Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0032463 (polycythemia vera)
 3,374 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A highly specific and sensitive PCR assay for the envelope glycoprotein gp50 has been developed for the detection of PRV-DNA sequences. Primer pairs from PRV gp50 gene were used with the enzyme uracil N-glycosylase and dUTP instead dTTP to prevent contamination due to PCR product carry-over. Biotinylated PCR products were captured in microtiter wells by specific oligonucleotide covalently linked to the polystyrene wells. After recognition of the biotinylated PCR product with a streptavidin phosphatase conjugate, a chemiluminescent detection was realised. Different factors influencing the binding, the hybridization and the detection efficiency have been tested.
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PMID:Chemiluminescent detection of amplified pseudorabies virus gp50 DNA with immobilized probes on microtiter wells. 781 Apr 34

To investigate the routes of neural spread of pseudorabies (Aujeszky's disease) virus (PRV), the effects of chemical sympathectomy by 6-hydroxydopamine (6-OHDA) on clinical signs and viral spread in mice inoculated intraocularly with PRV were examined. Similar to non-treated mice, the treated mice developed pruritus as a major clinical sign, followed by peracute death, but the time of death tended to be slightly delayed in about half of the treated mice. On immunohistological examination, viral antigens in treated mice were found to be markedly reduced in all the ipsilateral retinae; they were detected diffusely in the forebrain area with a localization in the mammillary area. In the treated mice, viral antigens were also reduced in the ipsilateral trigeminal nerve ganglia as well as in its central nuclei. These findings indicate that both the sympathetic nervous system and the trigeminal nervous system play an important role in the neural spread of PRV. Possible involvement of the dopaminergic nervous system, particularly in the eye, as the main site of viral growth was discussed.
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PMID:Effect of chemical sympathectomy on the neural spread of pseudorabies virus in mice. 788 31

We previously described a marked increase in the pathogenicity of a cell culture grown porcine rotavirus, PRV 4F, during serial passage in gnotobiotic piglets (Bridger et al., 1992). Here we report close temporal correlation between this change in pathogenicity and an amino acid change within a highly conserved hydrophobic domain of VP4 at position 469. Cell culture grown PRV 4F is unique in having a hydrophilic residue, glutamine, at amino acid 469; all previously sequenced VP4s have hydrophobic leucine or phenylalanine residues at the corresponding position. The detection of a point mutation causing a deduced amino acid change from glutamine to leucine at amino acid 469 of PRV 4F VP4 in virus obtained from one piglet at the second serial passage correlated exactly with the emergence of viral pathogenicity. However, given the multifactorial nature of virus pathogenicity, genetic studies are required to ascertain the degree to which this mutation is responsible for the observed change in pathogenicity.
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PMID:Temporal correlation between a single amino acid change in the VP4 of a porcine rotavirus and a marked change in pathogenicity. 803 Feb 38

Earlier studies have shown that retinohypothalamic projections terminate extensively within the hypothalamus of the rat. Recently, we identified a light retinal projection to the supraoptic nucleus as well as a larger, well-focused projection resulting in a peri-supraoptic nucleus terminal field. In this study, we employed a double labeling method with cholera toxin conjugated to horseradish peroxidase (CT-HRP) and pseudorabies virus, a transsynaptic neural tracer, to evaluate retinorecipient neurons in both the supraoptic nucleus and peri-supraoptic nucleus terminal field. In addition, we looked for evidence that cells in the peri-supraoptic nucleus terminal field project into the supraoptic nucleus. Three strains of pseudorabies virus were compared. A direct retinosupraoptic nucleus circuit was confirmed with all three strains. Retinorecipient neurons in the peri-supraoptic nucleus terminal field were also confirmed. However, there was a strain-based difference in the identification of these neurons. The wild-type Becker strain labeled cells in the peri-supraoptic nucleus terminal field in a manner paralleling the early, intermediate and late stages of infection of the suprachiasmatic nucleus. This parallel time course suggests that retinal ganglion cells terminate directly on cells in the peri-supraoptic nucleus terminal field. Conversely, the Bartha and PRV-91 strains showed appreciable labeling of peri-supraoptic neurons only at long survival times. This longer time course suggests that these mutant strains label neurons in the peri-supraoptic nucleus terminal field indirectly, after passing through additional neurons. In addition, experiments with monocular injection of CT-HRP and posterior pituitary injection of pseudorabies virus showed retrogradely labeled second-order cells in the peri-supraoptic nucleus amidst the CT-HRP labeled terminal field of the retinohypothalamic tract. These results demonstrate a direct projection from the retina to the supraoptic nucleus and provide evidence for an indirect circuit from the retina to the supraoptic nucleus via neurons located in the peri-supraoptic nucleus terminal field. The strain-based differences imply that those retinal ganglion cells that project to the peri-supraoptic nucleus terminal field differ from those that project to the suprachiasmatic nucleus. In addition, these results suggest a neuroanatomic basis for photic effects on physiological mechanisms that are not mediated by the circadian timing system.
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PMID:Direct and indirect retinohypothalamic projections to the supraoptic nucleus in the female albino rat. 816 25

