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

Nearly 40% of AIDS patients develop neurological complications during the course of their illness, and about 10% experience neurological symptoms as the initial manifestations of AIDS. The most common neurological complication (14% of AIDS patients) is human immunodeficiency virus (HIV) encephalopathy, but opportunistic viral and nonviral infections and neoplasms are also quite common; the most frequent among these are cryptococcal meningitis, toxoplasmosis, primary central nervous system (CNS) lymphoma, progressive multifocal leukoencephalopathy, and herpesvirus infections. Most of the nonviral infections and neoplasms are potentially treatable. Neurological syndromes include diffuse and regional encephalopathies, myelopathy, meningitis, intraaxial cranial neuropathies, and retinopathy. About 10% of AIDS patients develop a CNS mass lesion; the chief causes of these lesions are toxoplasmosis and primary CNS lymphoma. Since the clinical profiles of the various diseases overlap to a great extent, differential diagnosis requires a thorough workup, including magnetic resonance imaging or computed tomography brain scanning, examination of the cerebrospinal fluid, and, frequently, brain biopsy. Because AIDS patients have a high incidence of multiple intracranial pathologies, the diagnostic workup may have to be repeated to identify all of the diseases present.
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PMID:Central nervous system dysfunction in acquired immunodeficiency syndrome. 306 5

Eight children with acquired immunodeficiency syndrome (AIDS), aged four months to 12 years, were treated with zidovudine (azidothymidine) 100 mg/m2 intravenously every six hours for 14 days, followed by oral zidovudine at the same dose for a total of six months. Of the eight, six were infected at birth and two were contaminated by blood transfusion at ages eight and nine years, respectively; seven of the eight showed specific neurologic impairment consisting of encephalopathy (six children) and myelopathy (one child). In two children, a dramatic improvement of clinical status occurred, including neurologic progress in one; in three, the improvement was dissociate or transient and in the other three, no modification was observed. A marked increase of total lymphocyte and CD4(+) cell counts occurred in four children but was transient without modification of in vitro antigen-induced lymphocyte proliferation; p24 human immunodeficiency virus serum antigens were detected in seven of eight children, then transiently disappeared in all children during intravenous therapy but reappeared progressively during the oral regimen in all but one. Progressive modification of human immunodeficiency virus serology was noted in five children, mainly characterized by the finding of anti-core antibodies. The hematologic toxicity of zidovudine was comparable with that observed in adults. These preliminary results support the need for further studies in order to delineate the optimal regimen of zidovudine in children with AIDS.
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PMID:Zidovudine therapy in children with acquired immunodeficiency syndrome. 316 4

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

Human immunodeficiency virus type 1 (HIV-1) has been clearly associated with a variety of new illnesses, including profound immunodeficiency (acquired immune deficiency syndrome [AIDS]), wasting syndromes (formerly termed AIDS-related complex [ARC]) and neurologic syndromes, including neuropathy, myelopathy and encephalopathy (often termed subacute encephalitis or AIDS dementia complex). HIV-1 preferentially infects T lymphocytes by binding to a membrane receptor protein, CD4, associated with helper function. The virus can also attack macrophages and, possibly, other cells such as neuronal cells, colonic epithelial cells and B lymphocytes. Infection of macrophages or monocytes may be involved in neurologic disease. Knowledge about HIV-1 has rapidly increased, and investigators have characterized its structure, ways in which it infects cells, replicates and is cytopathic for certain cells, and how the immune system responds to it. The ideal vaccine would prevent adsorption of the virus into the cell, but it is difficult to develop stable resistance because the virus has many antigenic patterns and mutates frequently. The results of vaccine trials in animals have not been promising, but work is being done with monoclonal antibodies. Antiviral therapies being investigated include those to prevent virus binding and entry, to inhibit reverse transcription, to inhibit the virus's life cycle and to restore immune competence in immunocompromised patients.
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PMID:Vaccine and antiviral strategies against infections caused by human immunodeficiency virus. 328 28

A homosexual man, seropositive for human immunodeficiency virus, developed back and leg pain that evolved, over three weeks, into a T-10 anesthetic, areflexic paraplegia. Spinal fluid examination showed lymphocytosis, markedly elevated spinal fluid protein, and hypoglycorrhachia. A spinal cord biopsy specimen disclosed an intramedullary granuloma containing acid-fast bacilli. The patient was treated with antituberculous drugs and had no progression of neurologic deficit. He died, eight months after first becoming ill, of Klebsiella pyelonephritis and septicemia. Mycobacterial meningomyelitis is presently the only known acquired immunodeficiency syndrome-related myelopathy responsive to specific treatment.
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PMID:Mycobacterial meningomyelitis associated with human immunodeficiency virus infection. 274 40

