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)

We examined spinal cords, nerve roots, or peripheral nerves of 27 patients who died with acquired immunodeficiency syndrome (AIDS) for the presence of cytomegalovirus (CMV) and human immunodeficiency virus (HIV) by immunoperoxidase techniques in paraffin-embedded tissue. Vacuolar myelopathy was seen in 8 of 26 spinal cords (31%) and microglial nodules were seen in 13 (50%). All of the patients with lateral column vacuolar myelopathy showed severe brain pathology. HIV antigens had been detected in the brains of 15 (55%) of the 27 patients but were detected in only 3 (11%) of 26 spinal cords and were not localized to regions of vacuolar myelopathy. This suggests that the vacuolar myelopathy may be due to a remote or indirect effect of HIV or other infectious agent. CMV antigens were detected in none of the patients who showed vacuolar myelopathy but were detected in 2 of the 13 with microglial nodules. Focal nerve root or peripheral nerve inflammation was seen in 7 patients; 4 had CMV antigens and none had HIV antigens. CMV appears to be an important cause of inflammatory peripheral neuropathy in AIDS patients.
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PMID:Spinal cord and peripheral nerve pathology in AIDS: the roles of cytomegalovirus and human immunodeficiency virus. 254 60

The acquired immunodeficiency syndrome (AIDS) is caused by human immunodeficiency virus (HIV) and characterized by disorders of the nervous system in addition to opportunistic infection and cancer. Centers for Disease Control (CDC) recommend the classification system consisting of four major groups. Group I is patients with acute HIV infection, and Group II is asymptomatic carriers. Group III is those with persistent generalized lymphadenopathy (PGL). Group IV includes five subgroups: IVA with constitutional disease, IVB with neurologic disease, IVC with secondary infectious diseases, IVD with secondary cancers and IVE with other conditions. The nervous system disorders are classified into two types: one is produced by HIV itself and not directly related to immunodeficiency, and the other caused by opportunistic infectious agents and cancers. The former is further divided into two kinds: atypical aseptic meningitis and acute inflammatory demyelinating polyneuropathy (AIDP) occur mainly in Group I and II, whereas HIV encephalopathy, distal symmetric polyneuropathy (DSPN) and vacuolar myelopathy in Group III and IV. Group I or II patients have no apparent medical problems. Therefore, when neurologists see patients with risk factors for HIV infection presenting with atypical meningitis or AIDP, it is of utmost importance to have a high index of suspicion and to look for evidence of HIV infection.
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PMID:[Disorders of the nervous system associated with the acquired immunodeficiency syndrome (AIDS)-clinical approach]. 263 Jan 48

Spinal cord disease is common in patients infected with human immunodeficiency virus type 1 (HIV-1), and a characteristic vacuolar myelopathy is present at autopsy in approximately one-fourth of acquired immunodeficiency syndrome patients. Pathologic examination of the spinal cord shows vacuolation of white matter and infiltration by macrophages, a process distinct from HIV-1 encephalopathy. To determine the presence and localization of HIV-1 RNA in the spinal cords of acquired immunodeficiency syndrome patients with vacuolar myelopathy, we used the technique of combined in situ hybridization and immunohistochemical staining on the same slide. Spinal cord tissue sections were stained with markers for macrophages, endothelial cells, oligodendroglia, astrocytes, and myelin and then hybridized in situ with HIV-1-specific RNA probes. Combined in situ hybridization and immunohistochemical staining on three spinal cords showed HIV-1 expression in mononuclear and multinucleated macrophages localized mainly to areas of myelopathy in spinal cord white matter. Immunohistochemical staining and electron microscopy showed myelin within macrophages and electron microscopy revealed HIV-1 budding from macrophages. These data suggest a role for HIV-1-infected macrophages locally in the pathogenesis of vacuolar myelopathy and add to the body of evidence that these cells play a role systemically in the development of HIV-1-related disease.
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PMID:Human immunodeficiency virus type 1 in spinal cords of acquired immunodeficiency syndrome patients with myelopathy: expression and replication in macrophages. 271 18

