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:2.7.7.6 (RNA polymerase)
34,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A new approach to synthesis of oligoribonucleotides is suggested, based on transcription by E. coli RNA polymerase of synthetic immobilized DNA-templates with AUG as primer. The approach has been experimentally verified by synthesis of two oligonucleotides, viz., a RNA fragment of the fr phage (16 nucleotides long) and a RNA fragment of the tickborne encephalitis virus (18 nucleotides long). Fraction of the synthesized RNA fragments in the whole nucleotide material is about 20%. The templates can be used repeatedly. Sequences of the oligoribonucleotides were confirmed. Advantages of this approach and its usefulness for SP6 DNA-dependent RNA polymerase are discussed.
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PMID:[Synthesis of oligoribonucleotides with the use of RNA polymerases of E. coli and immobilized synthetic DNA-templates]. 266 54

We have developed a reverse-transcriptase polymerase chain reaction assay for rapid detection of Langat (LGT) virus, a flavivirus that is closely related to the highly pathogenic tick-borne encephalitis (TBE) viruses. Unlike TBE viruses, LGT virus exhibits a significantly lower virulence for man. The assay serves as a safe alternative for the development and optimization of specific assays for the highly pathogenic subtypes of TBE viruses that are endemic throughout much of Europe, the former Soviet Union, and China.
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PMID:The Langat model for tick-borne encephalitis virus. Specific detection by RT-PCR. 750 84

Intracerebral inoculation of the neurotropic murine picornavirus, Theiler's murine encephalomyelitis virus (TMEV), results either in an acute encephalitis (GDVII strain) or in the establishment of a persistent infection with the development of demyelinating lesions (BeAn strain). In this article, the expression of the viral RNA polymerase was studied in the central nervous system of both acutely and persistently infected mice and in infected cells in tissue culture. Similar numbers of acutely infected glial cells (80-85%) expressed both viral polymerase and structural proteins in vitro while a much smaller proportion of persistently infected glial cells (0.6-0.9%) expressed these proteins. Following infection of mice with GDVII, many cells in the brain were found to express polymerase. However, in the spinal cord of mice persistently infected with BeAn, very few cells were found to express the polymerase while many more cells showed the presence of viral structural proteins. This suggests that a restriction in viral replication, possibly at the level of polymerase expression, may be a feature of the persistent infection. However, enough polymerase was expressed to maintain a polymerase-specific antibody response in a number of infected animals as late as 21 months post-infection. Mechanisms that may be involved in the establishment and maintenance of TMEV persistence are discussed with reference to these findings.
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PMID:Theiler's murine encephalomyelitis virus 3D RNA polymerase: its expression in the CNS and the specific immune response generated in persistently infected mice. 759 84

Reverse transcriptase-polymerase chain reaction (RT-PCR) on 24 cerebrospinal fluid (CSF) specimens collected between February and August 1992 detected genome sequence of West Nile (WN) virus in 8 specimens and Japanese encephalitis (JE) virus in a single specimen. The results, combined with the data by IgM-ELISA on CSF indicated that a significant proportion of acute encephalitis cases in Karachi, Pakistan, were caused by WN virus infection, while JE virus caused a small fraction.
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PMID:Detection of west Nile and Japanese encephalitis viral genome sequences in cerebrospinal fluid from acute encephalitis cases in Karachi, Pakistan. 786 64