Feline herpesvirus 1 (FHV-1) is an important viral pathogen of cats. Like other alphaherpesviruses, FHV-1 contains a HSV-1 glycoprotein B (gB) homolog. In this study, monospecific antisera to HSV-1 gB reacted with three FHV-1 proteins (100, 64, and 58 kDa) present in virion lysates by immunoprecipitation and immunoblot analyses. Reduced stringency hybridization experiments using a HSV-1 gB probe localized the FHV-1 gB gene to a 9.6-kb Sa/l fragment in the unique long region of the genome. Northern blot analyses further localized the entire coding region within a 3.3-kb SacI fragment. The nucleotide sequence of this fragment was determined and two overlapping open reading frames (ORFs) encoding gB and ICP 18.5 were predicted. The amino acid sequence of the 2829 bp gB ORF was shown to have a high degree of homology with gB analogs of HSV-1, EHV-1, BHV-1, EHV-4, and especially PRV. Two unique characteristics of gB of FHV-1 were the unusually long signal sequence of 73 residues and two potential internal cleavage sites, RTRRS and RSRRS. An evolutionary tree based on gB homologs from 12 alphaherpesviruses suggests that feline herpesvirus-1 evolved along similar lines as the varicelloviruses, pseudorabies virus, bovine herpesvirus type 1, and equine herpesvirus types 1 and 4. The gB gene of FHV-1 was expressed in vaccinia virus (WR). This recombinant induced fairly high titers of virus neutralizing antibodies in rabbits. In Western blot analyses with potassium tartrate-purified virions, a 60-kDa polypeptide reacted with the rabbit antisera.
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PMID:Immunological characterization of the feline herpesvirus-1 glycoprotein B and analysis of its deduced amino acid sequence. 821 48

From 1984 to 1989 corrective operation circulation was performed under extracorporeal in 42 adults with trilogy of Fallot (6.2% of total intracardial operations under direct vision in patients with congenital heart disease in our hospital). The obstruction was relieved by resection of the hypertrophial and sclerotic muscle trabeculae of the Rt. ventricular outflow tract and pulmonary valvotomy and patching with a piece of artificial blood vessel lined internally by auto-pericardium so that a bougie (more than 1.6cm) could be passed through. The Rt. ventricular pressure was reduced satisfactorily (PRV/PLV < 0.75). There was one operative death.
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PMID:[Surgical treatment of trilogy of Fallot in 42 adults]. 822 4

We examined the responses of astrocytes, ramified microglia, and brain macrophages to CNS neuronal infection with virulent or attenuated strains of a swine alpha herpesvirus (pseudorabies virus, PRV). After PRV inoculation of the rat stomach or pancreas, the temporal course of viral replication and induced pathology of infected neurons were assessed in the dorsal motor nucleus of the vagus (DMV) and amygdala using an antiserum generated against PRV. Specific monoclonal antibodies against glial fibrillary acidic protein (GFAP), OX42, and ED1 and morphological criteria were used to classify non-neuronal cells. Both PRV strains infected DMV and motor neurons and then passed transneuronally to infect brainstem neurons that innervate the DMV. However, the onset of neuronal infection produced by the attenuated strain occurred approximately 20 hr later than infection with the virulent strain. Animals infected with the attenuated strain also survived longer, permitting transneuronal passage of virus into forebrain areas of the visceral neuraxis. Neuronal infection with both PRV strains produced consistent alterations in astrocytes, ramified microglia, and brain macrophages that correlated spatially and temporally with progressive stages of viral replication and neuronal pathology. Early stages of infection were characterized by increases in immunoreactivity for astrocytic GFAP and microglial OX42 that preceded overt signs of neuronal pathology. At later stages, GFAP immunoreactivity decreased dramatically in focal areas of neuronal infection while OX42 immunoreactivity continued to increase. Subsequently, ED1-immunoreactive brain macrophages infiltrated these infected areas. Double immunocytochemical labeling demonstrated that some astrocytes and brain macrophages were immunopositive for viral antigens but ramified microglia were not. The responses of glia and brain macrophages are consistent with a proposed role in restricting extracellular spread of virus by isolating or phagocytosing infected cells. These phenomena may contribute to the specific transneuronal transport exhibited by PRV.
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PMID:Spatiotemporal responses of astrocytes, ramified microglia, and brain macrophages to central neuronal infection with pseudorabies virus. 838 Nov 71

