Severe acute respiratory syndrome coronavirus infection causes neuronal death in the absence of encephalitis in mice transgenic for human ACE2.
Identifieur interne : 001C65 ( Ncbi/Merge ); précédent : 001C64; suivant : 001C66Severe acute respiratory syndrome coronavirus infection causes neuronal death in the absence of encephalitis in mice transgenic for human ACE2.
Auteurs : Jason Netland [États-Unis] ; David K. Meyerholz ; Steven Moore ; Martin Cassell ; Stanley PerlmanSource :
- Journal of virology [ 1098-5514 ] ; 2008.
Descripteurs français
- KwdFr :
- Animaux, Bulbe olfactif (anatomopathologie), Bulbe olfactif (virologie), Encéphale (anatomopathologie), Encéphale (virologie), Humains, Mort cellulaire, Neurones (virologie), Peptidyl-Dipeptidase A (génétique), Peptidyl-Dipeptidase A (physiologie), Poumon (anatomopathologie), Récepteurs viraux (génétique), Récepteurs viraux (physiologie), Souris, Souris de lignée C57BL, Souris transgéniques, Syndrome respiratoire aigu sévère (anatomopathologie), Virus du SRAS (pathogénicité).
- MESH :
- anatomopathologie : Bulbe olfactif, Encéphale, Poumon, Syndrome respiratoire aigu sévère.
- génétique : Peptidyl-Dipeptidase A, Récepteurs viraux.
- pathogénicité : Virus du SRAS.
- physiologie : Peptidyl-Dipeptidase A, Récepteurs viraux.
- virologie : Bulbe olfactif, Encéphale, Neurones.
- Animaux, Humains, Mort cellulaire, Souris, Souris de lignée C57BL, Souris transgéniques.
English descriptors
- KwdEn :
- Animals, Brain (pathology), Brain (virology), Cell Death, Humans, Lung (pathology), Mice, Mice, Inbred C57BL, Mice, Transgenic, Neurons (virology), Olfactory Bulb (pathology), Olfactory Bulb (virology), Peptidyl-Dipeptidase A (genetics), Peptidyl-Dipeptidase A (physiology), Receptors, Virus (genetics), Receptors, Virus (physiology), SARS Virus (pathogenicity), Severe Acute Respiratory Syndrome (pathology).
- MESH :
- chemical , genetics : Peptidyl-Dipeptidase A, Receptors, Virus.
- pathogenicity : SARS Virus.
- pathology : Brain, Lung, Olfactory Bulb, Severe Acute Respiratory Syndrome.
- chemical , physiology : Peptidyl-Dipeptidase A, Receptors, Virus.
- virology : Brain, Neurons, Olfactory Bulb.
- Animals, Cell Death, Humans, Mice, Mice, Inbred C57BL, Mice, Transgenic.
Abstract
Infection of humans with the severe acute respiratory syndrome coronavirus (SARS-CoV) results in substantial morbidity and mortality, with death resulting primarily from respiratory failure. While the lungs are the major site of infection, the brain is also infected in some patients. Brain infection may result in long-term neurological sequelae, but little is known about the pathogenesis of SARS-CoV in this organ. We previously showed that the brain was a major target organ for infection in mice that are transgenic for the SARS-CoV receptor (human angiotensin-converting enzyme 2). Herein, we use these mice to show that virus enters the brain primarily via the olfactory bulb, and infection results in rapid, transneuronal spread to connected areas of the brain. This extensive neuronal infection is the main cause of death because intracranial inoculation with low doses of virus results in a uniformly lethal disease even though little infection is detected in the lungs. Death of the animal likely results from dysfunction and/or death of infected neurons, especially those located in cardiorespiratory centers in the medulla. Remarkably, the virus induces minimal cellular infiltration in the brain. Our results show that neurons are a highly susceptible target for SARS-CoV and that only the absence of the host cell receptor prevents severe murine brain disease.
DOI: 10.1128/JVI.00737-08
PubMed: 18495771
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pubmed:18495771Le document en format XML
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Meyerholz</name></author><author><name sortKey="Moore, Steven" sort="Moore, Steven" uniqKey="Moore S" first="Steven" last="Moore">Steven Moore</name></author><author><name sortKey="Cassell, Martin" sort="Cassell, Martin" uniqKey="Cassell M" first="Martin" last="Cassell">Martin Cassell</name></author><author><name sortKey="Perlman, Stanley" sort="Perlman, Stanley" uniqKey="Perlman S" first="Stanley" last="Perlman">Stanley Perlman</name></author></analytic><series><title level="j">Journal of virology</title><idno type="eISSN">1098-5514</idno><imprint><date when="2008" type="published">2008</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Brain (pathology)</term><term>Brain (virology)</term><term>Cell Death</term><term>Humans</term><term>Lung (pathology)</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Mice, Transgenic</term><term>Neurons (virology)</term><term>Olfactory Bulb (pathology)</term><term>Olfactory Bulb (virology)</term><term>Peptidyl-Dipeptidase A (genetics)</term><term>Peptidyl-Dipeptidase A (physiology)</term><term>Receptors, Virus (genetics)</term><term>Receptors, Virus (physiology)</term><term>SARS Virus (pathogenicity)</term><term>Severe Acute Respiratory Syndrome (pathology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Bulbe olfactif (anatomopathologie)</term><term>Bulbe olfactif (virologie)</term><term>Encéphale (anatomopathologie)</term><term>Encéphale (virologie)</term><term>Humains</term><term>Mort cellulaire</term><term>Neurones (virologie)</term><term>Peptidyl-Dipeptidase A (génétique)</term><term>Peptidyl-Dipeptidase A (physiologie)</term><term>Poumon (anatomopathologie)</term><term>Récepteurs viraux (génétique)</term><term>Récepteurs viraux (physiologie)</term><term>Souris</term><term>Souris de lignée C57BL</term><term>Souris transgéniques</term><term>Syndrome respiratoire aigu sévère (anatomopathologie)</term><term>Virus du SRAS (pathogénicité)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Peptidyl-Dipeptidase A</term><term>Receptors, Virus</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Bulbe olfactif</term><term>Encéphale</term><term>Poumon</term><term>Syndrome respiratoire aigu sévère</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Peptidyl-Dipeptidase A</term><term>Récepteurs viraux</term></keywords><keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>SARS Virus</term></keywords><keywords scheme="MESH" qualifier="pathogénicité" xml:lang="fr"><term>Virus du