Viral infections of the developing nervous system
Identifieur interne : 000671 ( Istex/Corpus ); précédent : 000670; suivant : 000672Viral infections of the developing nervous system
Auteurs : P. K. CoyleSource :
- Seminars in Neuroscience [ 1044-5765 ] ; 1991.
English descriptors
- Teeft :
- Abnormality, Animal models, Apparent disease, Aqueductal stenosis, Bluetongue virus, Border disease, Brain atrophy, Brain malformations, Cell populations, Cerebellar hypoplasia, Cerebrospinal fluid, Chick embryos, Cholera virus, Chromosomal damage, Congenital, Congenital infection, Congenital infection results, Congenital infections, Consequent damage, Defect, Developmental stage, Different cell populations, Encephalitis, Ependymal cells, Epidermal growth factor, Fetal, Fetal brain, Fetal infection, Fetal tissue, Fetus, First half, First trimester, Focal areas, Genetic transmission, Germinal cells, Gestation, Hearing loss, Human immunodeficiency virus, Human immunodeficiency virus type, Human viruses, Immunodeficiency, Infection, Infectious diseases, Infects, Inflammatory changes, Intrauterine, Intrauterine growth retardation, Intrauterine infection, Louis encephalitis virus, Malformation, Maternal antibodies, Maternal infection, Maternal viremia, Mental retardation, Microcephaly, Mortality rate, Murine leukemia virus, Natural animal models, Natural infection, Nervous system, Neural tube defects, Neuronal migration defects, Newborn infant, Newcastle disease virus, Ontogenic development, Parvovirus, Pathogenic mechanisms, Perinatal, Perinatal infections, Persistent infection, Primary infection, Progressive disease, Rubella, Spontaneous ataxia, System damage, Viral, Viral clearance, Viral infection, Viral infections, Viral transmission, Virus, Virus infections, Virus infects, Weeks gestation.
Abstract
Abstract: Both clinical and experimental studies indicate that viruses can interact with the developing nervous system to produce a spectrum of neurological damage and brain malformations. Following infection of the pregnant woman, virus may indirectly or directly involve the fetus. Direct involvement is generally due to transplacental passage of the virus and invasion of fetal tissue. Resultant disease is determined by a variety of virus-host factors, including the developmental stage of the fetus at the time it is infected, the neural cell populations which are susceptible to infection, the consequent virus-infected cell interactions, and the mechanism and timing of viral clearance. There is a growing list of human viruses which injure the developing nervous system. There are also several experimental models in which congenital viral infections have been shown to result in a variety of brain malformations but with no evidence of the prior infection remaining at the time of birth.
Url:
DOI: 10.1016/1044-5765(91)90011-C
Links to Exploration step
ISTEX:A408296B93AAA77741833F7D9ED00D0DF5922FC3Le document en format XML
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Coyle</name><affiliation><mods:affiliation>From the Department of Neurology, Health Sciences Center, SUNY at Stony Brook, NY 11794, USA</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:A408296B93AAA77741833F7D9ED00D0DF5922FC3</idno><date when="1991" year="1991">1991</date><idno type="doi">10.1016/1044-5765(91)90011-C</idno><idno type="url">https://api.istex.fr/ark:/67375/6H6-K8CQTT34-R/fulltext.pdf</idno><idno type="wicri:Area/Istex/Corpus">000671</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">000671</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a">Viral infections of the developing nervous system</title><author><name sortKey="Coyle, P K" sort="Coyle, P K" uniqKey="Coyle P" first="P. K." last="Coyle">P. K. Coyle</name><affiliation><mods:affiliation>From the Department of Neurology, Health Sciences Center, SUNY at Stony Brook, NY 11794, USA</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Seminars in Neuroscience</title><title level="j" type="abbrev">YSMNS</title><idno type="ISSN">1044-5765</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1991">1991</date><biblScope unit="volume">3</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="157">157</biblScope><biblScope unit="page" to="163">163</biblScope></imprint><idno type="ISSN">1044-5765</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">1044-5765</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Abnormality</term><term>Animal models</term><term>Apparent disease</term><term>Aqueductal stenosis</term><term>Bluetongue virus</term><term>Border disease</term><term>Brain atrophy</term><term>Brain malformations</term><term>Cell populations</term><term>Cerebellar hypoplasia</term><term>Cerebrospinal fluid</term><term>Chick embryos</term><term>Cholera