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Query: UMLS:C0019693 (HIV)
 170,526 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It is well documented that human immunodeficiency virus (HIV) can infect the central nervous system. Neurological dysfunction occurs frequently in acquired immunodeficiency syndrome (AIDS) and most commonly in the form of a subacute HIV-encephalitis. The pathological abnormalities in patients with subacute HIV-encephalitis are most prominent in subcortical structures, notably in the cerebral white and deep gray matter. The patients frequently develop abnormalities in cognitive, motor and behavioral functions. The infected cells are predominant lymphocytes and macrophages. The production of cytokines by these cells appears to be a central factor in the pathogenesis of subacute HIV-encephalitis. The central nervous system can function as a reservoir of HIV infection. Neuropsychological assessment is a sensitive method for documentation of early brain involvement by HIV infection. The HIV-associated neurological abnormalities may be partially ameliorated by administration of zidovudine (AZT).
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PMID:[HIV and the central nervous system]. 277 97

HIV associated subacute, micronodular encephalitis and lymphadenopathy were compared with regard to demonstrable HIV antigens and characterization of HIV antigen expressing cells. In the brain, both gag- and env-coded antigens were confined to cells of micronodular lesions with immunophenotype of monocyte/macrophages (KiM6+, 9.4+, CD4+/-). The micronodular lesions were also infiltrated by some lymphoid cells, predominantly CD8+. In lymphadenopathic nodes, gag-encoded antigens were demonstrable almost exclusively in follicles/germinal centres in association with follicular dendritic cells, whereas env-antigens usually were not found. Follicular involution was related to destruction of follicular dendritic cells and infiltration of CD8+ lymphocytes within the germinal centres. During follicular involution, HIV-gag antigens diminished in parallel with destruction of the network of dendritic reticulum cells. These findings indicate important tissue related differences in HIV expression. In addition, a possible participation of CD8+ cells in the pathogenesis of HIV induced tissue lesions is suggested.
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PMID:HIV encephalopathy and lymphadenopathy: cells associated with viral antigens. 278 27

We assessed the capacity of cerebrospinal fluids (CSF) and sera from human immunodeficiency virus (HIV)-seropositive patients to neutralize HIV and to mediate specific antibody-dependent lysis of HIV-infected target cells. A local HIV-specific intrathecal antibody synthesis was found in all stages of HIV infection regardless of neurological manifestations. Virus-neutralizing antibodies could not be detected in the CSF of patients with primary encephalitis or polyneuropathy. Cytotoxic antibodies mediating HIV-specific antibody-dependent cellular cytotoxicity (ADCC) were demonstrable in the CSF of most patients without evidence of central nervous system (CNS) involvement, but only in 43% of cases with HIV encephalitis. In some cases, the exclusive detection of ADCC activity in either the CSF or serum compartment suggested the presence of non-identical target antigens in the CSF and serum of the same patient. Further studies are needed to clarify the significance of these findings for the manifestation of CNS involvement in HIV infection.
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PMID:Human immunodeficiency virus (HIV)-specific antibodies, neutralizing activity and antibody-dependent cellular cytotoxicity (ADCC) in the cerebrospinal fluid of HIV-infected patients. 280 87

The nervous system may be affected at any stage in the course of HIV-1 infection. Acute or subacute inflammatory demyelinating polyradiculoneuropathies occur often early and improve spontaneously. Distal symmetrical axonal, predominantly sensory, painful polyneuropathies occur in the late stages of the disease. Microvasculitis is frequent in the early neuropathies. Spastic and ataxic paraparesis associated with vacuolar myelopathy are rare and probably not related only to HIV-1. Aseptic lymphocytic meningitis may occur as the presenting or sole manifestation of HIV-1 infection. The more frequent subacute encephalitis, probably directly related to HIV-1, is late in the course of the disease. Microscopic changes are suggestive but non-specific (microglial nodules, multinucleated giant cells). According to some authors, HIV-1 infection of the central nervous system macrophages may be early and latent until associated pathologies (opportunistic infections, lymphoma) trigger the replication of HIV-1 by infected macrophages.
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PMID:[Neuropathology of human type 1 immunodeficiency virus infection]. 284 99

