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

The relative concentrations of human immunodeficiency virus (HIV) antibodies in relation to equal IgG contents of 46 serum cerebrospinal fluid (CSF) samples from 32 patients were determined by serial dilution in an anti-HIV enzyme-linked immunosorbent assay (ELISA). The ratio of CSF and the serum HIV antibody concentration was expressed as QHIV = CSF dilution/serum dilution. QHIV is regarded as a parameter for specific intrathecal HIV antibody production. The QHIV ranged from 0.7 to 16. Six of seven patients with clinical signs of acquired immunodeficiency syndrome (AIDS)-related dementia (ARD), but only seven of 25 patients without clinical diagnosis of ARD showed a QHIV greater than 2.
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PMID:Human immunodeficiency virus antibodies in cerebrospinal fluid. 319 35

Pathogenesis of HIV infection and expression of retroviral proteins are gradually being elucidated. Antibody to HIV is a marker of past or present viral infection. The virus can be isolated from cultured lymphocytes of seropositive but not seronegative patients. Sero-epidemiological studies show that the majority of infected patients are asymptomatic carriers without biological sign of immune depression. Some then show immune abnormalities such as a decrease of CD4 cells in the blood; some patients present with lymphadenopathies or signs of AIDS-related complexes. Frank AIDS is a late stage of the disease. Some cofactors increase the immunodeficiency and then accelerate the passage from asymptomatic carrier to persistent generalized lymphadenopathies or AIDS by spreading the virus into target cells, susceptible T4 cells, bone marrow precursors, or brain. These AIDS patients then present with opportunistic infections and/or malignancies like Kaposi's sarcoma, lymphoma, and/or brain diseases (dementia or encephalitis).
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PMID:HIV target cells: effect of their infection by HIV on the pathogenesis of AIDS. 326 Sep 82

Infection with human immunodeficiency virus type 1 (HIV-1) is frequently complicated in its late stages by the AIDS dementia complex, a neurological syndrome characterized by abnormalities in cognition, motor performance, and behavior. This dementia is due partially or wholly to a direct effect of the virus on the brain rather than to opportunistic infection, but its pathogenesis is not well understood. Productive HIV-1 brain infection is detected only in a subset of patients and is confined largely or exclusively to macrophages, microglia, and derivative multinucleated cells that are formed by virus-induced cell fusion. Absence of cytolytic infection of neurons, oligodentrocytes, and astrocytes has focused attention on the possible role of indirect mechanisms of brain dysfunction related to either virus or cell-coded toxins. Delayed development of the AIDS dementia complex, despite both early exposure of the nervous system to HIV-1 and chronic leptomeningeal infection, indicates that although this virus is "neurotropic," it is relatively nonpathogenic for the brain in the absence of immunosuppression. Within the context of the permissive effect of immunosuppression, genetic changes in HIV-1 may underlie the neuropathological heterogeneity of the AIDS dementia complex and its relatively independent course in relation to the systemic manifestations of AIDS noted in some patients.
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PMID:The brain in AIDS: central nervous system HIV-1 infection and AIDS dementia complex. 327 72

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

Toxoplasmosis as an opportunistic infection in patients with acquired immunodeficiency syndrome (AIDS) is a life-threatening condition. A review of the literature reveals over 140 cases of toxoplasmosis in AIDS victims, and there is sufficient clinical detail on 81 of these cases for in-depth evaluation. Toxoplasma infection in immunocompromised individuals generally affects the central nervous system and is the most common cause of focal brain lesions. Toxoplasmosis seems to be more frequent in AIDS patients in Africa than those from Europe or America. A clinical review of the 81 cases culled from the literature revealed deterioration in mental status in 42, neurological signs in 39, fever in 36, and persistent headache in 31. When human immunodeficiency virus (HIV) infection is associated with slowly evolving dementia and the preservation of consciousness, toxoplasmosis typically results in an acute deterioration in mental state. In AIDS, most cases of clinical toxoplasmosis result from an exacerbation of a chronic infection. Among the techniques that have been used to diagnose toxoplasmosis in AIDS patients are serology, cerebrospinal fluid samples, isolation of the parasite, radiology, and histology. Pyrimethamine plus a sulphonamide has been the traditional treatment for toxoplasma infection in AIDS patients and is associated with a greatly improved clinical state. Regardless of the drug therapy used, complete elimination of toxoplasma from viable cysts is unlikely and the subsequent emergence of trophozoites should be expected. A poor response to toxoplasmosis treatment is associated with failure to reach an early diagnosis, late initiation of drug therapy, and the lack of contrast enhancement of lesions detectable by computerized tomography.
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PMID:Toxoplasmosis and the acquired immune deficiency syndrome. 328 Jun 90