virus</term><term>Chromosomal damage</term><term>Congenital</term><term>Congenital infection</term><term>Congenital infection results</term><term>Congenital infections</term><term>Consequent damage</term><term>Defect</term><term>Developmental stage</term><term>Different cell populations</term><term>Encephalitis</term><term>Ependymal cells</term><term>Epidermal growth factor</term><term>Fetal</term><term>Fetal brain</term><term>Fetal infection</term><term>Fetal tissue</term><term>Fetus</term><term>First half</term><term>First trimester</term><term>Focal areas</term><term>Genetic transmission</term><term>Germinal cells</term><term>Gestation</term><term>Hearing loss</term><term>Human immunodeficiency virus</term><term>Human immunodeficiency virus type</term><term>Human viruses</term><term>Immunodeficiency</term><term>Infection</term><term>Infectious diseases</term><term>Infects</term><term>Inflammatory changes</term><term>Intrauterine</term><term>Intrauterine growth retardation</term><term>Intrauterine infection</term><term>Louis encephalitis virus</term><term>Malformation</term><term>Maternal antibodies</term><term>Maternal infection</term><term>Maternal viremia</term><term>Mental retardation</term><term>Microcephaly</term><term>Mortality rate</term><term>Murine leukemia virus</term><term>Natural animal models</term><term>Natural infection</term><term>Nervous system</term><term>Neural tube defects</term><term>Neuronal migration defects</term><term>Newborn infant</term><term>Newcastle disease virus</term><term>Ontogenic development</term><term>Parvovirus</term><term>Pathogenic mechanisms</term><term>Perinatal</term><term>Perinatal infections</term><term>Persistent infection</term><term>Primary infection</term><term>Progressive disease</term><term>Rubella</term><term>Spontaneous ataxia</term><term>System damage</term><term>Viral</term><term>Viral clearance</term><term>Viral infection</term><term>Viral infections</term><term>Viral transmission</term><term>Virus</term><term>Virus infections</term><term>Virus infects</term><term>Weeks gestation</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: Both clinical and experimental studies indicate that viruses can interact with the developing nervous system to produce a spectrum of neurological damage and brain malformations. Following infection of the pregnant woman, virus may indirectly or directly involve the fetus. Direct involvement is generally due to transplacental passage of the virus and invasion of fetal tissue. Resultant disease is determined by a variety of virus-host factors, including the developmental stage of the fetus at the time it is infected, the neural cell populations which are susceptible to infection, the consequent virus-infected cell interactions, and the mechanism and timing of viral clearance. There is a growing list of human viruses which injure the developing nervous system. There are also several experimental models in which congenital viral infections have been shown to result in a variety of brain malformations but with no evidence of the prior infection remaining at the time of birth.</div></front></TEI><istex><corpusName>elsevier</corpusName><keywords><teeft><json:string>fetal</json:string><json:string>viral</json:string><json:string>nervous system</json:string><json:string>fetus</json:string><json:string>rubella</json:string><json:string>perinatal</json:string><json:string>intrauterine</json:string><json:string>congenital</json:string><json:string>abnormality</json:string><json:string>infects</json:string><json:string>microcephaly</json:string><json:string>malformation</json:string><json:string>immunodeficiency</json:string><json:string>encephalitis</json:string><json:string>gestation</json:string><json:string>parvovirus</json:string><json:string>infection</json:string><json:string>viral infections</json:string><json:string>congenital infection</json:string><json:string>viral infection</json:string><json:string>fetal infection</json:string><json:string>persistent infection</json:string><json:string>virus infections</json:string><json:string>mental retardation</json:string><json:string>virus</json:string><json:string>fetal tissue</json:string><json:string>germinal cells</json:string><json:string>maternal antibodies</json:string><json:string>virus infects</json:string><json:string>fetal brain</json:string><json:string>perinatal infections</json:string><json:string>human immunodeficiency virus</json:string><json:string>first trimester</json:string><json:string>border disease</json:string><json:string>chick embryos</json:string><json:string>hearing loss</json:string><json:string>defect</json:string><json:string>neuronal migration defects</json:string><json:string>human immunodeficiency virus type</json:string><json:string>brain