Murine forebrain anomalies induced by coxsackievirus B3 variants
Neonatal or 7‐day‐old mice inoculated intracranially with either of two temperature‐sensitive mutants (tsl, ts6) or the parent coxsackievirus B3 (CVB3) subsequently developed porencephaly or hydranencephaly. The forebrain anomaly induced depended upon age of the animal at inoculation and virus varia...
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| Veröffentlicht in: | Journal of medical virology 1984, Vol.14 (4), p.341-355 |
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| creator | Gauntt, C. J. Jones, D. C. Huntington, H. W. Arizpe, H. M. Gudvangen, R. J. Deshambo, R. M. |
| description | Neonatal or 7‐day‐old mice inoculated intracranially with either of two temperature‐sensitive mutants (tsl, ts6) or the parent coxsackievirus B3 (CVB3) subsequently developed porencephaly or hydranencephaly. The forebrain anomaly induced depended upon age of the animal at inoculation and virus variant inoculated. Sections of brains from hydranencephalic mice revealed severe meningeal reactions, necrotizing encephalitis, and liquifactive necrosis in the cerebrum. No pathology was found in the pons, medulla, or cerebellum. Immunofluorescence studies with hyperimmune anti‐CVB3 antiserum showed a random distribution of virus‐infected cells in the cerebrum. Virus was recovered from several organs but little to no interferon and no anti‐CVB3 neutralizing antibody were present in brain tissues. Availability of cells for replication of virus at the time of inoculation and replicative properties of each virus likely contributed to the outcome. Thus, forebrain anomalies resembling those found in infants can be induced in a murine model by select variants of coxsackievirus B3. |
| doi_str_mv | 10.1002/jmv.1890140407 |
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J. ; Jones, D. C. ; Huntington, H. W. ; Arizpe, H. M. ; Gudvangen, R. J. ; Deshambo, R. M.</creator><creatorcontrib>Gauntt, C. J. ; Jones, D. C. ; Huntington, H. W. ; Arizpe, H. M. ; Gudvangen, R. J. ; Deshambo, R. M.</creatorcontrib><description>Neonatal or 7‐day‐old mice inoculated intracranially with either of two temperature‐sensitive mutants (tsl, ts6) or the parent coxsackievirus B3 (CVB3) subsequently developed porencephaly or hydranencephaly. The forebrain anomaly induced depended upon age of the animal at inoculation and virus variant inoculated. Sections of brains from hydranencephalic mice revealed severe meningeal reactions, necrotizing encephalitis, and liquifactive necrosis in the cerebrum. No pathology was found in the pons, medulla, or cerebellum. Immunofluorescence studies with hyperimmune anti‐CVB3 antiserum showed a random distribution of virus‐infected cells in the cerebrum. Virus was recovered from several organs but little to no interferon and no anti‐CVB3 neutralizing antibody were present in brain tissues. Availability of cells for replication of virus at the time of inoculation and replicative properties of each virus likely contributed to the outcome. Thus, forebrain anomalies resembling those found in infants can be induced in a murine model by select variants of coxsackievirus B3.</description><identifier>ISSN: 0146-6615</identifier><identifier>EISSN: 1096-9071</identifier><identifier>DOI: 10.1002/jmv.1890140407</identifier><identifier>PMID: 6096503</identifier><identifier>CODEN: JMVIDB</identifier><language>eng</language><publisher>New York: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Animals ; Animals, Newborn ; Antigens, Viral - analysis ; Biological and medical sciences ; Brain - microbiology ; Brain - pathology ; coxsackievirus ; coxsackievirus B3 ; Coxsackievirus Infections - pathology ; Enterovirus B, Human - isolation & purification ; Enterovirus B, Human - pathogenicity ; Experimental viral diseases and models ; Heart - microbiology ; HeLa Cells ; Humans ; hydranencephaly ; Infectious diseases ; Liver - microbiology ; Medical sciences ; Mice ; porencephaly ; Spleen - microbiology ; Viral diseases</subject><ispartof>Journal of medical virology, 1984, Vol.14 (4), p.341-355</ispartof><rights>Copyright © 1984 