Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.2.1.23 (beta-galactosidase)
14,648 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Among 102 brains obtained from patients with acquired immune deficiency syndrome (AIDS), 34 cases with subacute AIDS encephalitis were characterized by immunohistochemistry using an antibody that binds to a human immunodeficiency virus-1 (HIV-1) envelope glycoprotein, gp41. This glycoprotein was detected in mononucleated and/or multinucleated cells in 90% of adult and 50% of pediatric brains with subacute AIDS encephalitis. In addition, many gp41-positive cells with bipolar or multipolar processes were found in 10 cases, and these cells occurred most frequently in the basal ganglia and internal capsule. The phenotype of the gp41-positive cells was determined using an improved double-labeling immunohistochemical technique that employed beta-galactosidase and peroxidase conjugated reagents. Cell-type specific markers for double-labeling included: Ricinus communis agglutinin-1 (RCA-1) for macrophages and microglia; Ulex europaeus agglutinin-1 for endothelium; anti-glial fibrillary acidic protein (GFAP) for astrocytes; anti-amyloid precursor protein for neurons; and anti-leukocyte common antigen for leukocytes. Results of double-immunostaining revealed that gp41-positive cells of all morphologic types, including cells with bipolar or multipolar processes, were double-labeled with RCA-1, but not with markers for astrocytes, neurons, or endothelia. These findings support the contention that HIV-1 infection of the CNS is predominantly restricted to cells of the macrophage/microglia lineage.
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PMID:Cellular localization of an HIV-1 antigen in subacute AIDS encephalitis using an improved double-labeling immunohistochemical method. 169 70

Two possible forms of tick-borne encephalitis virus (TBE) gene NS1 (called NS1' and NS1) were constructed using two overlapping cDNA-fragments of TBE genome and synthetic DNA fragments. This genes were expressed in E. coli cells in expression vector pUR290 as individual proteins or fusion with bacterial beta-galactosidase. The proteins NS1 (Mw. 39 kDa), beta-galactosidase-NS1' (Mw. 162 kDa) and beta-galactosidase-NS1 (Mw. 155 kDa) were effectively synthesized under the Plgc-promoter induction conditions. Expression of NS1' gene results in the formation of two virus-specific proteins (Mw. 46 and 44 kDa). All bacterial analogs of NS1 protein fixed monoclonal and polyclonal antibodies specific to viral NS1.
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PMID:[Expression of gene coding for the NS1 protein of the tick-borne encephalitis virus in Escherichia coli cell]. 215 Dec 83

Agalactosyl IgG [Gal(0)] was first discovered in patients with rheumatoid arthritis (RA). However, the proportion of this glycoform is also raised in tuberculosis and leprosy. This has helped reinforce the suggestion that RA may be triggered by a mycobacterium-like slow bacterial infection. On the other hand, arthritis can occur in mycobacterial diseases, so raised Gal(0) could be associated with a tendency to arthritis, rather than with a particular type of infection. Therefore, we wished to find out whether the percentage of Gal(0) [%Gal(0)] is increased in sheep and goats following infection with maedi visna virus or caprine arthritis encephalitis virus (CAEV), both of which can lead to inflammatory synovitis. We found that the normal level of Gal(0) in these species is much lower than in humans. Goats infected with CAEV or Mycobacterium paratuberculosis (used as a control mycobacterial infection) had a significant increase in %Gal(0), though it was still below the level seen in normal humans. Studies by Western blot confirmed the presence of terminal N-acetylglucosamine on heavy chains, and percentages of Gal(0) comparable to those seen in human RA could be generated by exposing goat IgG to streptococcal beta-galactosidase. The rise in %Gal(0) was greatest in members of infected herds that were just starting to manifest arthritis, and tended to be lower in those in which severe carpitis had developed at the time of bleeding, implying the possibility that raise %Gal(0) may be an early or predisposing event for the development of arthritis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Glycosylation of IgG during potentially arthritogenic lentiviral infections. 759 80

Viral vectors are a means by which genes can be delivered to specific sites in the adult central nervous system. Nevertheless, the interaction between the viral vector and cells of the nervous system, which forms the basis for specific gene transfer, is not well understood. In this study a nonreplicating defective herpes simplex virus type 1 vector, expressing the marker gene lacZ, was stereotaxically injected at varying titers into the rat central nervous system. Three sites were targeted: the caudate nucleus, dentate gyrus, and cerebellar cortex, and the resulting patterns of beta-galactosidase activity were examined. Many cells of neuronal and glial morphology, and of differing neuronal subtypes, expressed beta-galactosidase at each of the injection sites. However, beta-galactosidase activity was also detected in distant secondary brain areas, the neurons of which make afferent connections with the primary sites. This strongly suggested that the retrograde transport of defective virus was the basis for the enzyme activity observed at a distance. Moreover, retrograde transport to secondary sites was found to be highly selective and restricted to certain retrograde neuroanatomical pathways in a specific and titer dependent fashion. The pathways observed were predominantly, but not exclusively, monoaminergic in origin. This finding is supported by reports of specific tropism by HSV for monoaminergic circuits in experimental encephalitis and transneuronal tracing studies. Our observations suggest that certain functional neuronal populations, which are permissive for the retrograde transfer of defective HSV-1 vectors, might be specifically targeted for gene transfer using this approach. Conversely, a knowledge of the pathways permissive for viral uptake, retrograde transfer, and subsequent gene expression will be essential in order to predict the consequences of gene transfer using viral vectors.
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PMID:Specific patterns of defective HSV-1 gene transfer in the adult central nervous system: implications for gene targeting. 782 88

