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

Eight of 13 children pre- or perinatally infected with the HIV virus subsequently developed neurological symptoms. Three children also had other nonspecific symptoms (fever, lymphadenopathy, diarrhoea, hepatosplenomegaly, failure to thrive and mucocutaneous thrush). Five children developed illnesses associated with AIDS (opportunistic infections, cachexia and lymphocytic interstitial pneumonia). The neurological abnormalities predominantly affected motor functions, only later also involving sensory ones. Motor, cognitive and language development was impaired in all eight children. A loss of developmental milestones occurred in three children with HIV encephalopathy: they have since died. In all the children the HIV infection caused symptoms within the first year, progressing more quickly in the three with encephalopathy. There were no discernible risk factors to account for the difference in the course of the disease.
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PMID:[Cerebral symptoms in pre- or perinatally HIV-infected children]. 768 71

HIV infection is associated with abnormalities of cytokine production. A number of cytokines (IL-1, IL-6, TNF-alpha, interferons-alpha and -gamma) are produced at an increased level in vivo, whereas the production of IL-2 is decreased. This latter abnormality certainly plays an important role in the immunodeficiency of AIDS patients. Monokines (IL-1, IL-6, TNF-alpha) stimulate HIV replication in vitro, whereas the interferons decrease it. Cytokine effects on the in vivo spreading of HIV remain however to be determined. Cytokines may also be mediators of the clinical manifestations of AIDS. IL-1, IL-6 and TNF-alpha may induce tissue lesions of opportunistic infections and HIV encephalopathy. Cytokines, and mainly IL-6, may stimulate the growth of malignant cells in Kaposi sarcomas and in lymphomas. A better knowledge of the roles of cytokines in HIV infection may allow new therapeutic approaches using either recombinant cytokines or specific antagonists, with the aim of inhibiting both HIV spreading and the clinical manifestations of the infection.
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PMID:[Cytokines and AIDS]. 768 34

To describe the clinico-pathological aspect of HIV/AIDS inpatients, we reviewed HIV/AIDS inpatients in our hospital since 1988. We evaluated risk factors, CD4 counts, CD4/8 ratio, cause of death and the survival time after diagnosis of AIDS. A total of 13 HIV sero-positive subjects were admitted to our hospital, including 11 cases (85%) with AIDS. One patient was a foreigner. All cases were male; age range 18-70 years. Hemophiliacs and sexually transmitted patients account for 62% and 38% of cases, respectively. There were no cases of intravenous drug users. In all cases with AIDS, CD4+ cells and CD4/8 ratio significantly decreased with median value of 73/microns and 0.18, respectively. Six cases (54%) were decreased and autopsy were done in four cases. Findings of autopsy revealed HIV encephalopathy and systemic various infection, including Pneumocystis carinii, cytomegalovirus, papilloma virus and pox virus. Cytomegalovirus infection was found in all cases; one had innumerable inclusion bodies in lung, adrenal gland and intestines. The median survival time after diagnosis of AIDS were 26 months.
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PMID:[Clinico-pathological aspect of HIV-sero positive inpatients]. 775 47

Complications of human immunodeficiency virus type 1 infection and acquired immunodeficiency syndrome may involve any level of the central or peripheral nervous system. Acute encephalitis, aseptic meningitis and acute demyelinating polyneuropathy may occur early in the course of HIV infection, while dementia, central nervous system-related cancer, opportunistic infections and autonomic neuropathy typically present later. Headache and mental status changes are common early manifestations of central nervous system involvement. Most severe headaches are related to an identifiable cause, including a mass lesion, opportunistic cerebral infection and medication side effect. Memory deficits, concentration difficulties and abnormalities on mental status testing may represent early AIDS dementia complex (HIV encephalopathy), the most common neurologic complication. In patients with AIDs, the differential diagnosis of cerebral mass lesions on computed tomography or magnetic resonance imaging includes cerebral toxoplasmosis, tuberculous or fungal abscess, focal viral encephalitis, metastatic resonance imaging includes cerebral toxoplasmosis, tuberculous or fungal abscess, focal viral encephalitis, metastatic Kaposi's sarcoma and primary CNS lymphoma. Peripheral neuromuscular disease, including distal symmetric polyneuropathy, autonomic neuropathy, and HIV and chronic zidovudine myopathy, affects 15 to 40 percent of all persons with HIV infection or AIDS.
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PMID:Common neurologic complications of HIV-1 infection and AIDS. 784 35