Although merging clinically within the spectrum of the AIDS dementia complex, vacuolar myelopathy is a pathologically distinct entity detected in up to 30% of autopsied patients succumbing to the late complications of human immunodeficiency virus type 1 (HIV-1) infection. Using immunohistochemistry and in situ hybridization to detect an HIV-1 core protein and viral mRNA, respectively, in tissue sections, and culture isolation to assess infectious virus in tissue homogenates, we found that vacuolar myelopathy was independent of productive HIV-1 infection of the spinal cord and brain. These results indicate that AIDS-associated vacuolar myelopathy is either not related directly to spinal cord HIV-1 infection or involves nonproductive infection and pathobiological processes distinct from those responsible for the multinucleated-cell inflammatory infiltrates that serve as histopathologic markers of productive CNS HIV-1 infection.
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PMID:Dissociation of AIDS-related vacuolar myelopathy and productive HIV-1 infection of the spinal cord. 273 16

Tropical spastic paraparesis (TSP), a chronic myelopathy of unknown etiology, was studied in the Seychelles. Human T-lymphotropic virus type I (HTLV-I) and human immunodeficiency virus antibodies were determined using an enzyme-linked immunosorbent assay and confirmed with an indirect fluorescent antibody test in serum samples of 20 patients with TSP and 16 controls. Test results indicated that 17 patients (85%) and two controls (transverse myelopathy and clinically probable multiple sclerosis) were positive for HTLV-I. Serum samples of nine healthy controls and five with other neurologic diseases were negative for HTLV-I. No serum samples were positive for human immunodeficiency virus. Estimated relative risk for TSP in those subjects whose serum is positive for HTLV-I antibodies is 40. This result is highly statistically significant. Although primarily associated with adult T-cell leukemia and non-Hodgkin's lymphoma, HTLV-I could also be an etiologic agent of TSP.
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PMID:Human T-lymphotropic virus type I antibodies in the serum of patients with tropical spastic paraparesis in the Seychelles. 288 62

Human T-lymphotropic virus type I (HTLV-I), the causative agent of adult T-cell leukemia and non-Hodgkin's lymphoma (ATLL)--or a cross-reacting retrovirus--has been associated with tropical spastic paraparesis in Martinique, Jamaica, Colombia, Trinidad and Tobago, the Seychelles, and probably also in Zaire. The Caribbean basin and sub-Saharan Africa are endemic for ATLL. A similar etiology has been invoked in a chronic spastic myelopathy occurring in areas of high ATLL endemicity in Japan. An HTLV-I viral antigen has been demonstrated in cerebrospinal fluid lymphocytes of a Japanese patient with myelopathy. Human T-lymphotropic virus type I antibodies have occurred in patients in Florida and Japan (areas of HTLV-I endemicity) who were diagnosed as having clinically definite multiple sclerosis (MS), but not in patients with MS in other parts of the world. Human T-lymphotropic virus type I, like some lentiviruses--visna and human immunodeficiency virus, in particular--may be both lymphotropic and neurotropic. Tropical spastic paraparesis, the Japanese myelopathy, and, perhaps, an MS-like neurologic syndrome, may represent clinical variants of the same disease, a retroviral myelopathy.
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PMID:Retrovirus-associated myelopathies. 288 64

A 29 year old white homosexual man presented with a two and a half week history of severe sore throat, fever, and extreme fatigue. His symptoms did not respond to antibiotics. He had mild bilateral conjunctivitis, a rash over his chest and back, and enlarged lymph nodes, but examination of the nervous system yielded normal results. He had low total white cell and platelet counts. The results of enzyme linked immunosorbent assay for human immunodeficiency virus (HIV) were equivocal when HIV IgM was detected in serum. Despite treatment with ampicillin his temperature remained high and he developed abnormal neurological signs, including a paraparesis and hyperreflexia of the arms. HIV was isolated from lymphocytes from blood and cerebrospinal fluid. Over the next six weeks the patient improved and was discharged. Two months later abnormal neurological signs persisted in his legs. Although various neurological syndromes associated with seroconversion to HIV have been described, this is probably the first report of a patient with myelopathy at the time of seroconversion.
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PMID:Acute myelopathy associated with primary infection with human immunodeficiency virus. 288 58

