Viral infections of the developing nervous system
Identifieur interne : 001409 ( Main/Exploration ); précédent : 001408; suivant : 001410Viral infections of the developing nervous system
Auteurs : P. K. Coyle [États-Unis]Source :
- 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
Affiliations:
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Le document en format XML
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K." last="Coyle">P. K. Coyle</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>From the Department of Neurology, Health Sciences Center, SUNY at Stony Brook, NY 11794</wicri:regionArea><placeName><region type="state">État de New York</region></placeName></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><affiliations><list><country><li>États-Unis</li></country><region><li>État de New York</li></region></list><tree><country name="États-Unis"><region name="État de New York"><name sortKey="Coyle, P K" sort="Coyle, P K" uniqKey="Coyle P" first="P. K." last="Coyle">P. K. Coyle</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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