It may be postulated that the encephalopathy induced by the human immunodeficiency virus HIV-1, in particular, the characteristic "myelin pallor," may result from binding of the envelope glycoprotein gp120 to galactosylceramide and/or its metabolite sulfatide in the plasma membrane of oligodendrocytes, the myelin forming cells in the central nervous system. (1) gp120 has been reported to have a high affinity for these molecules in vitro. (2) The binding of antibodies to these molecules increases intracellular free calcium levels, which may be cytotoxic. (3) The binding of gp120 to the CD4 receptor in the immune system has the same effect. We have investigated the binding of gp120 to rat oligodendrocytes in vitro by indirect immunofluorescence and have monitored changes in intracellular free calcium with the calcium-sensitive dye INDO-1, in individual oligodendrocytes exposed to the glycoprotein. Antibodies against galatosylceramide and sulfatide bound to the cell membrane, but gp120 did not. The antibodies also increased intracellular free calcium levels in the oligodendrocytes, whereas gp120 did not. It, therefore, seems highly improbable that the demyelination observed during HIV encephalopathy is a direct cytotoxic effect of gp120 on oligodendrocytes.
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PMID:HIV-1 envelope glycoprotein gp120 does not bind to galactosylceramide-expressing rat oligodendrocytes. 785 83

Prior to the onset of immunodeficiency disease, neurochemical and neuropathological events associated with motor and/or cognitive impairment can be identified in rhesus monkeys infected with simian immunodeficiency virus (SIV). These are astrocytosis, up-regulation of mRNA encoding the neuropeptide somatostatin (SRIF) and an increased expression of MHC Class II antigen. End-stage immunodeficiency disease has been associated with robust viral expression in the CNS frequently observed as multinucleated giant cell formation. SIV encephalitis has not been observed in animals whose only clinical signs of SIV disease were motor and/or cognitive impairment. These data suggest that neuronal dysfunction discernable as altered neuropeptide expression in cortical neurons precedes frank structural damage to the CNS in SIV encephalopathy. This model is consistent with the mechanism of neuropathogenesis in human HIV encephalopathy that can be partially inferred from neurochemical and neuropathological examination of autopsy material in HIV disease.
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PMID:Neuronal substrates for SIV encephalopathy. 787 94

We measured levels of soluble intercellular adhesion molecule 1 (sICAM-1) in paired serum and CSF samples of 110 HIV-1-positive patients with and without neurological symptoms and 40 HIV-negative non-immune neurological controls, and in sera of 26 asymptomatic HIV-1-positive patients. Serum sICAM-1 levels in asymptomatic HIV-1-positive patients were significantly increased in comparison to HIV-negative controls. Moreover, they were significantly higher in HIV-1-positive patients with AIDS-defining diseases than in the asymptomatic HIV-1-positive group. In subgroups of patients with neurological disease, the highest serum values were found in HIV encephalopathy. CSF levels of sICAM-1 were elevated only in HIV-1-positive patients with neurological disease mainly due to passive diffusion through a defective blood-brain barrier. An sICAM-1 index was calculated as a measure for intrathecal production of sICAM-1 but showed no significant differences between patients with and without neurological involvement. However, increased levels of the sICAM-1 index were found in some patients with opportunistic CNS infection of bacterial or fungal origin. Serum and CSF levels of sICAM-1 correlated with neopterin levels, a marker of interferon-gamma-mediated macrophage activation and CSF sICAM-1 levels were inversely correlated to numbers of CD4+ T cells. Elevated serum sICAM-1 levels already in asymptomatic HIV-1-positive individuals add to the evidence for an early immune activation in HIV infection. With the further increase of serum and CSF s-ICAM-1 in patients with AIDS-defining diseases sICAM-1 could serve as a new surrogate marker similar to neopterin.
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PMID:Serum and cerebrospinal fluid levels of soluble intercellular adhesion molecule 1 (sICAM-1) in patients with HIV-1 associated neurological diseases. 791 74