We have mutagenized and mapped the gene encoding the large subunit of ribonucleotide reductase (RR1) in pseudorabies virus (PRV; synonyms Aujeszky's disease virus, suid herpesvirus type 1). PRV strains carrying an oligonucleotide that leads to termination of translation of the RR1 gene are avirulent for mice. We subsequently constructed a PRV strain carrying a deletion in the RR1 gene and also a PRV strain carrying both the deletion in the RR1 gene and a deletion in the glycoprotein g1 gene, which is a marker for PRV virulence. Both PRV strains were assayed for virulence and immunogenicity in pigs, the natural host for PRV. In contrast to a marker-rescued PRV strain, these RR1-deleted mutants were avirulent, were shed in very low titres in the oropharyngeal fluid by the animals, and induced low titres of neutralizing antibodies. However, protection against clinical signs after infection with virulent PRV was induced by both RR1-deleted mutants. The relative importance of viral RR and thymidine kinase enzymes for deoxynucleotide synthesis in viral replication is discussed. In addition, we discuss the potential use of RR as a target for anti-herpesviral drugs and the use of PRV strains, deleted for the RR1 gene, as vaccine strains.
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PMID:Ribonucleotide reductase-deficient mutants of pseudorabies virus are avirulent for pigs and induce partial protective immunity. 838 70

I have examined the state of phosphorylation of the envelope glycoproteins of two neurotropic herpesviruses, HSV-2 and PRV. HSV-2 gE2 and PRV gI, which are the homologues to HSV-1 gE, were found to be phosphorylated and phosphoaminoacid analysis revealed that both contained phosphoserine. These findings are consistent with a conserved phosphorylation of the glycoprotein homologues to HSV gE among the neurotropic alphaherpesviruses.
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PMID:Phosphorylation of neurotropic alphaherpesvirus envelope glycoproteins: herpes simplex virus type 2 gE2 and pseudorabies virus gI. 839 Nov 84

We investigated the function of antigenic domains on gI in virulence and immunogenicity. Three PRV gI mutants were constructed by deleting nucleotides coding for the following amino acids: valine-125 and cysteine-126, located in a discontinuous antigenic domain (M 303); glycine-59 and aspartic acid-60 located in a continuous antigenic domain (M304); and arginine-67 and alanine-68, located in a discontinuous antigenic domain (M305). Mismatch primers in the polymerase chain reaction were used to introduce the deletions. Anti-gI monoclonal antibodies were used in an immunoperoxidase monolayer assay to distinguish PRV gI mutants from wild-type PRV. The gI mutant viruses were tested for their growth in vitro and for their virulence in mice. The growth properties of PRV gI mutant virus M303 were comparable to the growth properties of a PRV gI-negative mutant (M301): both mutants produced small plaques in various cells, and when grown on swine kidney cells and chicken embryo fibroblasts, their growth was disadvantaged compared to wild-type PRV. However, in embryonal Balb/c mouse cells expressing gI, gI mutant viruses and wild-type PRV produced plaques of the same size, confirming that the mutations in gI are responsible for the small plaque phenotype. The growth properties of PRV gI mutant viruses M 304 and M 305 were comparable to the growth properties of wild-type PRV. When the mean time to death was used as the criterion, the gI mutant viruses M 301 and M 303 were significantly less virulent in mice than wild-type PRV. Four other, independently obtained, PRV mutants all carrying the valine-125 and cysteine-126 deletion (M 308, M 309, M 310 and M 311 respectively) exhibit the same phenotype. Our results show that deleting valine-125 and cysteine-126 in gI decreases plaque size and reduces virulence in mice to the same degree as deleting the gI protein.
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PMID:Deleting valine-125 and cysteine-126 in glycoprotein gI of pseudorabies virus strain NIA-3 decreases plaque size and reduces virulence in mice. 839 68


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