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Query: UMLS:C0085584 (encephalopathy)
 18,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Adherent human embryo brain cells have been infected with HIV. Cells replicating HIV were maintained in culture for seven sequential passes over 7 months and continued to produce HIV during that time. Human embryo brain cells displayed glial-cell morphology and expressed glial fibrillary acidic protein. Electron microscopy showed clusters of virus particles around these cells as well as budding virus. Extracted, infected glial cells revealed bands for three major gag proteins, p18, p24 and p55, in Western blotting. It was not possible to detect CD4 antigen on the surface of these cells by indirect immunofluorescence or alkaline phosphatase staining with CD4 monoclonal antibodies. The results of these experiments indicate that HIV replicates in non-malignant brain cells. This observation strengthens the postulated aetiological link between HIV and the encephalopathy, dementia and other neurological symptoms observed in HIV-infected patients.
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PMID:HIV replicates in cultured human brain cells. 312 70

Evaluation of HIV disease status includes physical examination (anthropomorphic measurements, neurological assessment, etc.) and laboratory examination. Consideration should be given to changes from baseline values, age adjusted normal values and the rapidity of changes. Here we compare results of neuroophthalmologic assessment with Western Blo (WB) profiles in cerebrospinal fluids (CSF) of 54 children with AIDS. Children were classified by Denver Developmental Screening Test (DDST) administration in encephalopathy positive (n = 44) and encephalopathy negative (n = 10) groups. Neuroophthalmological examination which included nine items with good test-retest reliability showed that two of them (nystagmus on following and visual memory impairment) appeared early in the encephalopathy free group and correlated with the loss of some gag band in Western Blot (lower gag score). No correlation was however, found with respect to p24 antigen level in cerebrospinal fluid, a marker which reflects CNS viral load.
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PMID:Neuroophthalmological examination in children with AIDS. 782 69

Since the pathogenesis of SIVmac disease complex is thought to be explained by the tropism of the infecting virus for either CD4+ T-lymphocytes or macrophages or both types of cells, we compared the infection in primary macaque macrophages with molecularly cloned, lymphocyte-tropic SIVmac239 and a cloned, macrophage-tropic chimeric virus (SIVmac239/17E) whose env gene was derived from brain of a macaque (17E) dying from SIV-induced encephalopathy. SIVmac239/17E caused a productive, syncytial cytopathic infection accompanied by accumulation of virus particles within cytoplasmic vesicles of the macrophages. Pulse-chase and immune precipitation studies showed that both the viral glycoprotein precursor (gp160) and the gag precursor (p57) were cleaved into gp120 and p27, respectively, and both were released into the culture medium of infected cells, although most of the p27 remained cell associated. SIVmac239 also infected macrophages, but in comparison to SIVmac239/17E, minimal virus replication occurred. Immunocytostaining revealed that while occasional syncytia were observed in cultures, the majority of the infected cells were not associated with syncytium formation. Ultrastructural studies did not reveal the accumulation of virions within infected macrophages. Pulse-chase studies showed that both gp160 and p57 were produced but were cleaved inefficiently and only minimal amounts of gp120 and p27 were released into the culture medium, even after prolonged incubation times. The processing of proteins of the two viruses was indistinguishable in lymphocytes. Since these two viruses are identical except for changes within the env gene, these results indicate that efficient assembly and release of SIV from blood-derived macrophages is mediated by changes in the envelope glycoprotein.
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PMID:The proteins of lymphocyte- and macrophage-tropic strains of simian immunodeficiency virus are processed differently in macrophages. 783 8

Immunological and viral studies were conducted on cerebrospinal fluid from 31 HIV-1-infected children, of whom 23 were neurologically asymptomatic and 8 had progressive encephalopathy. After AZT treatment, a second cerebrospinal fluid specimen was obtained from 15 children, 11 of whom were neurologically asymptomatic and 4 had progressive encephalopathy. Virus isolation and p24Ag detection were more frequent in children with progressive encephalopathy than in asymptomatic children (66% versus 12%) and were inversely correlated with intrathecal HIV-1-antibody detection (anti-gag AB: 25% versus 70%). High concentrations of interleukin-1 beta (IL-1 beta) and IL-6 were found in children with progressive encephalopathy (50% and 37%, respectively), but low levels were also detected in some asymptomatic children (13% and 9%, respectively). Tumour necrosis factor-alpha (TNF alpha) was not found. AZT treatment induced disappearance of p24Ag in cerebrospinal fluid, as well as a marked reduction in cytokine levels. Cytokine determination may be useful in monitoring AZT treatment in children with progressive encephalopathy.
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PMID:Cerebrospinal fluid analysis in HIV-1-infected children: immunological and virological findings before and after AZT therapy. 784 99