malformations</json:string><json:string>human viruses</json:string><json:string>consequent damage</json:string><json:string>viral transmission</json:string><json:string>murine leukemia virus</json:string><json:string>animal models</json:string><json:string>weeks gestation</json:string><json:string>maternal infection</json:string><json:string>developmental stage</json:string><json:string>cell populations</json:string><json:string>ontogenic development</json:string><json:string>pathogenic mechanisms</json:string><json:string>first half</json:string><json:string>chromosomal damage</json:string><json:string>natural animal models</json:string><json:string>cerebellar hypoplasia</json:string><json:string>neural tube defects</json:string><json:string>inflammatory changes</json:string><json:string>spontaneous ataxia</json:string><json:string>bluetongue virus</json:string><json:string>intrauterine growth retardation</json:string><json:string>congenital infection results</json:string><json:string>maternal viremia</json:string><json:string>cholera virus</json:string><json:string>louis encephalitis virus</json:string><json:string>newcastle disease virus</json:string><json:string>natural infection</json:string><json:string>ependymal cells</json:string><json:string>cerebrospinal fluid</json:string><json:string>aqueductal stenosis</json:string><json:string>different cell populations</json:string><json:string>viral clearance</json:string><json:string>focal areas</json:string><json:string>genetic transmission</json:string><json:string>primary infection</json:string><json:string>apparent disease</json:string><json:string>mortality rate</json:string><json:string>intrauterine infection</json:string><json:string>progressive disease</json:string><json:string>system damage</json:string><json:string>epidermal growth factor</json:string><json:string>congenital infections</json:string><json:string>infectious diseases</json:string><json:string>newborn infant</json:string><json:string>brain atrophy</json:string></teeft></keywords><author><json:item><name>P.K. 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Following infection of the pregnant woman, virus may indirectly or directly involve the fetus. Direct involvement is generally due to transplacental passage of the virus and invasion of fetal tissue. Resultant disease is determined by a variety of virus-host factors, including the developmental stage of the fetus at the time it is infected, the neural cell populations which are susceptible to infection, the consequent virus-infected cell interactions, and the mechanism and timing of viral clearance. There is a growing list of human viruses which injure the developing nervous system. 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Following infection of the pregnant woman, virus may indirectly or directly involve the fetus. Direct involvement is generally due to transplacental passage of the virus and invasion of fetal tissue. Resultant disease is determined by a variety of virus-host factors, including the developmental stage of the fetus at the time it is infected, the neural cell populations which are susceptible to infection, the consequent virus-infected cell interactions, and the mechanism and timing of viral clearance. There is a growing list of human viruses which injure the developing nervous system. There are also several experimental models in which congenital viral infections have been shown to result in a variety of brain malformations but with no evidence of the prior infection remaining at the time of birth.</p></abstract><textClass><keywords scheme="keyword"><list><head>Keywords</head><item><term>congenital viral infection</term></item><item><term>fetus</term></item><item><term>brain malformations</term></item><item><term>developing nervous system</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1991">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-K8CQTT34-R/fulltext.txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier, elements deleted: tail"><istex:xmlDeclaration>version="1.0" encoding="utf-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//ES//DTD journal article DTD version 4.5.2//EN//XML" URI="art452.dtd" name="istex:docType"></istex:docType><istex:document><converted-article version="4.5.2" docsubtype="fla"><item-info><jid>YSMNS</jid><aid>9190011C</aid><ce:pii>1044-5765(91)90011-C</ce:pii><ce:doi>10.1016/1044-5765(91)90011-C</ce:doi><ce:copyright type="unknown" year="1991"></ce:copyright></item-info><head><ce:title>Viral infections of the developing nervous system</ce:title><ce:author-group><ce:author><ce:given-name>P.K.