Ribonucleoprotein (RNP) cores extracted from virions of wild-type (Edmonston strain) measles virus (MV) or obtained from MV-infected cells (cRNP) were shown to be capable of transcribing RNA in vitro but at relatively low efficiency. The tightly bound matrix (M) protein could be effectively removed from virion RNP (vRNP) and from cRNP by exposure to buffers of high ionic strength (0.5 to 1.0 M KCl) but only at pH 8.0 or higher. The vRNP and cRNP cores complexed with M protein exhibited markedly reduced transcriptional activity at increasing concentrations, whereas vRNP and cRNP cores free of M protein exhibited linear and substantially higher transcriptional activity; these data suggest that M protein is the endogenous inhibitor of MV RNP transcription. M-gene cDNA clones derived from three strains of wild-type (wt) MV and 10 clones from mRNAs isolated from the brain tissue of patients who had died from subacute sclerosing panencephalitis (SSPE) and from measles inclusion body encephalitis (MIBE) were recloned in the pTM-1 expression vector driven by the bacteriophage T7 RNA polymerase expressed by a coinfecting vaccinia virus recombinant. All 10 mutant SSPE and MIBE clones expressed in vitro and in vivo M proteins that reacted with monospecific anti-M polyclonal antibody and migrated on polyacrylamide gels to positions identical to or only slightly different from those of the M proteins expressed by wt MV clones. When reconstituted with cRNP cores, the three expressed wt M proteins and 6 of the 10 mutant-expressed M proteins showed equivalent capacity to down-regulate MV transcription. Three of the M proteins from SSPE clones and one from the MIBE clone showed little or no capacity to down-regulate transcription when reconstituted with cRNP cores. The only plausible explanations for loss of transcription inhibition activity by the four SSPE/MIBE M proteins were exceedingly high degrees of hypermutations leading to U-->C transitions and cloning-corrected mutations in the initiator codon (ATG-->ACG) of the four M genes. However, only the hypermutated M protein expressed by the MIBE cDNA clone exhibited virtually no capacity to bind cRNP cores in a reconstitution assay. These experiments provide some preliminary data to support the hypothesis that MV encephalitis may result from certain selective mutations in the M gene.
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PMID:Transcription inhibition and other properties of matrix proteins expressed by M genes cloned from measles viruses and diseased human brain tissue. 810 16

IFN-gamma is critical for prevention of development of toxoplasmic encephalitis (TE). Since IL-4 down-regulates production of IFN-gamma, we examined its role in the pathogenesis of TE in IL-4-targeted mutant (IL-4-/-) mice. IL-4-/- mice all died from 6 to 20 wk after peroral infection with cysts of the ME49 strain of Toxoplasma gondii; control mice survived. At 4 and 8 wk after infection, significantly greater numbers of T. gondii cysts and foci of acute inflammation, and greater amounts of tachyzoite-specific mRNA (by reverse-transcriptase PCR) were in brains of IL-4-/- mice than controls. Toxoplasma IgG2b and IgG3 Ab levels were slightly but significantly higher in sera of IL-4-/- than control mice, whereas IgM and IgG2a levels did not differ between these mice. Toxoplasma IgG1 and IgE Abs were not detected in sera of either strain. Amounts of IFN-gamma, TNF-alpha, IL-6, and IL-10 mRNA detected by reverse-transcriptase PCR did not differ between brains of infected IL-4-/- and controls, although brains of the former mice had greater numbers of inflammatory mononuclear cell infiltrates. IL-4 mRNA was detected only in infected control mice. Spleen cells of control mice at 8 wk after infection produced significantly greater amounts of IFN-gamma following stimulation in vitro with soluble T. gondii Ags than did those from IL-4-/- mice. These results indicate that IL-4 is protective against development of TE by preventing formation of T. gondii cysts and proliferation of tachyzoites in the brain. The impaired ability of IL-4-/- mice in the late stage of T. gondii infection to produce IFN-gamma most likely contributes to their susceptibility for development of severe TE.
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PMID:IL-4 is protective against development of toxoplasmic encephalitis. 880 58

The use of in situ hybridization (ISH) for the detection of caprine arthritis-encephalitis virus (CAEV) RNA with fluorescein-11-UTP-labelled single-stranded RNA probes is described. Three different probes were made by PCR amplification of proviral CAEV DNA (strain 75-G63). The PCR products were cloned into the plasmid pAM-18, and labelled single-stranded RNA probes were synthesized by the use of RNA polymerase. The LTR probe was able to detect viral RNA in CAEV-infected, cultured caprine macrophages, while probes based on the genes for the matrix and transmembrane proteins failed to do so. A few macrophages were positive for CAEV RNA 24 h post infection (p.i.) while most cells were positive 96 h p.i. The use of fluorescein-labelled RNA probes made this method feasible for kinetic in vitro studies of CAEV.
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PMID:Detection of caprine arthritis--encephalitis virus RNA in macrophages by in situ hybridization using fluorescein-labelled single-stranded RNA probes. 891 48

