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

Central Nervous System (CNS) involvement, whether primary by the Human Immunodeficiency Virus--HIV--itself, or secondary (toxoplasmosis or lymphoma) is remarkably frequent in AIDS, in 40 to 70% of cases, depending upon the author. In order to study the natural history of this illness, a cohort of 25 asymptomatic seropositive patients have been established. Every 6 months these patients undergo biological and clinical examinations, as well as Magnetic Resonance brain scans. After two examinations at a 6 month's interval, the first results are reported. Out of these 25 cases, 9 present anomalies: One patient with diffuse cerebral atrophy and 8 others with high signal intensity areas on T2 weighted sequences, like those of the Multiple Sclerosis. No relationship could be demonstrated between the existence of these lesions and various criteria such as age, sex, risk factors and T4 cells count. The nature of these lesions is not clear. They certainly indicate early involvement of the CNS after primary infection by the HIV virus. They may either represent scars of the primary infection or early alterations announcing developing encephalopathy.
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PMID:[Magnetic resonance imaging: early detection of involvement of the central nervous system in acquired immunodeficiency syndrome]. 314 38

This case report is about an eleven year old boy with new developed symptoms of a cellular immundeficiency and a positive HIV-serology 33 months after a CNS-leukemia relapse. After 18 weeks a progredient neurological symptomatology is beginning with motor, cognitive and behavioral disturbances and a brain atrophy in the CT-scan. These cerebral manifestations are explainable as an encephalopathy both through HIV and after CNS-leukemia. A SSPE has been excluded. CT, EEG, Evoked Potentials do not show differential diagnostic pathognomonic findings regarding both diseases. The CSF findings hint at a persistent virus infection compatibel with the postulated slow virus pathogenesis of the AIDS-Encephalopathy. We conclude, that in this case an etiological diagnoses is only possible through histological brain examination and through demonstration of HIV or HIV-antigen in brain tissue respectively. AZT, which is reported to be effective against the cerebral AIDS-manifestations could not be applicated because of the existing pancytopenia.
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PMID:[AIDS encephalopathy in childhood or the late sequela of central nervous system leukemia?]. 316 63

To produce concentrations of zidovudine (AZT) in plasma and cerebrospinal fluid that would provide constant inhibition of the replication of human immunodeficiency virus (HIV), we gave AZT by continuous intravenous infusion to 21 children ranging in age from 14 months to 12 years who had acquired HIV infection through transfusions or perinatally. All patients were symptomatic before AZT treatment (Class P2 of the Centers for Disease Control); 13 (62 percent) had evidence of neurodevelopmental abnormalities. The mean CD4/CD8 ratio was 0.18; 11 patients had CD4 counts below 0.2 x 10(9) per liter. We administered AZT at four dose levels: 0.5, 0.9, 1.4, and 1.8 mg per kilogram of body weight per hour. The plasma drug concentrations achieved at the respective dose levels were 1.9 +/- 0.3, 2.8 +/- 1.4, 3.1 +/- 1.1, and 4.5 +/- 1.0 microM. The steady-state cerebrospinal fluid:plasma ratio was 0.24 +/- 0.07. The only evidence of toxicity was bone marrow suppression. Transfusion was required in 14 patients because of low levels of hemoglobin (5 mmol per liter [less than 8 g per deciliter]). Dose-limiting neutropenia (less than 0.5 x 10(9) polymorphonuclear leukocytes per cubic millimeter) occurred in most patients who received doses of 1.4 mg per kilogram per hour or more. Improvement in neurodevelopmental abnormalities occurred in all 13 children who had presented with encephalopathy before treatment. Serial measurements of IQ before therapy and after three and six months of continuous therapy with AZT showed that IQ scores, including those for verbal and performance IQ, rose in these 13 patients and in 5 other children who had no detectable evidence of encephalopathy before treatment. Most patients also had increased appetite and weight, decreased lymphadenopathy and hepatosplenomegaly, decreased immunoglobulin levels, and increased numbers of CD4 cells. In some patients the improvement in the features of encephalopathy occurred despite the absence of immunologic improvement. We conclude that AZT is beneficial in children with symptomatic HIV infection, especially those with encephalopathy (which may be subclinical), and that the optimal continuous intravenous dose of AZT in children is between 0.9 and 1.4 mg per kilogram per hour.
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PMID:Effect of continuous intravenous infusion of zidovudine (AZT) in children with symptomatic HIV infection. 263 49

The autopsied brains of three homosexual men with acquired immune deficiency syndrome (AIDS), progressive encephalopathy and widespread multinucleated giant cell encephalitis were investigated by lectin and immunohistochemical methods to ascertain the cellular distribution of a human immunodeficiency virus (HIV) core protein, p25. Abundant viral antigen was present in all brains, limited to perivascular macrophages, microglial and multinucleated cells, some bearing elongated cytoplasmic processes. The multinucleated cells were consistently labelled by the lectin Ricinus communis agglutinin-1, a marker for microglia, which demonstrated process-bearing variants of these cells. The prominent staining of microglia for viral antigen and the morphological suggestion that they fuse with other microglia and/or macrophages to form the multinucleated cells characteristic of HIV encephalitis indicate that microglia are probably direct targets of HIV infection and serve to propagate and amplify this retroviral encephalitis.
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PMID:Microglia in the giant cell encephalitis of acquired immune deficiency syndrome: proliferation, infection and fusion. 317 3