In order to review the clinical course, laboratory findings, and outcome of children with vertically acquired HIV infection and Pneumocystis carinii pneumonia, questionnaires were sent to paediatricians in the British Isles who had reported P carinii pneumonia and HIV infection through the British Paediatric Surveillance Unit (BPSU). Paediatric reports from the BPSU are linked to reports of pregnancies in HIV positive women and laboratory reports. P carinii pneumonia was the most frequently reported AIDS indicator disease at AIDS diagnosis, occurring in 22/56 (40%) children born in the British Isles; in a further two children P carinii pneumonia occurred after another AIDS indicator disease. The median age at P carinii pneumonia diagnosis was 4.1 (1.4-27.3) months and in 48% it occurred with other AIDS indicator diseases. Despite intensive treatment the three month survival was only 38%. The nine children surviving P carinii pneumonia subsequently developed further AIDS indicator diseases, in particular HIV encephalopathy and four have since died. P carinii pneumonia was present at AIDS diagnosis in 65% of children developing AIDS in the first year of life and caused 82% of infant deaths. Most children were not known to be at risk of HIV until they presented with P carinii pneumonia. Children with HIV infection develop P carinii pneumonia at an early age and have a poor outcome. Increased awareness of the condition is required to initiate early treatment. Prevention may be a compelling incentive for screening in pregnancy, but further study is required to quantify the risks and benefits of initiating early P carinii pneumonia prophylaxis as well as the impact this might have on life expectancy.
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PMID:Pneumocystis carinii pneumonia in vertically acquired HIV infection in the British Isles. 813 71

In previous studies, using polymerase chain reaction amplification of HIV-1 genes directly from pathologic tissues of children who died with AIDS encephalopathy, we showed that the reading frame of the HIV-1 regulatory nef gene is open, suggesting that the nef protein was expressed. We now show, using immunocytochemistry and in situ hybridization with nef-specific probes in postmortem pediatric CNS tissues, that nef mRNA and protein are present in up to 20% of astrocytes in tissue sections selected for extensive histopathology. By contrast, HIV-1 structural proteins such as gag and their coding mRNAs are present in multinucleated giant cells that harbor productive infection and are the hallmark of HIV-1 infection in the CNS. These findings are consistent with the nonproductive infection of glial cells observed in vitro, and imply that HIV-1 infection of astrocytes is restricted to early regulatory gene products, of which nef is the best target as it is expressed at high levels and is membrane-anchored. In developing central nervous tissues of children, restricted and latent HIV-1 infection of astrocytes may be extensive and contribute significantly to HIV-1 neuropathogenesis.
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PMID:Overexpression of nef as a marker for restricted HIV-1 infection of astrocytes in postmortem pediatric central nervous tissues. 814 18

The growing incidence of AIDS in children and newborns has been related to increasing incidence of AIDS in women. Case records were composed by 14 children with death occurring at different ages--from 1 hour to 12 years--and 1 female fetus, all with serological confirmation of AIDS. Brain and internal organs samples were collected at autopsy for morphological, immunohistochemical and "in situ" hybridization's technical examination. The prevailing extracerebral pathology observed at autopsy consisted of opportunistic infections. The cerebral findings were HIV-encephalopathy; cytomegalovirus encephalitis; vascular alterations such as necrosis and hemorrhage; calcifications and edema. Neurologic symptoms were reported in 3 children of intravenous drug-abuser mothers as drug withdrawal syndrome. HIV positivity in one or both the intravenous drug-abuser parents is the main risk factor of congenital AIDS. This factor means lack of care during the gestational stage and may determine relevant differences in the course of disease. The cerebral changes due to opportunistic infection must be differentiated from HIV-specific lesions; it has to be stressed that "diffuse" leukoencephalopathy is not AIDS-specific but can be found in every chronic encephalitis/encephalopathy especially in newborns and children. Chronologically, HIV encephalopathy appears as late manifestation of the disease, due to an infiltration of CNS of HIV-infected macrophages and not to an impairment of neuronal or glial cells infected by HIV in the early stages of the disease.
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PMID:Autoptic findings in HIV-1 positive children. 815 6


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