Wiley‐Liss, Inc., A Wiley Company</rights><rights>1985 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5047-3e4db407ef9b6ed48f7969f8f0e63bd0c45f803872055707772de9b6b8b3b5093</citedby><cites>FETCH-LOGICAL-c5047-3e4db407ef9b6ed48f7969f8f0e63bd0c45f803872055707772de9b6b8b3b5093</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fjmv.1890140407$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fjmv.1890140407$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,4024,27923,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=9130003$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/6096503$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Gauntt, C. J.</creatorcontrib><creatorcontrib>Jones, D. C.</creatorcontrib><creatorcontrib>Huntington, H. W.</creatorcontrib><creatorcontrib>Arizpe, H. M.</creatorcontrib><creatorcontrib>Gudvangen, R. J.</creatorcontrib><creatorcontrib>Deshambo, R. M.</creatorcontrib><title>Murine forebrain anomalies induced by coxsackievirus B3 variants</title><title>Journal of medical virology</title><addtitle>J. Med. Virol</addtitle><description>Neonatal or 7‐day‐old mice inoculated intracranially with either of two temperature‐sensitive mutants (tsl, ts6) or the parent coxsackievirus B3 (CVB3) subsequently developed porencephaly or hydranencephaly. The forebrain anomaly induced depended upon age of the animal at inoculation and virus variant inoculated. Sections of brains from hydranencephalic mice revealed severe meningeal reactions, necrotizing encephalitis, and liquifactive necrosis in the cerebrum. No pathology was found in the pons, medulla, or cerebellum. Immunofluorescence studies with hyperimmune anti‐CVB3 antiserum showed a random distribution of virus‐infected cells in the cerebrum. Virus was recovered from several organs but little to no interferon and no anti‐CVB3 neutralizing antibody were present in brain tissues. Availability of cells for replication of virus at the time of inoculation and replicative properties of each virus likely contributed to the outcome. Thus, forebrain anomalies resembling those found in infants can be induced in a murine model by select variants of coxsackievirus B3.</description><subject>Animals</subject><subject>Animals, Newborn</subject><subject>Antigens, Viral - analysis</subject><subject>Biological and medical sciences</subject><subject>Brain - microbiology</subject><subject>Brain - pathology</subject><subject>coxsackievirus</subject><subject>coxsackievirus B3</subject><subject>Coxsackievirus Infections - pathology</subject><subject>Enterovirus B, Human - isolation & purification</subject><subject>Enterovirus B, Human - pathogenicity</subject><subject>Experimental viral diseases and models</subject><subject>Heart - microbiology</subject><subject>HeLa Cells</subject><subject>Humans</subject><subject>hydranencephaly</subject><subject>Infectious diseases</subject><subject>Liver - microbiology</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>porencephaly</subject><subject>Spleen - microbiology</subject><subject>Viral diseases</subject><issn>0146-6615</issn><issn>1096-9071</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1984</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkUtvGyEURlHVKnXTbrurNIuqu3EvwwDDLmmU5iEn6aIPqRsEzEUimUcCHif-98Gy5aqrrJC45_u4OhDykcKcAlRfb_vVnDYKaA01yFdkRkGJUoGkr8ks34pSCMrfkncp3QJAo6rqgByIDHFgM3J0NcUwYOHHiDaaMBRmGHvTBUxFGNrJYVvYdeHGp2TcXcBViFMqvrFiZWIwwzK9J2-86RJ-2J2H5Nf3058n5-Xi5uzi5HhROg61LBnWrc0LoldWYFs3XiqhfOMBBbMtuJr7BlgjK-BcgpSyajGjtrHMclDskHzZ9t7H8WHCtNR9SA67zgw4TklL3tCNgxfBDFWMqU3jfAu6OKYU0ev7GHoT15qC3rjV2a3-5zYHPu2aJ9tju8d3MvP8825ukjOdj2ZwIe0xRVn-gA2mtthj6HD9wqP68ur3fyuU22xIS3zaZ02800IyyfWf6zO9-CsZkz-k5uwZozCf6g</recordid><startdate>1984</startdate><enddate>1984</enddate><creator>Gauntt, C. J.</creator><creator>Jones, D. C.</creator><creator>Huntington, H. W.</creator><creator>Arizpe, H. M.</creator><creator>Gudvangen, R. J.</creator><creator>Deshambo, R. M.