A progressive encephalopathy occurs in 30 to 50% of infants and children infected with the human immunodeficiency virus (HIV). The expression of HIV antigen in the cerebrospinal fluid appears to correlate with the clinical occurrence of progressive encephalopathy. The signs of progressive encephalopathy in children with HIV infection, including loss of developmental milestones, impaired brain growth, and progressive motor dysfunction, indicate a poor prognosis and almost invariably a fatal outcome. Neuropathological findings in these children, including virus-laden macrophages and multinucleated giant cells are unique to this condition. Opportunistic or reactivated latent infections and neoplasms of brain occur in children with HIV infection but are uncommon. These findings support the hypothesis that the progressive encephalopathy observed in HIV-infected children is caused by primary infection of the brain with this virus. Epidemiological data predict increasing numbers of HIV-infected women and children. Research aimed at an understanding of the mechanism(s) of mother-to-infant transmission of HIV infection is urgently needed so that strategies for the prevention and treatment of such infection in children may be planned.
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PMID:Neurological and neuropathological features of human immunodeficiency virus infection in children. 327 2

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

AIDS, presumably caused by the human retrovirus, human immunodeficiency virus (HIV), is a disease with multiple pathologies, most of which are the consequence of a profound immunodeficiency. The first two sections of this review focus primarily on the normal development and function of the cells of the immune system and the known abnormalities that occur in this system in AIDS patients. Very little is known of the pathogenesis, in humans, of the four major clinical manifestations of AIDS--immunodeficiency, encephalopathy, Kaposi's sarcoma, and lymphoma. Because most pathologic studies derive from autopsy findings in terminal AIDS patients, it has been difficult to track the course of HIV infection from the time of initial contact with the virus through the evolution of the disease. Therefore, the final section of this review focuses on actual and potential animal models of AIDS and how such models might be valuable for studies on the pathogenesis of the disease, the development of relevant vaccines, and the testing of potential therapies.
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PMID:Approaches to an understanding of pathogenetic mechanisms in AIDS. 328 66

In an attempt to determine factors of predictive value in HIV (human immuno-deficiency virus) seropositive patients, particular attention was payed to symptoms indicating early involvement of the central nervous system (CNS). A cohort of healthy carriers was thus constituted. Follow-up will be carried out every six month including clinical, biological as well as CNS imaging by NMR. Among the first 15 of them, abnormalities could be observed in 4 individuals. Lesions consisted in nodules of high signal in T2 which were localized either in the white matter or thalamic nuclei. No relationship could be demonstrated between the existence of these lesions and various criteria such as age, sex, risk factors and T4 cells count. Such lesions appeared similar to the localizations observed in multiple sclerosis or to the scars of limited vascular accidents. The nature of these lesions is not clear. They certainly indicate early involvement of CNS after primary infection by the HIV virus. They may either represent sequellae of this primary infection or early alterations announcing developing encephalopathy.
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PMID:[Cerebral MRI in the study of prognostic factors in AIDS. Hypotheses from tests on 15 patients]. 339 92

In addition to central nervous system (CNS) opportunistic infections and neoplasms, patients with acquired immunodeficiency syndrome (AIDS) develop unexplained dementia and encephalopathy and degeneration of the white matter. We studied autopsied brains from 20 adult patients who expired from AIDS to determine the relationship of human immunodeficiency virus (HIV) infection to white matter lesions and to clinical findings. In four patients with dementia/encephalopathy and abnormalities of the white matter, there was evidence of HIV infection as shown by in situ hybridization. In contrast, the remaining 16 patients who had no evidence of white matter degeneration revealed no hybridization to the HIV probe. The cells infected with HIV included endothelial cells, perivascular macrophages/monocytes, and multinucleated giant cells and were found in or adjacent to white matter degeneration. These results demonstrate a correlation between HIV-infected cells and AIDS leukoencephalopathy and provide further evidence for HIV-related dementia/encephalopathy.
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PMID:Human immunodeficiency virus (HIV) infection in brains with AIDS-related leukoencephalopathy. 344 27

The retrovirus that causes acquired immune deficiency syndrome (AIDS) is now designated the human immunodeficiency virus (HIV). The cerebrospinal fluid (CSF) of 27 children with HIV infection was assayed for intra-blood-brain barrier (IBBB) synthesis of HIV-specific antibodies and for the presence of HIV antigen. In this cohort, 11 children had a progressive encephalopathy (PE), 9 had a static encephalopathy (SE), and 7 had normal neurological findings (N). IBBB synthesis of HIV-specific antibodies was identified (using matched serum and CSF specimens) in 7 of 11 children with PE, 4 of 9 children with SE, and 2 of 7 children with N. HIV antigen was found (using a highly sensitive solid-phase enzyme immunoassay) in the CSF of 8 of 11 children with PE, none of the children with SE, and none of the 7 children with N. On the basis of these data, we conclude that: IBBB synthesis of HIV antibodies indicates invasion of the central nervous system but may reflect prior or current infection; and HIV antigen in CSF indicates viral expression and correlates with the occurrence of PE. These findings strongly implicate HIV as the causative agent of PE in these children. The assay for HIV antigen in the CSF may be of value in determining the prognosis of children with HIV infection and for evaluating the efficacy of therapeutic agents against this retrovirus.
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PMID:Expression of human immunodeficiency virus in cerebrospinal fluid of children with progressive encephalopathy. 347 86


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