Replication defective retroviral vectors are regularly used for transfer and expression of exogenous genes into dividing cells and in animals. Since lentiviruses are able to infect terminally differentiated and non-dividing cells, their use to produce replication defective vectors may overcome this limitation. We developed two replication-defective lentiviral vectors based on the genome of Caprine Arthritis Encephalitis Virus (CAEV). The first vector (pBNL2) carries the neo and lacZ marker genes. Neo gene is expressed from a genomic RNA and lacZ gene from a subgenomic RNA. The second vector (pCSHL) carries a single fusion gene encoding both phleomycin resistance and beta-galactosidase activity. Replication-competent CAEV was used as helper virus to provide the viral proteins for transcomplementation of these vectors. Our data demonstrated that the genomes of both vectors were packaged into CAEV virions and transduced into goat synovial membrane cells following infection. However, the vector titers remained 3 to 4 logs lower than those of CAEV. Further analysis showed a lack of accumulation of unspliced pBNL2 RNA into the cytoplasm of producer cells resulting in the packaging of pBNL2 sub-genomic RNA only. In contrast, RNA produced from pCSHL vector was correctly transported to the cytoplasm and more efficiently packaged than the pBNL2 sub-genomic RNA as revealed by slot-blot and quantitative RT/PCR analyses. However this higher packaging efficiency of pCSHL genome did not result in a higher transduction efficiency of lacZ gene.
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PMID:Defective RNA packaging is responsible for low transduction efficiency of CAEV-based vectors. 963 41

Infection with Japanese encephalitis virus (JEV), a mosquito-borne flavivirus, may cause acute encephalitis in humans and induce severe cytopathic effects in various types of cultured cells. We observed that JEV replication rendered infected baby hamster kidney (BHK-21) cells sensitive to the translational inhibitor hygromycin B or alpha-sarcine, to which mock-infected cells were insensitive. However, little is known about whether any JEV nonstructural (NS) proteins contribute to virus-induced changes in membrane permeability. Using an inducible Escherichia coli system, we investigated which parts of JEV NS1 to NS4 are capable of modifying membrane penetrability. We found that overexpression of NS2B-NS3, the JEV protease, permeabilized bacterial cells to hygromycin B whereas NS1 expression failed to do so. When expressed separately, NS2B alone, but not NS3, was sufficient to alter bacterial membrane permeability. Similarly, expression of NS4A or NS4B also rendered bacteria susceptible to hygromycin B inhibition. Examination of the effect of NS1 to NS4 expression on bacterial growth rate showed that NS2B exhibited the greatest inhibitory capability, followed by a modest repression from NS2A and NS4A, whereas NS1, NS3, and NS4B had only trivial influence with respect to the vector control. Furthermore, when cotransfected with a reporter gene luciferase or beta-galactosidase, transient expression of NS2A, NS2B, and NS4B markedly reduced the reporter activity in BHK-21 cells. Together, our results suggest that upon JEV infection, these four small hydrophobic NS proteins have various modification effects on host cell membrane permeability, thereby contributing in part to virus-induced cytopathic effects in infected cells.
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PMID:Membrane permeabilization by small hydrophobic nonstructural proteins of Japanese encephalitis virus. 1040 Jul 16

West Nile virus (WNV) is a member of the Flavivirus family and induces febrile illness, sporadic encephalitis, and paralysis. The capsid (Cp) of WNV is thought to play a role in inducing these symptoms through caspase-3- and caspase-9-dependent apoptosis. Using WNVCp as bait for a yeast two-hybrid assay, we identified that Hsp70 interacted with WNVCp. The interaction between Hsp70 and WNVCp was further substantiated using purified proteins. Deletion analysis of Hsp70 indicated that WNVCp could bind to the substrate binding domain of Hsp70. The presence of WNVCp in the Hsp70-dependent folding system inhibited the refolding of beta-galactosidase (beta-gal), which showed that WNVCp might function as a negative regulator of Hsp70. Finally, the cytotoxic effect of WNVCp in 293T cells was prevented by ectopic Hsp70, suggesting a negative regulatory role of Hsp70 on WNVCp. Our findings suggest a possible negative regulatory role of Hps70 in the pathway of WNV infection.
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PMID:Hsp70 functions as a negative regulator of West Nile virus capsid protein through direct interaction. 1685 74

To study early events of neonatal herpes simplex virus (HSV) encephalitis and its sequelae, the authors induced a controlled infection in the brains of mice using HSVgH, a genetically modified Disabled Infective Single Cycle virus. Neonatal Balb/C mice were infected with various amounts of HSVgH- virus by intracerebral injection. Results showed that the survival of infected mice was dependent on the amount of virus injected. Infection with 200,000 plaque forming units (pfu) of HSVgH-, virus resulted in 0% survival, whereas 25,000 pfu resulted in 75% survival. If the mice died, 98% of the deaths occurred between 3 and 7 days after infection. Replication competent virus was recovered from 20% of mice brains infected with 25,000 pfu of HSVgH-. Neutralizing antibodies were not detected 6 weeks post infection in sera of mice, which survived infection with 25,000 pfu of HSVgH-. LacZ histochemistry and immunoperoxidase staining using anti-HSV and anti- beta-galactosidase antibodies revealed that the infection was limited to the site of injection. Tissue destruction was observed at the site of inoculation 3 days post infection using cresyl violet staining. At 3 days post infection adjacent sections showed positive cells for viral antigens and apoptotic cells in the infected area. Immunoperoxidase staining using antibodies to surface markers showed microglial activation beginning on day 1 and astrocyte proliferation beginning on day 3 post infection. B and T lymphocytes were not detected on day 1 through 7 post infection. This controlled experimental HSV infection suggests a limited non-specific early host response in the neonate to HSV encephalitis.
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PMID:Innate and adaptive host response during the initial phase of herpes simplex virus encephalitis in the neonatal mouse. 1706 29

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