.05, and 3.06 +/- 0.92 ng/ml, respectively. Although the level of sFas in patient groups with HAM/TSP, ATL, and AIDS was significantly high in comparison to that of normal controls (p < 0.01), the individual values were highly variable within the groups. The sFas level was statistically correlated to the soluble interleukin-2 receptor (sIL-2R) level, as well as to cells expressing membrane Fas (mFas), indicating the same cellular origin. In some ATL cases, however, serum sFas levels and mFas expression density on leukemic T-cells were discrepant, with especially high levels of the soluble form and a lack of expression of the membrane form observed in 2 cases, sFas detection could serve as a putative marker for active diseases in patients with ATL and AIDS.
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PMID:Serum levels of soluble Fas/APO-1 receptor in human retroviral infection and associated diseases. 914 6

To study the epidemiology of the neurologic manifestations of human immunodeficiency virus (HIV)-1 infection in Japan, we conducted two nationwide surveys. Of 1854 HIV-1 carriers, 578 had acquired immunodeficiency syndrome (AIDS) and 166 (28.7% of AIDS patients) had neurologic manifestations including HIV dementia (11.8%), myelopathy (3.6%) and peripheral neuropathy (2.6%). The incidence of neurologic manifestations in patients with HIV-1 infection through blood products was about 60% of that in patients with HIV-1 infection through sex or unknown routes. This nationwide survey showed that the incidence of neurologic manifestations in AIDS patients in Japan was consistent with that in other countries.
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PMID:Nationwide survey of neurologic manifestations of acquired immunodeficiency syndrome in Japan. 914 4

The localization of mammalian retroviruses to specified immune organs has significant implications on the pathophysiology of retroviral associated diseases. Human T-cell Lymphotropic Virus Type I (HTLV-I) is considered a CD4+ lymphotropic virus although the virus has been shown to infect a large variety of cells in vitro. Similarly, the human immunodeficiency virus (HIV), once thought to be harbored only in CD4+ peripheral blood lymphocytes (PBL) has been shown to be present in latent form in lymph nodes of HIV infected patients. HTLV-I Associated Myelopathy/Tropical Spastic Paraparesis (HAM/TSP) is a chronic progressive neurologic disorder of the central nervous system and is believed to result from infection of HTLV-I in association with an immunopathogenic or autoimmune mechanism. Here we describe experiments which utilize the in situ hybridization/polymerase chain reaction technology to demonstrate extensive HTLV-I infection of bone marrow in HAM/TSP patients. We discuss these results in the context of HTLV-I associated neurologic disease and extend these observations to other disorders of potential retroviral etiology and autoimmune involvement.
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PMID:Immunopathogenesis of HTLV-I associated neurologic disease: massive latent HTLV-I infection in bone marrow of HAM/TSP patients. 920 3

Since the onset of the acquired immune deficiency syndrome (AIDS) epidemic fifteen years ago, much has been learned about the effects of the human immunodeficiency virus (HIV) in the nervous system. This review summarizes the pathology findings in the central nervous system (CNS). There is now abundant evidence that HIV can infect the CNS directly, leading to a characteristic HIV encephalitis (HIVE) which occurs in 10-50 p. 100 of AIDS autopsy series. Multinucleated giant cells are the pathognomonic feature of HIVE and are found predominantly in the central white matter and deep grey matter. Evidence of productive HIV infection in the CNS is confined to cells of the microglial/macrophage lineage, from which the giant cells are almost certainly derived. These cells are known to express both CD4 and beta-chemokine receptors, which act in conjunction to permit HIV entry. Restricted infection of astrocytes has also been identified by a variety of methods. HIVE is frequently associated with white matter damage ranging from inflammatory (microglia, macrophages and sparse lymphocytes) to degenerative (myelin loss and axonal damage) pathology. Although giant cells are seen less frequently in neocortical grey matter, significant neuronal loss has been established in a number of studies. Recent investigations using markers of apoptosis, (including TUNEL, Bcl-2 and BAX), have established the presence of DNA damage in some neurons and in other cell types. Axonal damage has also been confirmed by evidence of amyloid precursor protein expression. The CNS is also vulnerable to opportunistic infections and high grade B-cell lymphomas as a result of the immune suppression of advanced HIV infection. Cytomegalovirus (CMV) infection is reported in 10-30 p. 100 of AIDS cases at autopsy, toxoplasma in 10-25 p. 100, progressive multifocal leucoencephalopathy in about 5 p. 100 and lymphomas, usually primary, in up to 10 p. 100. A wide variety of other infections has also been reported. These may coexist with HIVE and may be difficult to diagnose in life. CMV gives rise to microglial nodular encephalitis, ventriculitis, necrotising encephalitis and myelo-radiculitis. Presymptomatic HIV positive patients do not show HIVE or opportunistic infections or lymphomas in the CNS. They frequently display a low-grade T-cell infiltrate in the leptomeninges and parenchyma, particularly around vessels. This lymphocytic infiltrate has been attributed to presumed early invasion of the CNS by HIV although the exact timing of entry is uncertain. It is possible that reported abnormalities in presymptomatic cases such as gliosis, microglial activation and rising proviral load may anticipate the onset of HIVE but most studies show that significant CNS damage and HIV-related pathology is confined to patients with AIDS. HIV-related pathology in the spinal cord includes not only HIV myelitis, opportunistic infections and lymphomas, but also vacuolar myelopathy (VM) which affects predominantly the dorsolateral white matter tracts. The cause of VM is not understood and has not been unequivocally linked with HIV infection. It is noted that none of these neuropathological features (including HIVE) correlates exactly with the clinical expression of AIDS-related dementia (ARD). The exact contribution of macrophage activation and cytokine release, astrocytic infection, neuronal loss and axonal damage to the neuropsychiatric syndromes of advanced HIV infection remain to be determined. While the current understanding of the pathogenesis of HIVE and ARD is beyond the scope of this review it is axiomatic that accurate documentation of neuropathology findings will help to resolve the outstanding dilemmas relating to HIV infection of the CNS. There is considerable optimism that progress in therapeutic regimes for HIV-infected patients will succeed in eliminating the virus from the blood and from lymphoid tissue. (ABSTRACT TRUNCATED)
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PMID:The neuropathology of adult HIV infection. 993 3

