Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0085584 (encephalopathy)
 18,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
 ...
PMID:The proteins of lymphocyte- and macrophage-tropic strains of simian immunodeficiency virus are processed differently in macrophages. 783 8

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.
 ...
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.
 ...
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.
 ...
PMID:The foamy virus family: molecular biology, epidemiology and neuropathology. 838

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.
 ...
PMID:Simian immunodeficiency virus mac251 infection of astrocytes. 1087 8

Xenotropic murine leukemia virus-related virus (XMRV) has been considered a possible trigger of myalgic encephalomyelitis/ chronic fatigue syndrome (ME/CFS) and could also be linked with unspecified encephalopathy. The aim of this study was to analyse the frequency of XMRV proviral sequences in peripheral blood leukocyte (PBL) DNA from 150 patients with ME/CFS and 30 apparently healthy individuals, as well as in PBL and brain tissue DNA from 61 individuals with/without unspecified encephalopathy. Targeting the XMRV proviral gag gene sequence by nested polymerase chain reaction (nPCR) with previously reported primer sets, provirus was not detected either in DNA from patients with ME/CFS and individuals with unspecified encephalopathy, or in apparently healthy individuals. Only the positive control gave the amplimer of 410 base pairs (bp) after the second round that corresponds to the expected XMRV gag gene fragment. In addition, DNA was found to be negative in nPCR assays, targeting XMRV specific env gene sequence, using previously described primer sets. Also only positive control gave the amplimer of 218 bp after the second round, corresponding to the expected XMRV env gene fragment. Using nPCR we found no evidence of XMRV infection either in apparently healthy individuals or in patients with ME/CFS and individuals with unspecified encephalopathy.
...
PMID:No evidence of XMRV provirus sequences in patients with myalgic encephalomyelitis/chronic fatigue syndrome and individuals with unspecified encephalopathy. 2453 Nov 67