Differential accumulation of herpes simplex virus type 1 latency-associated transcripts in sensory and autonomic ganglia
Identifieur interne : 000C92 ( Istex/Corpus ); précédent : 000C91; suivant : 000C93Differential accumulation of herpes simplex virus type 1 latency-associated transcripts in sensory and autonomic ganglia
Auteurs : Eyvind R Dahl ; Jack G. StevensSource :
- Virology [ 0042-6822 ] ; 1992.
English descriptors
- Teeft :
- Acute phase, Anterior chamber, Anterior chamber inoculation, Autonomic ganglia, Autonomic neurons, Average number, Brain research, Cell culture medium, Detection limit, Essential medium, Further details, Ganglion, Genome, Genome equivalents, Herpes simplex virus type, Hybridization signal, Latent infection, Latent phase, Lats, Neuron, Normal goat serum, Polymerase gene, Positive neurons, Pterygopalatine ganglion, Reaction products, Sensory ganglia, Short communications, Substantial amounts, Trigeminal ganglion, Uninfected mice, Viral, Viral antigens, Viral genome equivalents.
Abstract
Abstract: We have analyzed the capacity of sensory and autonomic ganglia to demonstrate latency-associated transcripts (LATs) following inoculation of the anterior chamber of the mouse eye with Herpes simplex virus type 1 (HSV-1). In autonomic ganglia, the number of LAT-containing neurons decreased 50-fold or more from the acute to the latent phase, while in the trigeminal ganglion, the decrease was less than 2-fold. The decrease in autonomic ganglia could not be related to destruction of neurons expressing LATs, since these ganglia harbored substantial amounts of viral DNA. The data demonstrate that during the latent phase of the infection, accumulation of LATs varies depending on the type of infected neuron and suggest that some neurons may harbor a latent infection in the absence of LAT expression.
Url:
DOI: 10.1016/0042-6822(92)90721-Z
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ISTEX:B54559997BA29B36A677E03CC59FBCFE64E91B22Le document en format XML
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Stevens</name><affiliation><mods:affiliation>Department of Microbiology and Immunology, UCLA School of Medicine, Center for the Health Sciences, 10833 Le Conte Avenue, Los Angeles, California 90024-1747, USA</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Virology</title><title level="j" type="abbrev">YVIRO</title><idno type="ISSN">0042-6822</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1992">1992</date><biblScope unit="volume">189</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="385">385</biblScope><biblScope unit="page" to="388">388</biblScope></imprint><idno type="ISSN">0042-6822</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0042-6822</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Acute phase</term><term>Anterior chamber</term><term>Anterior chamber inoculation</term><term>Autonomic ganglia</term><term>Autonomic neurons</term><term>Average number</term><term>Brain research</term><term>Cell culture medium</term><term>Detection limit</term><term>Essential medium</term><term>Further details</term><term>Ganglion</term><term>Genome</term><term>Genome equivalents</term><term>Herpes simplex virus type</term><term>Hybridization signal</term><term>Latent infection</term><term>Latent phase</term><term>Lats</term><term>Neuron</term><term>Normal goat serum</term><term>Polymerase gene</term><term>Positive neurons</term><term>Pterygopalatine ganglion</term><term>Reaction products</term><term>Sensory ganglia</term><term>Short communications</term><term>Substantial amounts</term><term>Trigeminal ganglion</term><term>Uninfected mice</term><term>Viral</term><term>Viral antigens</term><term>Viral genome equivalents</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: We have analyzed the capacity of sensory and autonomic ganglia to demonstrate latency-associated transcripts (LATs) following inoculation of the anterior chamber of the mouse eye with Herpes simplex virus type 1 (HSV-1). In autonomic ganglia, the number of LAT-containing neurons decreased 50-fold or more from the acute to the latent phase, while in the trigeminal ganglion, the decrease was less than 2-fold. The decrease in autonomic ganglia could not be related to destruction of neurons expressing LATs, since these ganglia harbored substantial amounts of viral DNA. The data demonstrate that during the latent phase of the infection, accumulation of LATs varies depending on the type of infected neuron and suggest that some neurons may harbor a latent infection in the absence of LAT expression.