</ce:given-name><ce:surname>Coyle</ce:surname></ce:author><ce:affiliation><ce:textfn>From the Department of Neurology, Health Sciences Center, SUNY at Stony Brook, NY 11794, USA</ce:textfn></ce:affiliation></ce:author-group><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para>Both clinical and experimental studies indicate that viruses can interact with the developing nervous system to produce a spectrum of neurological damage and brain malformations. Following infection of the pregnant woman, virus may indirectly or directly involve the fetus. Direct involvement is generally due to transplacental passage of the virus and invasion of fetal tissue. Resultant disease is determined by a variety of virus-host factors, including the developmental stage of the fetus at the time it is infected, the neural cell populations which are susceptible to infection, the consequent virus-infected cell interactions, and the mechanism and timing of viral clearance. There is a growing list of human viruses which injure the developing nervous system. There are also several experimental models in which congenital viral infections have been shown to result in a variety of brain malformations but with no evidence of the prior infection remaining at the time of birth.</ce:simple-para></ce:abstract-sec></ce:abstract><ce:keywords><ce:section-title>Keywords</ce:section-title><ce:keyword><ce:text>congenital viral infection</ce:text></ce:keyword><ce:keyword><ce:text>fetus</ce:text></ce:keyword><ce:keyword><ce:text>brain malformations</ce:text></ce:keyword><ce:keyword><ce:text>developing nervous system</ce:text></ce:keyword></ce:keywords></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>Viral infections of the developing nervous system</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Viral infections of the developing nervous system</title></titleInfo><name type="personal"><namePart type="given">P.K.</namePart><namePart type="family">Coyle</namePart><affiliation>From the Department of Neurology, Health Sciences Center, SUNY at Stony Brook, NY 11794, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="Full-length article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-1JC4F85T-7">research-article</genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1991</dateIssued><copyrightDate encoding="w3cdtf">1991</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><abstract lang="en">Abstract: Both clinical and experimental studies indicate that viruses can interact with the developing nervous system to produce a spectrum of neurological damage and brain malformations. Following infection of the pregnant woman, virus may indirectly or directly involve the fetus. Direct involvement is generally due to transplacental passage of the virus and invasion of fetal tissue. Resultant disease is determined by a variety of virus-host factors, including the developmental stage of the fetus at the time it is infected, the neural cell populations which are susceptible to infection, the consequent virus-infected cell interactions, and the mechanism and timing of viral clearance. There is a growing list of human viruses which injure the developing nervous system. There are also several experimental models in which congenital viral infections have been shown to result in a variety of brain malformations but with no evidence of the prior infection remaining at the time of birth.</abstract><subject><genre>Keywords</genre><topic>congenital viral infection</topic><topic>fetus</topic><topic>brain malformations</topic><topic>developing nervous system</topic></subject><relatedItem type="host"><titleInfo><title>Seminars in Neuroscience</title></titleInfo><titleInfo type="abbreviated"><title>YSMNS</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1991</dateIssued></originInfo><identifier type="ISSN">1044-5765</identifier><identifier type="PII">S1044-5765(00)X0020-6</identifier><part><date>1991</date><detail type="issue"><title>Virus-Cell Interactions in the Nervous System</title></detail><detail type="volume"><number>3</number><caption>vol.</caption></detail><detail type="issue"><number>2</number><caption>no.</caption></detail><extent unit="issue-pages"><start>81</start><end>173</end></extent><extent unit="pages"><start>157</start><end>163</end></extent></part></relatedItem><identifier type="istex">A408296B93AAA77741833F7D9ED00D0DF5922FC3</identifier><identifier type="ark">ark:/67375/6H6-K8CQTT34-R</identifier><identifier type="DOI">10.1016/1044-5765(91)90011-C</identifier><identifier type="PII">1044-5765(91)90011-C</identifier><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-HKKZVM7B-M">elsevier</recordContentSource></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-K8CQTT34-R/record.json</uri></json:item></metadata></istex></record>Pour manipuler ce document sous Unix (Dilib)
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