Multinucleated giant cells (MNGCs) expressing the human immunodeficiency virus (HIV) are characteristically found in hyperplastic tonsils and adenoids, acquired immunodeficiency syndrome encephalitis, vacuolar myelopathy, and lymph nodes coinfected with opportunistic pathogens. We identified similar polykaryons in the hyperplastic gut-associated immune system of an HIV-infected patient. Colonic biopsy specimens from this patient with heme-positive stools were studied by light and transmission electron microscopy (TEM), immunohistochemistry, and in situ hybridization for HIV-specific RNA. No bleeding source was identified by endoscopic or light microscopic examination of the biopsied tissues. There was diffuse and nodular lymphoid hyperplasia with germinal centers. HIV RNA-positive and p24 gag-positive Langhans'-type MNGCs and mononuclear cells (MNCs) were present within the lamina propria The MNGCs and MNCs were identified as macrophages on the basis of TEM and expression of CD68, HAM56, and lysozyme markers. They also expressed S100 protein, a marker of dendritic/Langerhans' cells, but they lacked Birbeck granules by TEM. In situ hybridization demonstrated RNA expression by MNGCs, MNCs, and follicular dendritic cells. TEM revealed budding and mature HIV particles on the plasma membranes of MNGCs, MNCs, and follicular dendritic cells. We conclude, therefore, that hyperplastic gut-associated immune systems can contain HIV-positive MNGCs and MNCs of the type seen in tonsils and adenoids and opportunistic pathogen-infected lymph nodes. Associated with immune activation, macrophages can express markers of dendritic/Langerhans' cells, cell types derived from the same CD34-positive bone marrow progenitor.
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PMID:Human immunodeficiency virus-rich multinucleated giant cells in the colon: a case report with transmission electron microscopy, immunohistochemistry, and in situ hybridization. 995 Jan 66

We examined the neurological differences between human immunodeficiency virus (HIV)-infected men (n = 193) and women (n = 41) receiving primary medical care. There was no difference between men and women in the rate of HIV-related neurological syndromes (i.e. polyneuropathy, myelopathy, myopathy, HIV- dementia [HAD]). A logistic regression analysis indicated that low CD4+ cell count predicted all neurological syndromes. In addition, HAD was predicted by intravenous-drug use and lower education level, while neuropathy was associated with older age and with race. These findings indicate that there are no differences in the rate of neuropsychiatric disorders attributable to gender. The presence of other factors (e.g. drug abuse) could explain previously reported gender differences in neurological manifestations of HIV infection.
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PMID:Neurological characteristics of HIV-infected men and women seeking primary medical care. 1005 33

The purpose of this review is to present some concepts on the etiology of tropical spastic paraparesis or human T-cell lymphotropic virus-I (HTLV-I)-associated myelopathy (TSP/HAM). The large number of syndromes that have been associated with HTLV-I (60 to date), the existence of TSP/HAM cases associated with other retroviruses (human immunodeficiency virus-2 [HIV-2], HTLV-II), the existence of many TSPs without HTLV-I, and the evidence of clear epidemiologic contradictions in TSP/HAM indicate that the etiopathogenesis of TSP/HAM is not yet clear. Tropical spastic paraparesis/HAM affects patients of all human ethnic groups, but usually in well localized and relatively isolated geographic regions where HTLV-I has been endemic for a long time. Environmental factors and geographic locations appear to be critical factors. Because the neuropathology of TSP/HAM suggests a toxometabolic, rather than a viral cause, it is proposed that an intoxication similar to neurolathyrism could account for some of TSP/HAM cases, mainly in tropical and subtropical countries. If this were the case, HTLV-I could be a cofactor or act as a bystander. it is possible that co-infection with another agent is necessary to produce TSP/HAM and most of the syndromes associated with HTLV-I.
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PMID:On the etiology of tropical spastic paraparesis and human T-cell lymphotropic virus-I-associated myelopathy. 1046 Sep 31

The most common disease of the spinal cord in human immunodeficiency virus (HIV) infection is vacuolar myelopathy. Pathology studies have demonstrated that vacuolization in the thoracic spinal cord is present in more than a third of patients with AIDS. The disease, however, manifests clinically only when the vacuolization in the spinal cord has become severe, with prominent myelin loss in the lateral and posterior columns. Vacuolar myelopathy presents usually with slowly progressing spastic paraparesis, accompanied by loss of vibratory and position sense and urinary frequency and urgency. In males, erectile dysfunction can be an early manifestation of the disease. The pathogenesis of vacuolar myelopathy is unknown but may be related to abnormal trans-methylation mechanisms induced by the HIV virus and cytokines. There is no known treatment for the disease, although therapy with methylating agents is being investigated. There are other rarer causes of spinal cord disease in AIDS, including a number of infectious myelitis and neoplastic and vascular myelopathies.
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PMID:Diseases of the spinal cord in human immunodeficiency virus infection. 1071 35


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