We have isolated a new foamy virus from blood samples taken from two apparently healthy orangutans (Pongo pygmaeus). The older orangutan has since died with encephalopathy after a brief acute illness, while the younger one, his grandson, remains well. These animals and 12 other orangutans had specific antibodies to foamy virus as measured by immunofluorescence. The new foamy virus and the antisera showed strong and specific neutralization, with only weak cross-reaction with other simian foamy virus strains. Southern blotting with gag and env probes of human foamy virus and PCR amplification showed that the new foamy virus, designated SFV-11, is related to, yet distinct from, previously characterized strains from humans, chimpanzees, and monkeys.
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PMID:Isolation of a new foamy retrovirus from orangutans. 793 94

Human foamy virus (HFV) is a retrovirus encoding structural genes and, like human immunodeficiency virus and human T cell leukemia virus I, several ancillary reading frames collectively termed the be1 genes. We have previously shown that HFV transgenic mice develop an encephalopathy with neuronal loss in hippocampus and cerebral cortex. We have now raised and characterized rabbit antisera to various recombinant portions of gag, pol, env, and bel-1, the viral trans-activator. Immunoreactivity for gag and bel-1 was observed in nuclei and processes of hippocampal and cortical neurons before the onset of morphological lesions and correlated with the appearance of HFV mRNA. Astrocyte-derived multinucleated giant cells containing HFV proteins were present in the brain of transgenic mice coexpressing full-length HFV genes but not in mice expressing truncated gag and env, suggesting that these genes contain a fusogenic domain. Expression of full-length structural genes decreased the life expectancy of transgenic mice, implying an adjuvant role for these proteins in HFV-induced brain damage.
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PMID:Human foamy virus proteins accumulate in neurons and induce multinucleated giant cells in the brain of transgenic mice. 838 40

The family of foamy viruses designates a group of retroviruses which share a specific morphology and provoke characteristic cytopathic effects in cultured cells. Like HTLV and HIV, foamy viruses are complex viruses encoding a number of ancillary genes in addition to gag, pol and env, including a transcriptional transactivator. Foamy viruses are endemic in various primate species, and human foamy viruses (HFV) have been isolated from patients with various neoplastic and degenerative diseases. Despite a growing body of knowledge on the biology of foamy viruses, it has not yet been possible to identify a disease specifically caused by foamy virus infection. After reviewing the epidemiology and molecular biology of the various animal foamy viruses, this article focuses on the pathogenic properties of HFV in transgenic mouse systems. HFV transgenes exhibit a striking neurotropism and elicit a progressive degenerative disease of the central nervous system and striated muscle. Similarly to patients with HIV-associated encephalopathy, HFV transgenic mice develop accumulations of syncytial giant cells in their brains. The relevance of these findings for human neuropathology is discussed.
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PMID:The foamy virus family: molecular biology, epidemiology and neuropathology. 838