An understanding of the biologic characteristics and cellular tropism of human immunodeficiency virus (HIV) is critical to appreciate the diverse neurologic manifestations of HIV infection in patients with the acquired immunodeficiency syndrome (AIDS). Only carefully designed prospective studies can provide information regarding prevalence, incidence, and natural history of the full spectrum of neurologic complications of HIV infection. A degree of tropism for monocyte/macrophages and possibly for cells within the CNS seems certain. One of the most frequent complications is AIDS-related dementia, which reflects central nervous system invasion by HIV. Despite the evidence linking unchecked viral replication within the brain and progressive dementia, the basic pathogenetic mechanisms remain obscure. Further characterization of the cellular targets of HIV within the brain, and the mechanisms which ultimately lead to the dementia, is critical. The demonstration that HIV enters the central nervous system during the earliest stages of infection has major implications for antiviral agents which must penetrate brain parenchyma to clear the virus effectively. Other neurologic complications occur frequently, including myelopathies, peripheral neuropathies, opportunistic CNS infections, and CNS neoplasms. Many of these disorders are novel and incompletely characterized and their etiology is uncertain. While treatment is available for several of these conditions, it is generally not curative, and is often poorly tolerated because of adverse effects. Research directions will focus on better understanding of pathogenetic mechanisms, on earlier and more precise detection of these diverse conditions, and on improved therapeutic agents. For the future, efforts toward the development of a safe, effective vaccine are of critical importance. There are, however, already up to 2 million individuals in the United States who are already infected with HIV and who are thus at risk for developing 1 or several of these neurologic complications. Vaccination, even if it were available now, is not likely to benefit these individuals. While it is hoped that only a fraction of this infected population will develop neurologic symptoms, the prospects of an epidemic of AIDS-related dementia are ominous, particularly as antiviral therapy alone is unlikely to either eradicate the virus or restore brain function. In Africa and worldwide the numbers at risk for HIV-related diseases are enormous, and the risk factors for transmission of HIV less well defined. There, economic and medical resources are less than adequate to deal with a problem of this magnitude.
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PMID:Neurologic manifestations of AIDS. 331 21

Mental disturbances associated with acquired immunodeficiency syndrome (AIDS) are related not only to profound psychosocial stress, systemic diseases, and neoplasms or opportunistic infections within the central nervous system (CNS); they are also related to the direct neurotoxicity of the etiologic human immunodeficiency virus (HIV), producing an array of both insidious and acute affective, cognitive, and behavioral dysfunction that can mimic many neuropsychiatric disorders. The precise mechanism of this direct neurotoxicity is not known, nor have the frequency, clinical course, or methods of early diagnosis been clearly established; however, a critique of 56 clinical reviews or case reports regarding approximately 800 subjects suggest that at some point following infection an HIV-induced dementia is extremely common, as are marked histopathological changes throughout the CNS. Treatment strategies are discussed.
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PMID:AIDS dementia: a review of the literature. 333 Nov 19

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

The acquired immunodeficiency syndrome (AIDS) dementia complex (ADC) commonly complicates the course of human immunodeficiency virus (HIV) infection and AIDS. Although many of its clinical aspects have recently been brought into clearer focus, and pathogenetic evidence has accrued implicating direct HIV brain infection, there remain a number of fundamental aspects of ADC and HIV nervous system infection that require clarification. These include clearer definition of the clinical syndrome and its variants; development of instrumentation for diagnosis and monitoring the disorder; definition of the epidemiology and natural history of both central nervous system HIV infection and ADC, which may seemingly be discordant; and understanding of both the viral pathogenesis and the biology of resultant brain dysfunction. Elucidation of these fundamental issues will enhance rational development and evaluation of therapy.
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PMID:The AIDS dementia complex: some current questions. 334 98

A human immunodeficiency virus (HIV-I) was isolated from the brain of a patient with progressive dementia but no obvious immunosuppression. This isolate, designated as HIV-IBR, was molecularly cloned and sequenced, and its long terminal repeat (LTR) and envelope sequences were compared with those of other HIV isolates not uniquely associated with dementia. The HIV-IBR LTR showed marked homology with the LTR sequences of the other HIV-I isolates. The predicted amino acid sequence of the external glycoprotein (gp120) of HIV-IBR revealed a pattern of conserved and variable regions similar to that of other HIV isolates. The sequence of the transmembrane portion of envelope, gp 41, was highly homologous to the counterpart region of other isolates. Further analysis is required to determine whether specific sequence variation can account for neurological manifestations of HIV-IBR infection.
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PMID:Preliminary molecular characterization of a human immunodeficiency virus (HIV-I) associated with neuropathology. 334


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