</div></front></TEI><istex><corpusName>elsevier</corpusName><keywords><teeft><json:string>ganglion</json:string><json:string>neuron</json:string><json:string>genome</json:string><json:string>viral</json:string><json:string>anterior chamber</json:string><json:string>autonomic ganglia</json:string><json:string>genome equivalents</json:string><json:string>positive neurons</json:string><json:string>latent infection</json:string><json:string>trigeminal ganglion</json:string><json:string>anterior chamber inoculation</json:string><json:string>latent phase</json:string><json:string>average number</json:string><json:string>autonomic neurons</json:string><json:string>brain research</json:string><json:string>lats</json:string><json:string>herpes simplex virus type</json:string><json:string>substantial amounts</json:string><json:string>pterygopalatine ganglion</json:string><json:string>sensory ganglia</json:string><json:string>short communications</json:string><json:string>acute phase</json:string><json:string>hybridization signal</json:string><json:string>cell culture medium</json:string><json:string>essential medium</json:string><json:string>further details</json:string><json:string>normal goat serum</json:string><json:string>uninfected mice</json:string><json:string>polymerase gene</json:string><json:string>reaction products</json:string><json:string>viral genome equivalents</json:string><json:string>detection limit</json:string><json:string>viral antigens</json:string></teeft></keywords><author><json:item><name>Eyvind Rødahl</name><affiliations><json:string>Department of Microbiology and Immunology, UCLA School of Medicine, Center for the Health Sciences, 10833 Le Conte Avenue, Los Angeles, California 90024-1747, USA</json:string></affiliations></json:item><json:item><name>Jack G. 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The decrease in autonomic ganglia could not be related to destruction of neurons expressing LATs, since these ganglia harbored substantial amounts of viral DNA. 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In autonomic ganglia, the number of LAT-containing neurons decreased 50-fold or more from the acute to the latent phase, while in the trigeminal ganglion, the decrease was less than 2-fold. The decrease in autonomic ganglia could not be related to destruction of neurons expressing LATs, since these ganglia harbored substantial amounts of viral DNA. 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In autonomic ganglia, the number of LAT-containing neurons decreased 50-fold or more from the acute to the latent phase, while in the trigeminal ganglion, the decrease was less than 2-fold. The decrease in autonomic ganglia could not be related to destruction of neurons expressing LATs, since these ganglia harbored substantial amounts of viral DNA. The data demonstrate that during the latent phase of the infection, accumulation of LATs varies depending on the type of infected neuron and suggest that some neurons may harbor a latent infection in the absence of LAT expression.</ce:simple-para></ce:abstract-sec></ce:abstract></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>Differential accumulation of herpes simplex virus type 1 latency-associated transcripts in sensory and autonomic ganglia</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Differential accumulation of herpes simplex virus type 1 latency-associated transcripts in sensory and autonomic ganglia</title></titleInfo><name type="personal"><namePart type="given">Eyvind</namePart><namePart type="family">Rødahl</namePart><affiliation>Department of Microbiology and Immunology, UCLA School of Medicine, Center for the Health Sciences, 10833 Le Conte Avenue, Los Angeles, California 90024-1747, USA</affiliation><description>Present address: National Centre for Research in Virology, University of Bergen, N-5020 Bergen, Norway.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jack G.</namePart><namePart type="family">Stevens</namePart><affiliation>Department of Microbiology and Immunology, UCLA School of Medicine, Center for the Health Sciences, 10833 Le Conte Avenue, Los Angeles, California 90024-1747, USA</affiliation><description>To whom reprint requests should be addressed.</description><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="brief-communication" displayLabel="Short communication" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-S9SX2MFS-0">brief-communication</genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1992</dateIssued><copyrightDate encoding="w3cdtf">1992</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><abstract lang="en">Abstract: We have analyzed the capacity of sensory and autonomic ganglia to demonstrate latency-associated transcripts (LATs) following inoculation of the anterior chamber of the mouse eye with Herpes simplex virus type 1 (HSV-1). In autonomic ganglia, the number of LAT-containing neurons decreased 50-fold or more from the acute to the latent phase, while in the trigeminal ganglion, the decrease was less than 2-fold. The decrease in autonomic ganglia could not be related to destruction of neurons expressing LATs, since these ganglia harbored substantial amounts of viral DNA. 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