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

Dementia is common in patients with AIDS, but the mechanism by which the human immunodeficiency virus type 1 (HIV-1) causes the neurological impairment is unknown. In this study the possibility that an antigen of HIV-1 suppresses neuronal responses to neurotrophic factors was examined. Both HIV-1 and a related retrovirus, simian immunodeficiency virus (SIV), inhibited the growth of sensory neurons from chick dorsal root ganglia in medium containing neuroleukin (NLK) but not in medium containing nerve growth factor. An unrelated type D retrovirus, simian acquired immunodeficiency syndrome virus, did not affect the growth of neurons in the presence of either neurotrophic factor. The inhibition by HIV-1 of neuron growth in the presence of NLK was found to be due to the gp120 envelope glycoprotein. Regions of sequence homology between gp120 and NLK may account for this inhibitory property of gp120 and functional interactions between gp120 and NLK may be important in the pathogenesis of the AIDS dementia complex.
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PMID:Functional interaction and partial homology between human immunodeficiency virus and neuroleukin. 303 62

The protean neurological manifestations of human immunodeficiency virus (HIV) infection are reviewed. Both the central nervous system and peripheral nervous system may be affected and many of the complications may occur in individuals with acquired immunodeficiency syndrome (AIDS)-related complex, or who are seropositive for HIV alone as well as those with the established AIDS syndrome. Specific therapy is available for certain of these neurological conditions, but the clinical course in others is untreatable and progressive. Although it seems likely that the pathogenesis of some of these syndromes such as the AIDS-dementia complex are due to the direct effect of HIV on the nervous system, in others the neurological injury probably occurs as a consequence of the immunosuppression which HIV induces, or immune-mediated mechanisms.
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PMID:Neurological complications of human immunodeficiency virus infection. 305 Sep 40

For the geriatrician who commonly evaluates cognitive and psychiatric disorders in the elderly, the neurologic consequences of infection with the human immunodeficiency virus (HIV) are of particular importance. The most frequent neurologic disease is the AIDS dementia complex characterized by cognitive, behavioral, and motor changes, occurring in two-thirds of AIDS patients. The pathophysiology of central nervous system HIV infection has been advanced with important implications for both the diagnosis and the potential treatment of this devastating disease.
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PMID:AIDS dementia. 306 66

A review of the magnetic resonance (MR) images of 365 patients with acquired immunodeficiency syndrome (AIDS) revealed that 112 (31%) had signal abnormalities confined to the white matter. Four patterns were observed: (a) diffuse: widespread involvement of a large area; (b) patchy: localized involvement with ill-defined margins; (c) focal: well-defined areas of involvement; and (d) punctate: small foci less than 1 cm in diameter. Clinical or pathologic findings were available in 60 of the 112 patients and were correlated with the white matter patterns seen on MR images. The diffuse pattern correlated with AIDS dementia complex (ADC), which was the most common clinical diagnosis. Patchy or punctate lesions may be seen with ADC but are less common. Focal white matter lesions were not seen in patients with ADC but were seen in all six patients with progressive multifocal leukoencephalopathy, in both patients with lymphoma, and in one patient with toxoplasmosis. The authors conclude that white matter lesions are are common in AIDS and are often secondary to direct infection of the brain with human immunodeficiency virus, which causes the ADC and usually produces a diffuse white matter pattern. Biopsy is probably not indicated in these patients. Focal white matter lesions suggest a focal infection or tumor, and biopsy may be warranted.
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PMID:White matter disease in AIDS: findings at MR imaging. 317 91

The AIDS Dementia Complex (ADC) frequently occurs in individuals with Acquired Immunodeficiency Syndrome (AIDS). We report on a clinical series of 33 patients with either AIDS or AIDS-Related Complex (ARC), who were referred for neuropsychological evaluation. This clinical series supports the developing understanding that AIDS spectrum patients often demonstrate impairment on tasks involving abstract reasoning, memory, speeded mental processing and motoric slowing. This series helps to draw attention to a small subgroup of patients, with no previous psychiatric history, who after infection with the human immunodeficiency virus (HIV), present with hyperactivity, euphoria and grandiose delusions. ADC would appear to bear with it the increased possibility of the development of secondary mania.
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PMID:Neuropsychiatric aspects of AIDS dementia complex: a report on a clinical series. 320 May 6

Human immunodeficiency virus (HIV) has selective T4-cell tropism and is cytocidal to cells with the helper-inducer phenotype. Central nervous system dysfunctions can complicate full-blown acquired immunodeficiency syndrome (AIDS) but can also be present either in isolation or in the context of AIDS-related complex. Remarkably bland histopathological findings have been reported in some patients with AIDS dementia in the presence of severe clinical dysfunction. Thus, to understand the cytopathic properties of HIV, we recovered five viral isolates from 4 patients with neurological symptoms of AIDS and identified them as HIVs. The replication and cytocidal properties of these isolates were compared with lymphadenopathy-associated virus in vitro. All five isolates exhibited replication efficiency equivalent to lymphadenopathy-associated virus, but four isolates did not kill CD4 (T4+) cells. These findings provide evidence for the existence of replication-competent noncytocidal natural variants of HIV and raise the possibility that, in some AIDS patients, neurological disorders might be caused by HIV variants that are noncytocidal to T4 cells.
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PMID:Natural variants of human immunodeficiency virus from patients with neurological disorders do not kill T4+ cells. 325 41

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

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

Neurological complications in the acquired immunodeficiency syndrome (AIDS) are an important aspect of this new infectious disease and occur frequently. The existence of neurotropic variants of the human immunodeficiency virus (HIV), the causative agent of AIDS, is probable. Direct infection of the nervous system with HIV leads to a variety of HIV-induced neurological syndromes, the AIDS dementia complex being its most important representative. In addition, a large number of opportunistic infections and malignancies of the nervous system may complicate the disease. Major aspects of the clinical pictures, rational diagnostic approaches and treatment options of the most important sequels of HIV infection of the nervous system are discussed.
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PMID:Neurological complications in AIDS. 330 20

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


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