We analyzed brain tissue from 39 patients for the presence of proviral HIV-1 sequences, using the polymerase chain reaction (PCR) for the amplification of segments of the viral LTR and gag genes. A novel primer extension procedure allowed the detection of a single HIV-1 copy in 1 micrograms DNA. We detected proviral HIV-1 DNA in 16 of 25 brain samples from AIDS patients. Semiquantitative evaluation of the amplified DNAs indicated considerable variation in viral load. Highest levels of proviral DNA were present in brain samples from six patients with clinical evidence of HIV-associated cognitive/motor complex and the histopathologic correlate of HIV leukoencephalopathy or HIV encephalitis. An additional 11 brain samples contained smaller amounts of proviral DNA. In these patients, clinical data were inconclusive regarding the diagnosis of HIV-1 encephalopathy and histopathologically there was no evidence of HIV-1-induced tissue lesions. In nine of 25 seropositive patients with AIDS (36%), brain samples scored negative or did not contain an unequivocal signal indicating the presence of proviral DNA. HIV-1 sequences were not detected in any of 14 control brain samples from HIV-1 seronegative patients. Our data indicate that HIV-1 is present in the central nervous system of the majority (two thirds) of AIDS patients and that the highest levels of proviral DNA in brain tissue are associated with HIV encephalopathy.
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PMID:PCR identification of HIV-1 DNA sequences in brain tissue of patients with AIDS encephalopathy. 841 37

Human immunodeficiency virus type 1 (HIV-1) infection of astrocytes has been demonstrated in the brains of patients with AIDS dementia complex (ADC) and may play an important role in neuropathological pathways of HIV-related encephalopathy. SIVmac-infected monkeys develop an acquired immunodeficiency syndrome (AIDS) with CNS involvement which is quite similar to that seen in human AIDS. We investigated the in vitro infection of primary astrocytes derived from adult macaques with SIVmac251 or an isogenic virus that expresses a non-functional Nef protein (SIVmac251-DeltaNef). In both cases we observed that viral expression was mostly limited to early regulatory genes after a transient phase of late viral gene expression (i.e. env and gag), as reported for HIV-1-infected astrocytes in vivo. Late viral gene expression could be reactivated by TNF-alpha, GM-CSF and IFN-gamma treatment of SIVmac251-infected astrocytes but not by similarly treated SIVmac251-DeltaNef-infected cells. Our findings suggest that Nef is not involved in the restricted expression of SIV in astrocytes, but may be important for astrocytes to function as a viral reservoir in the CNS. In additional experiments, we demonstrated Rev and Nef expression in 17 of 27 primary astrocyte cultures derived from macaques infected by SIVmac251. Nef was located in the cytoplasm of astrocytes infected by SIVmac251 in vivo, but displayed perinuclear localisation after infection in vitro. Attempts to activate late viral gene expression by astrocytes infected in vivo using cytokines or by coculture with human cord blood mononuclear cells were unsuccessful.
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PMID:Simian immunodeficiency virus mac251 infection of astrocytes. 1087 8

In order to obtain information on neurologic AIDS, 54 white caucasian children infected by nosocomial route with a median age of 46.2 +/- 7 months were followed up prospectively for a median of 12 months with three months Denver tests neurologic evaluation and six months serologic investigations in CSF and sera. Paired CSF and serum samples, collected on the same day, from children with AIDS encephalopathy, were analysed for the permeability of the blood brain barrier (BBB) and for intrathecal production of anti HIV specific antibodies. A prospective follow-up and repeated comparison of WB profiles and the presence of anti V3 antibodies in CSF and sera was done, as well as an evaluation of the modification in the CSF antibody specificity (anti gag Western Blot scoring) with disease progression. An increased intrathecal synthesis of IgG was recorded in all subjects, in spite of an unaltered BBB permeability. No significant differences were recorded for the anti gag score in the serum samples, which was stable between 9.1-10.4. By contrast, the score for CSF samples decreases significantly with disease progression, from 8.7 in children without encephalopathy, to 6.5 in those with stationary disease and 3.6 in the progressive encephalopathy group. A strong correlation was found between the level of anti p24 antibodies determined by ELISA and the anti gag score quantified by WB for the same CSF samples. The p24 antigen was found to be positive only in 3 cases, even after immune complex dissociation. Anti V3 antibodies were not detected in CSF samples from patients with functional BBB. The decline in anti-gag antibody reactivity in CSF is an early indicator of disease progression, reflecting a severe course of neurological impairments. The absence of anti V3 antibodies in the CSF samples suggests that the PND of neurotropic strains mapped in distinct positions into the V3 loop. These results reflect the selection of antigenic escape mutants which evolve in the CNS, distinct from the blood lymphotropic isolates.
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PMID:Cerebrospinal fluid western Blot profiles in the evolution of HIV-1 pediatric encephalopathy. 1089 27


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