SRAS</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Brain</term><term>Lung</term><term>Olfactory Bulb</term><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Peptidyl-Dipeptidase A</term><term>Récepteurs viraux</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Peptidyl-Dipeptidase A</term><term>Receptors, Virus</term></keywords><keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Bulbe olfactif</term><term>Encéphale</term><term>Neurones</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Brain</term><term>Neurons</term><term>Olfactory Bulb</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cell Death</term><term>Humans</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Mice, Transgenic</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Humains</term><term>Mort cellulaire</term><term>Souris</term><term>Souris de lignée C57BL</term><term>Souris transgéniques</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Infection of humans with the severe acute respiratory syndrome coronavirus (SARS-CoV) results in substantial morbidity and mortality, with death resulting primarily from respiratory failure. While the lungs are the major site of infection, the brain is also infected in some patients. Brain infection may result in long-term neurological sequelae, but little is known about the pathogenesis of SARS-CoV in this organ. We previously showed that the brain was a major target organ for infection in mice that are transgenic for the SARS-CoV receptor (human angiotensin-converting enzyme 2). Herein, we use these mice to show that virus enters the brain primarily via the olfactory bulb, and infection results in rapid, transneuronal spread to connected areas of the brain. This extensive neuronal infection is the main cause of death because intracranial inoculation with low doses of virus results in a uniformly lethal disease even though little infection is detected in the lungs. Death of the animal likely results from dysfunction and/or death of infected neurons, especially those located in cardiorespiratory centers in the medulla. Remarkably, the virus induces minimal cellular infiltration in the brain. Our results show that neurons are a highly susceptible target for SARS-CoV and that only the absence of the host cell receptor prevents severe murine brain disease.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">18495771</PMID><DateCompleted><Year>2008</Year><Month>08</Month><Day>01</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1098-5514</ISSN><JournalIssue CitedMedium="Internet"><Volume>82</Volume><Issue>15</Issue><PubDate><Year>2008</Year><Month>Aug</Month></PubDate></JournalIssue><Title>Journal of virology</Title><ISOAbbreviation>J. Virol.</ISOAbbreviation></Journal><ArticleTitle>Severe acute respiratory syndrome coronavirus infection causes neuronal death in the absence of encephalitis in mice transgenic for human ACE2.</ArticleTitle><Pagination><MedlinePgn>7264-75</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1128/JVI.00737-08</ELocationID><Abstract><AbstractText>Infection of humans with the severe acute respiratory syndrome coronavirus (SARS-CoV) results in substantial morbidity and mortality, with death resulting primarily from respiratory failure. While the lungs are the major site of infection, the brain is also infected in some patients. Brain infection may result in long-term neurological sequelae, but little is known about the pathogenesis of SARS-CoV in this organ. We previously showed that the brain was a major target organ for infection in mice that are transgenic for the SARS-CoV receptor (human angiotensin-converting enzyme 2). Herein, we use these mice to show that virus enters the brain primarily via the olfactory bulb, and infection results in rapid, transneuronal spread to connected areas of the brain. This extensive neuronal infection is the main cause of death because intracranial inoculation with low doses of virus results in a uniformly lethal disease even though little infection is detected in the lungs. Death of the animal likely results from dysfunction and/or death of infected neurons, especially those located in cardiorespiratory centers in the medulla. Remarkably, the virus induces minimal cellular infiltration in the brain. Our results show that neurons are a highly susceptible target for SARS-CoV and that only the absence of the host cell receptor prevents severe murine brain disease.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Netland</LastName><ForeName>Jason</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Interdisciplinary Program in Immunology, University of Iowa,Iowa City, IA 52242, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Meyerholz</LastName><ForeName>David K</ForeName><Initials>DK</Initials></Author><Author ValidYN="Y"><LastName>Moore</LastName><ForeName>Steven</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Cassell</LastName><ForeName>Martin</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Perlman</LastName><ForeName>Stanley</ForeName><Initials>S</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>P01 AI060699</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>T32 AI007533</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2008</Year><Month>05</Month><Day>21</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Virol</MedlineTA><NlmUniqueID>0113724</NlmUniqueID><ISSNLinking>0022-538X</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D011991">Receptors, Virus</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.4.15.1</RegistryNumber><NameOfSubstance UI="D007703">Peptidyl-Dipeptidase 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K" sort="Meyerholz, David K" uniqKey="Meyerholz D" first="David K" last="Meyerholz">David K. Meyerholz</name><name sortKey="Moore, Steven" sort="Moore, Steven" uniqKey="Moore S" first="Steven" last="Moore">Steven Moore</name><name sortKey="Perlman, Stanley" sort="Perlman, Stanley" uniqKey="Perlman S" first="Stanley" last="Perlman">Stanley Perlman</name></noCountry><country name="États-Unis"><region name="Iowa"><name sortKey="Netland, Jason" sort="Netland, Jason" uniqKey="Netland J" first="Jason" last="Netland">Jason Netland</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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