HIV-infected patients are at markedly increased risk for neurological dysfunction, which may occur at any level of the neuraxis (see Table 1). The most common syndromes--AIDS dementia complex, vacuolar myelopathy, and possibly distal symmetric peripheral neuropathy--appear to be related to HIV infection within the nervous system, rather than due to the immunoincompetence caused by HIV. However, the mechanism(s) by which HIV causes these syndromes, e.g., infecting neurons or oligodendroglia directly, interfering with neurotrophic factors, effecting toxic monokine production, etc., is unknown. Early, albeit incomplete, success with azidothymidine is encouraging. Less commonly, neurological syndromes may be secondary to the immunoincompetence produced by HIV. Many different etiologies--most of which are treatable--have been encountered, but a few of these (cerebral toxoplasmosis, cryptococcal meningitis, primary CNS lymphoma, and progressive multifocal leukoencephalopathy) are responsible for most of the opportunistic complications. Marked differences in symptoms and signs between AIDS patients and immunologically normal patients may complicate recognition of some of these diseases (e.g., herpes simplex encephalitis). Finally, some HIV-associated syndromes, e.g., inflammatory demyelinating polyradiculoneuropathy and retinal microvasculopathy, are of unknown etiology.
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PMID:The neurology of human immunodeficiency virus infection. 285 54

Of subjects with asymptomatic HIV infection or Lymphoadenopathy Syndrome, 185 were studied by means of electroencephalography coupled with computerized spectral analysis and mapping (EEG-CSA). Abnormal EEGs were found in 30 of 118 (25.4%) patients with asymptomatic infection (CDC Group II) and in 20 of 67 (29.9%) patients with Lymphoadenopathy Syndrome (CDC Group III). The most common EEG abnormalities were represented by theta slowing on the frontal and fronto-temporal lobes and, in some cases, by delta slowing and paroxysmal sharp activity on the forebrain. Among 50 patients with abnormal EEGs, 16 showed some abnormalities on neuropsychological testing, whereas mild signs of cerebral atrophy were evident on CT scan in only 12 patients. These findings suggest that EEG-CSA could be a useful and sensitive method in the early detection and monitoring of HIV-related subacute encephalitis.
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PMID:Electroencephalography in the early diagnosis of HIV-related subacute encephalitis: analysis of 185 patients. 292 23

Reported in this paper are postmortem findings recorded from the central nervous system of 51 HIV carriers, among them 43 with clinically manifest AIDS. Opportunistic infections and tumours were established in 24 cases, including toxoplasmosis, cytomegaly, progressive multifocal leucoencephalopathy, and lymphomas. Findings obtained from 5 patients were restricted to unspecific alterations. No pathological findings at all were recordable from 8 HIV carriers without AIDS. So-called subacute microglial encephalitis (SME) was detected in 26 cases. SME was found to provide for the morphological substrate of genuine HIV encephalopathy. It was characterised by occurrence of mononuclear and even multinucleated cells which were macrophages and obviously served as virus carriers. Multinucleated cells are pathognomonic of HIV encephalopathy. No unambiguous evidence has so far been produced to primary invasion of neurons or glial cells by HI viruses.
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PMID:[The morphology of HIV encephalopathy]. 292 83

Primary manifestations of HIV infection may present as a mononucleosis-like syndrome. Cases have also been reported where it presents with symptoms of encephalitis, meningitis or acute polyneuropathy. When no cause is found for such clinical symptoms, they should suggest the possibility of primary HIV infection even in a patient who is not at risk. HIV antibody will appear in the following weeks and serum studies should be done within the three months that follow. The patient should then be warned that he is contagious. Short term prognostic is usually good. But long term progosis remains uncertain.
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PMID:[Acute symptomatology in HIV virus primo-infection. 2 cases]. 295 Apr 84

Dysfunction of the central nervous system (CNS) is a prominent feature of the acquired immune deficiency syndrome (AIDS). Many of these patients have a subacute encephalitis consistent with a viral infection of the CNS. We studied the brains of 12 AIDS patients using in situ hybridization to identify human immunodeficiency virus [HIV, referred to by others as human T-cell lymphotropic virus type III (HTLV-III), lymphadenopathy-associated virus (LAV), AIDS-associated retrovirus (ARV)] nucleic acid sequences and immunocytochemistry to identify viral and cellular proteins. Nine patients had significant HIV infection in the CNS. In all examined brains, the white matter was more severely involved than the grey matter. In most cases the infection was restricted to capillary endothelial cells, mononuclear inflammatory cells, and giant cells. In a single case with severe CNS involvement, a low-level infection was seen in some astrocytes and neurons. These results suggest that CNS dysfunction is due to indirect effects rather than neuronal or glial infection.
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PMID:Cellular localization of human immunodeficiency virus infection within the brains of acquired immune deficiency syndrome patients. 301 55

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


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