</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><general>Wiley-Liss</general><scope>BSCLL</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TK</scope><scope>7U9</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>1984</creationdate><title>Murine forebrain anomalies induced by coxsackievirus B3 variants</title><author>Gauntt, C. J. ; Jones, D. C. ; Huntington, H. W. ; Arizpe, H. M. ; Gudvangen, R. J. ; Deshambo, R. M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5047-3e4db407ef9b6ed48f7969f8f0e63bd0c45f803872055707772de9b6b8b3b5093</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1984</creationdate><topic>Animals</topic><topic>Animals, Newborn</topic><topic>Antigens, Viral - analysis</topic><topic>Biological and medical sciences</topic><topic>Brain - microbiology</topic><topic>Brain - pathology</topic><topic>coxsackievirus</topic><topic>coxsackievirus B3</topic><topic>Coxsackievirus Infections - pathology</topic><topic>Enterovirus B, Human - isolation & purification</topic><topic>Enterovirus B, Human - pathogenicity</topic><topic>Experimental viral diseases and models</topic><topic>Heart - microbiology</topic><topic>HeLa Cells</topic><topic>Humans</topic><topic>hydranencephaly</topic><topic>Infectious diseases</topic><topic>Liver - microbiology</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>porencephaly</topic><topic>Spleen - microbiology</topic><topic>Viral diseases</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Gauntt, C. J.</creatorcontrib><creatorcontrib>Jones, D. C.</creatorcontrib><creatorcontrib>Huntington, H. W.</creatorcontrib><creatorcontrib>Arizpe, H. M.</creatorcontrib><creatorcontrib>Gudvangen, R. J.</creatorcontrib><creatorcontrib>Deshambo, R. M.</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of medical virology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Gauntt, C. J.</au><au>Jones, D. C.</au><au>Huntington, H. W.</au><au>Arizpe, H. M.</au><au>Gudvangen, R. J.</au><au>Deshambo, R. M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Murine forebrain anomalies induced by coxsackievirus B3 variants</atitle><jtitle>Journal of medical virology</jtitle><addtitle>J. Med. Virol</addtitle><date>1984</date><risdate>1984</risdate><volume>14</volume><issue>4</issue><spage>341</spage><epage>355</epage><pages>341-355</pages><issn>0146-6615</issn><eissn>1096-9071</eissn><coden>JMVIDB</coden><abstract>Neonatal or 7‐day‐old mice inoculated intracranially with either of two temperature‐sensitive mutants (tsl, ts6) or the parent coxsackievirus B3 (CVB3) subsequently developed porencephaly or hydranencephaly. The forebrain anomaly induced depended upon age of the animal at inoculation and virus variant inoculated. Sections of brains from hydranencephalic mice revealed severe meningeal reactions, necrotizing encephalitis, and liquifactive necrosis in the cerebrum. No pathology was found in the pons, medulla, or cerebellum. Immunofluorescence studies with hyperimmune anti‐CVB3 antiserum showed a random distribution of virus‐infected cells in the cerebrum. Virus was recovered from several organs but little to no interferon and no anti‐CVB3 neutralizing antibody were present in brain tissues. Availability of cells for replication of virus at the time of inoculation and replicative properties of each virus likely contributed to the outcome. Thus, forebrain anomalies resembling those found in infants can be induced in a murine model by select variants of coxsackievirus B3.</abstract><cop>New York</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>6096503</pmid><doi>10.1002/jmv.1890140407</doi><tpages>15</tpages></addata></record> |
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| subjects | Animals Animals, Newborn Antigens, Viral - analysis Biological and medical sciences Brain - microbiology Brain - pathology coxsackievirus coxsackievirus B3 Coxsackievirus Infections - pathology Enterovirus B, Human - isolation & purification Enterovirus B, Human - pathogenicity Experimental viral diseases and models Heart - microbiology HeLa Cells Humans hydranencephaly Infectious diseases Liver - microbiology Medical sciences Mice porencephaly Spleen - microbiology Viral diseases |
| title | Murine forebrain anomalies induced by coxsackievirus B3 variants |
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