Congenital viral infections of the brain: lessons learned from lymphocytic choriomeningitis virus in the neonatal rat.

The fetal brain is highly vulnerable to teratogens, including many infectious agents. As a consequence of prenatal infection, many children suffer severe and permanent brain injury and dysfunction. Because most animal models of congenital brain infection do not strongly mirror human disease, the mod...

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Autores principales:	Daniel J Bonthius, Stanley Perlman
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2007
Materias:	Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/ff2855801fd1490d9cbca1f9a553b991
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spelling	oai:doaj.org-article:ff2855801fd1490d9cbca1f9a553b9912021-11-25T05:46:49ZCongenital viral infections of the brain: lessons learned from lymphocytic choriomeningitis virus in the neonatal rat.1553-73661553-737410.1371/journal.ppat.0030149https://doaj.org/article/ff2855801fd1490d9cbca1f9a553b9912007-11-01T00:00:00Zhttps://doi.org/10.1371/journal.ppat.0030149https://doaj.org/toc/1553-7366https://doaj.org/toc/1553-7374The fetal brain is highly vulnerable to teratogens, including many infectious agents. As a consequence of prenatal infection, many children suffer severe and permanent brain injury and dysfunction. Because most animal models of congenital brain infection do not strongly mirror human disease, the models are highly limited in their abilities to shed light on the pathogenesis of these diseases. The animal model for congenital lymphocytic choriomeningitis virus (LCMV) infection, however, does not suffer from this limitation. LCMV is a well-known human pathogen. When the infection occurs during pregnancy, the virus can infect the fetus, and the developing brain is particularly vulnerable. Children with congenital LCMV infection often have substantial neurological deficits. The neonatal rat inoculated with LCMV is a superb model system of human congenital LCMV infection. Virtually all of the neuropathologic changes observed in humans congenitally infected with LCMV, including microencephaly, encephalomalacia, chorioretinitis, porencephalic cysts, neuronal migration disturbances, periventricular infection, and cerebellar hypoplasia, are reproduced in the rat model. Within the developing rat brain, LCMV selectively targets mitotically active neuronal precursors. Thus, the targets of infection and sites of pathology depend on host age at the time of infection. The rat model has further shown that the pathogenic changes induced by LCMV infection are both virus-mediated and immune-mediated. Furthermore, different brain regions simultaneously infected with LCMV can undergo widely different pathologic changes, reflecting different brain region-virus-immune system interactions. Because the neonatal rat inoculated with LCMV so faithfully reproduces the diverse neuropathology observed in the human counterpart, the rat model system is a highly valuable tool for the study of congenital LCMV infection and of all prenatal brain infections In addition, because LCMV induces delayed-onset neuronal loss after the virus has been cleared, the neonatal rat infected with LCMV may be an excellent model system to study neurodegenerative or psychiatric diseases whose etiologies are hypothesized to be virus-induced, such as autism, schizophrenia, and temporal lobe epilepsy.Daniel J BonthiusStanley PerlmanPublic Library of Science (PLoS)articleImmunologic diseases. AllergyRC581-607Biology (General)QH301-705.5ENPLoS Pathogens, Vol 3, Iss 11, p e149 (2007)
institution	DOAJ
collection	DOAJ
language	EN
topic	Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5
spellingShingle	Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5 Daniel J Bonthius Stanley Perlman Congenital viral infections of the brain: lessons learned from lymphocytic choriomeningitis virus in the neonatal rat.
description	The fetal brain is highly vulnerable to teratogens, including many infectious agents. As a consequence of prenatal infection, many children suffer severe and permanent brain injury and dysfunction. Because most animal models of congenital brain infection do not strongly mirror human disease, the models are highly limited in their abilities to shed light on the pathogenesis of these diseases. The animal model for congenital lymphocytic choriomeningitis virus (LCMV) infection, however, does not suffer from this limitation. LCMV is a well-known human pathogen. When the infection occurs during pregnancy, the virus can infect the fetus, and the developing brain is particularly vulnerable. Children with congenital LCMV infection often have substantial neurological deficits. The neonatal rat inoculated with LCMV is a superb model system of human congenital LCMV infection. Virtually all of the neuropathologic changes observed in humans congenitally infected with LCMV, including microencephaly, encephalomalacia, chorioretinitis, porencephalic cysts, neuronal migration disturbances, periventricular infection, and cerebellar hypoplasia, are reproduced in the rat model. Within the developing rat brain, LCMV selectively targets mitotically active neuronal precursors. Thus, the targets of infection and sites of pathology depend on host age at the time of infection. The rat model has further shown that the pathogenic changes induced by LCMV infection are both virus-mediated and immune-mediated. Furthermore, different brain regions simultaneously infected with LCMV can undergo widely different pathologic changes, reflecting different brain region-virus-immune system interactions. Because the neonatal rat inoculated with LCMV so faithfully reproduces the diverse neuropathology observed in the human counterpart, the rat model system is a highly valuable tool for the study of congenital LCMV infection and of all prenatal brain infections In addition, because LCMV induces delayed-onset neuronal loss after the virus has been cleared, the neonatal rat infected with LCMV may be an excellent model system to study neurodegenerative or psychiatric diseases whose etiologies are hypothesized to be virus-induced, such as autism, schizophrenia, and temporal lobe epilepsy.
format	article
author	Daniel J Bonthius Stanley Perlman
author_facet	Daniel J Bonthius Stanley Perlman
author_sort	Daniel J Bonthius
title	Congenital viral infections of the brain: lessons learned from lymphocytic choriomeningitis virus in the neonatal rat.
title_short	Congenital viral infections of the brain: lessons learned from lymphocytic choriomeningitis virus in the neonatal rat.
title_full	Congenital viral infections of the brain: lessons learned from lymphocytic choriomeningitis virus in the neonatal rat.
title_fullStr	Congenital viral infections of the brain: lessons learned from lymphocytic choriomeningitis virus in the neonatal rat.
title_full_unstemmed	Congenital viral infections of the brain: lessons learned from lymphocytic choriomeningitis virus in the neonatal rat.
title_sort	congenital viral infections of the brain: lessons learned from lymphocytic choriomeningitis virus in the neonatal rat.
publisher	Public Library of Science (PLoS)
publishDate	2007
url	https://doaj.org/article/ff2855801fd1490d9cbca1f9a553b991
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Congenital viral infections of the brain: lessons learned from lymphocytic choriomeningitis virus in the neonatal rat.

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