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

Eventually, gene therapy may be a valid option for chronic viral infections, including retroviral infections. Human retroviral diseases fit two categories: (1) those that result from a monoclonal outgrowth of a human T-cell leukemia virus type I (HTLV-I)-infected cell, as in the case of adult T cell leukemia (ATL); and (2) those that appear to result directly from virus load rather than monoclonal outgrowth--such as tropical spastic paraparesis/HTLV-I associated myelopathy (TSP/HAM) and human immunodeficiency virus (HIV)-associated acquired immune deficiency syndrome (AIDS). For ATL gene therapy, corrective mechanisms directed at regulatory sequences rather than viral sequences may be most important, though perhaps anti-tax therapy would be useful. For TSP/HAM and AIDS, gene therapy directed to control virus replication may be most useful. For anti-retroviral therapy, one may use dominant negative mutants and a variety of other approaches that direct toxins or compete out viral regulatory gene signal sequences. For maximum benefit, such therapy should be directed to different essential genes (eg gag, pol, env, tat or rev) involved in the virus replication cycle and utilize different toxic approaches. A major impediment to the use of gene therapy for AIDS is our inability to transfect a significant fraction of target cells in vivo. Except for reconstituted mice, retroviral systems of animals have been under-utilized as models for gene therapy. Naturally occurring retroviral diseases of cats, goats, horses, and other species provide models for future development.
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PMID:Gene therapy against retroviral diseases. 747 20

The post-mortem pathology in 20 spinal cords of human immunodeficiency virus (HIV) infected patients with vacuolar myelopathy was quantified by evaluating (i) the intensity of myelin change, vacuolation and macrophage density; and (ii) the areas of white matter covered by each feature. Severity scores were constructed for (i) the anterior, lateral, and posterior white matter columns; (ii) each level of spinal cord; and (iii) the whole spinal cord [Cord Total and Cord Average Severity Scores (CTSS, CASS)]. Astroglial activation was scored separately. In 14 cords with mild-moderate vacuolar myelopathy (CASS = 23-259), macrophages were the most prominent pathological feature, and level severity scores were higher at mid-thoracic than cervical levels (P = 0.009). In six cords with severe vacuolar myelopathy (CASS = 396-614), vacuolation, demyelination and macrophages were equally evident and thoracic and cervical level severity scores were similar. The most severe lesions showed evidence of clearing of macrophages from the collapsed centres. A clinical lower limb score correlated with the anterior (P = 0.03) and lateral (P = 0.04) column total scores and with the CTSS (P = 0.04) in the nine patients who had had both myelopathy related disability and all cord levels available. There was no significant longitudinal gradient in score severity in the posterior, lateral or anterior columns and no evidence of a dying-back phenomenon. There was no evidence of Wallerian degeneration occurring as a primary process. Astroglial activation did not correlate with the severity or duration of the vacuolar myelopathy. Detection of HIV p24 antigen in the spinal cord related to the local presence of multinucleated giant cells and to antigen expression in the brain but not with the severity of vacuolar myelopathy. The pathology in vacuolar myelopathy appeared to start in the mid-low thoracic cord, with increasing rostral involvement as the disease became more severe. The relative prominence of macrophages in mild-moderate lesions suggests they may be involved early in the pathogenesis of vacuolar myelopathy.
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PMID:AIDS-associated vacuolar myelopathy. A morphometric study. 749 84

The vast majority of patients with human immunodeficiency virus (HIV) and acquired immune deficiency syndrome (AIDS) have symptoms or signs involving the feet and lower extremities. Patients presenting to podiatrists with foot complaints may, in fact, have neurologic complications of HIV originating in any level of the neuraxis, and multiple levels may be involved. These include multiple classes of peripheral neuropathy and myopathy, inflammatory radiculopathy, myelopathy, and central nervous system lesions caused by direct HIV infection or opportunistic infections. Common complaints such as pain, numbness, burning, tingling, weakness, cramps, unsteady gait, and others should be systematically evaluated with both podiatric and neurologic etiologies in mind for early diagnosis and intervention.
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PMID:Neurologic conditions affecting the lower extremities in HIV infection. 764 14

Human T-lymphotropic virus type I (HTLV-I) is a pathogenic retrovirus associated with a chronic progressive myelopathy, termed HTLV-I-associated myelopathy (HAM). A chronic inflammatory process has been implicated in HAM by a pathological study, but the exact mechanism still remains to be elucidated. Our quantitative polymerase chain reaction study indicated that the large increase in the HLTV-I proviral DNA in peripheral blood is associated with the development of HAM. The nucleotide sequence analysis of HTLV-I in central nervous system (CNS) tissue of HAM patients revealed that the sequences of HTLV-I genome were heterogenous in all cases, and that the pX-defective mutants were found frequently in the CNS. Thus, HTLV-I exists as quasispecies in vivo, as shown in the case of human immunodeficiency virus. It is possible that the HTLV-I pX microvariants contribute to the neural damage, since the pX gene products are essential for the transactivation of various cellular genes as well as for viral replication.
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PMID:[The nervous system involvement in human retroviral infection]. 777 30


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