Semliki Forest virus (SFV) infection of mice is used as a model to study pathogenic processes occurring in viral encephalitis and demyelinating disease. In this study, the long-term effects of infection by the avirulent M9 mutant of SPV on the central nervous system (CNS) of BALB/c and SJL mice were determined. The presence of infectious virus, viral RNA and cytokine mRNA in the brains of individual mice and the presence of lesions in the spinal cords of the same mice up to 360 days post-infection (d.p.i.) were analysed in order to detect any correlation between these parameters of pathogenesis. Infectious virus could not be detected beyond 7 d.p.i. for either mouse strain. Reverse transcriptase polymerase chain reaction (RT-PCR) was used to detect the presence of the E2 and nsP1 regions of the virus genome and mRNA for interferon-gamma and tumour necrosis factor-alpha. Viral RNA could be detected up to 90 d.p.i. for both mouse strains. Cytokine mRNA could be detected up to 28 d.p.i. for BALB/c mice but up to 360 d.p.i. for SJL mice. Inflammatory lesions, which were associated with cytokine mRNA expression, were not detected in BALB/c mice beyond 28 d.p.i. but were detected in two SJL mice at 90 d.p.i. It is concluded that M9-SFV infection induces long-term prolonged expression of pro-inflammatory cytokines in the CNS of the majority of SJL (but not BALB/c) mice which is not associated with persistence of the virus genome. M9-SFV infection of SJL mice may be a relevant model for the pathogenesis of multiple sclerosis in man.
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PMID:Long-term effects of Semliki Forest virus infection in the mouse central nervous system. 922 33

Borna disease virus (BDV) is a neurotropic enveloped virus with a nonsegmented, single-, negative-stranded RNA genome. This virus induced encephalitis in experimentally infected adult rats, but in newborn rats BDV established a persistent, tolerant infection with no apparent clinical signs. Here, we report evidence that newborn Mongolian gerbils (Meriones unguiculatus) are more susceptible to experimental intracranial inoculation of horse-derived BDV in persistently infected MDCK cells, compared with similar inoculation in newborn rats. All inoculated newborn gerbils, but not rats, died 30 days after infection. Reverse transcriptase-polymerase chain reaction amplified BDV-specific sequences in several regions including the brain. Histopathological analysis revealed apparent inflammatory reactions in the brains of inoculated gerbils but not rats, although similar levels of BDV RNA were detected in both gerbil and rat brains. BDV-specific antigen and RNA were identified predominantly in neurons in the brains by immunohistochemistry with antibodies to BDV and in situ hybridization with BDV-specific riboprobes, respectively. BDV in the gerbil brain was easily rescued by co-cultivation of the brain homogenate with human oligodendroglioma cells. Thus, gerbils seem to be a useful animal model for studying BDV-induced pathogenesis in the brain.
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PMID:High susceptibility of Mongolian gerbil (Meriones unguiculatus) to Borna disease virus. 1007 27

Molecular determinants of neuropathogenesis have been shown to be present in the hemagglutinin (H) protein of measles virus (MV). An H gene insertion vector has been generated from the Edmonston B vaccine full-length infectious clone of MV. Using this vector, it is possible to insert complete H open reading frames into the parental (Edtag) background. The H gene from a rodent brain-adapted MV strain (CAM/RB) was inserted into this vector, and a recombinant virus (EdtagCAMH) was rescued by using a modified vaccinia virus which expresses T7 RNA polymerase (MVA-T7). The recombinant virus grew at an equivalent rate and to similar titers as the CAM/RB and Edtag parental viruses. Neurovirulence was assayed in a mouse model for MV encephalitis. Viruses were injected intracerebrally into the right cortex of C57/BL/6 suckling mice. After infection mice inoculated with the CAM/RB strain developed hind limb paralysis and ataxia. Clinical symptoms were never observed with an equivalent dose of Edtag virus or in sham infections. Immunohistochemistry (IHC) was used to detect viral antigen in formalin-fixed brain sections. Measles antigen was observed in neurons and neuronal processes of the hippocampus, frontal, temporal, and olfactory cortices and neostriatum on both sides of symmetrical structures. Viral antigen was not detected in mice infected with Edtag virus. Mice infected with the recombinant virus, EdtagCAMH, became clinically ill, and virus was detected by IHC in regions of the brain similar to those in which it was detected in animals infected with CAM/RB. The EdtagCAMH infection had, however, progressed much less than the CAM/RB virus at 4 days postinfection. It therefore appears that additional determinants are encoded in other regions of the MV genome which are required for full neurovirulence equivalent to CAM/RB. Nevertheless, replacement of the H gene alone is sufficient to cause neuropathology.
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PMID:The H gene of rodent brain-adapted measles virus confers neurovirulence to the Edmonston vaccine strain. 1040 Jul 89


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