To investigate the possible occurrence of human immunodeficiency virus (HIV) or human T-cell lymphotropic virus, type I (HTLV-I) infections in the United States prior to 1979-1981, when acquired immune deficiency syndrome (AIDS) was first recognized, we tested sera from 310 pregnant women who participated in the Collaborative Perinatal Project during the period 1959-1964 for HIV and HTLV-I antibody. These samples included sera from 53 pregnant women who were intravenous drug users. The remainder were from women who had cervical epithelial abnormalities, who developed cervical carcinomas, who had had children with erythroblastosis fetalis, who had had children that developed malignant neoplasms early in life, or normal pregnant women. None of the 310 women had confirmed HIV or HTLV-I antibody. The rate of false-positive reactions with the HIV enzyme-linked immunosorbent assay (ELISA) antibody test in these long-frozen samples was similar to that observed in fresh sera. HIV antibody was detected in homosexual patients with AIDS; HTLV-I antibody was not detected in any of these sera. HTLV-I antibody was detected in 17 of 20 patients with tropical spastic paraparesis (TSP) and in two of seven patients with other neurological diseases diagnosed as transverse myelopathy and multiple sclerosis, and in none of nine normal controls; HIV antibody was not detected in any of these sera patients. Thus, we conclude that there was no serological evidence of infection with HIV or HTLV-I in the pregnant women studied; however, HIV antibody was present in all AIDS patients tested, and HTLV-I antibody was found in the majority of patients with TSP.
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PMID:HIV and HTLV-I antibody studies: pregnant women in the 1960s, patients with AIDS, homosexuals, and individuals with tropical spastic paraparesis. 289 97

Subacute encephalitis caused by infection of the central nervous system by the human immunodeficiency virus (HIV) is the most frequent cause of neurologic dysfunction in patients with the acquired immunodeficiency syndrome (AIDS). This disorder results in progressive cognitive, motor, and behavioral abnormalities in at least two thirds of patients with AIDS. Pathologic evidence of subacute encephalitis is found in 90% of these patients at autopsy. Human immunodeficiency virus is also the etiologic agent of aseptic meningitis, a disease that can occur at the time of seroconversion. Other neurologic disorders frequently associated with HIV include peripheral neuropathies and vacuolar myelopathy. Thus, HIV is neurotropic and may enter the central nervous system early in the course of infection. Neurologic disease may be the only clinical manifestation of HIV infection. Although mechanisms of pathogenesis are unclear, cells of monocyte-macrophage lineage may be important in viral spread to and within the central nervous system. Effective antiviral therapy will probably require penetration of drugs across the blood-brain barrier.
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PMID:Neurologic manifestations of infection with human immunodeficiency virus. Clinical features and pathogenesis. 303 90

Clinical symptoms of the central and peripheral nervous system occur in about 40% of patients wit HIV infection. At autopsy, CNS lesions can be demonstrated in even higher percentages. Primary sequelae of HIV infection--either due to direct viral effects or the immunopathologic response of the human host--are acute aseptic meningitis or mengingo-encephalitis, HIV encephalopathy, myelopathy, neuropathy, and myositis. Secondary consequences of immunodeficiency in AIDS are opportunistic infections with other viruses, bacteria, fungi, and protozoa, e.g. CMV, HSV and HZV encephalitis, mycobacterial CNS infections, neurosyphilis, cryptococcal meningitis, and last but not least cerebral toxoplasmosis. The main secondary malignoma of the CNS is lymphoma. Together these disorders form a complex spectrum of central and peripheral neurological symptoms.
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PMID:[Neurologic complications of AIDS]. 304 48


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