Measles Virus Replication in Lymphatic Cells and Organs of CD150 (SLAM) Transgenic Mice
A transgenic mouse containing the complete human SLAM (hSLAM/CD150) gene, including its endogenous promoter for transcription, was generated by using human genomic DNA cloned into a bacterial artificial chromosome. hSLAM, the primary receptor for measles viruses (MV), was expressed on activated B, T...
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| Veröffentlicht in: | Proceedings of the National Academy of Sciences - PNAS 2005-11, Vol.102 (45), p.16415-16420 |
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| container_title | Proceedings of the National Academy of Sciences - PNAS |
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| creator | G. Grant Welstead Caterina Iorio Ryan Draker Jane Bayani Squire, Jeremy Sompong Vongpunsawad Cattaneo, Roberto Richardson, Christopher D. |
| description | A transgenic mouse containing the complete human SLAM (hSLAM/CD150) gene, including its endogenous promoter for transcription, was generated by using human genomic DNA cloned into a bacterial artificial chromosome. hSLAM, the primary receptor for measles viruses (MV), was expressed on activated B, T, and dendritic cells with an expression profile equivalent to that of humans. We demonstrated that$hSLAM^+$cells obtained from the transgenic mouse, including activated B, T, and dendritic cells, were susceptible to MV infection in a receptor-dependent manner. Evidence was provided for transient infection in the nasal lymph nodes of$hSLAM^+$mice after intranasal inoculation. Virus was rapidly cleared without signs of secondary replication. To improve the efficiency of MV production, the$hSLAM^+$mice were bred with mice having a Stat7-deficient background. These mice were more susceptible to MV infection and produced more virus particles. After intranasal and intraperitoneal inoculation of these mice with MV, infections of the thymus, spleen, nasal, mesenteric, and leg lymph nodes were detected. Upon necropsy, enlarged lymph nodes and spleen were apparent. Flow cytometric analysis showed that abnormally large numbers of mature neutrophils and natural killer cells caused the splenomegaly. The hSLAM transgenic mouse constitutes an improved rodent model for studying the interaction of MV with immune cells that more accurately reflects the infection pattern found in humans. |
| doi_str_mv | 10.1073/pnas.0505945102 |
| format | Article |
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Grant Welstead ; Caterina Iorio ; Ryan Draker ; Jane Bayani ; Squire, Jeremy ; Sompong Vongpunsawad ; Cattaneo, Roberto ; Richardson, Christopher D.</creator><creatorcontrib>G. Grant Welstead ; Caterina Iorio ; Ryan Draker ; Jane Bayani ; Squire, Jeremy ; Sompong Vongpunsawad ; Cattaneo, Roberto ; Richardson, Christopher D.</creatorcontrib><description>A transgenic mouse containing the complete human SLAM (hSLAM/CD150) gene, including its endogenous promoter for transcription, was generated by using human genomic DNA cloned into a bacterial artificial chromosome. hSLAM, the primary receptor for measles viruses (MV), was expressed on activated B, T, and dendritic cells with an expression profile equivalent to that of humans. We demonstrated that$hSLAM^+$cells obtained from the transgenic mouse, including activated B, T, and dendritic cells, were susceptible to MV infection in a receptor-dependent manner. Evidence was provided for transient infection in the nasal lymph nodes of$hSLAM^+$mice after intranasal inoculation. Virus was rapidly cleared without signs of secondary replication. To improve the efficiency of MV production, the$hSLAM^+$mice were bred with mice having a Stat7-deficient background. These mice were more susceptible to MV infection and produced more virus particles. After intranasal and intraperitoneal inoculation of these mice with MV, infections of the thymus, spleen, nasal, mesenteric, and leg lymph nodes were detected. Upon necropsy, enlarged lymph nodes and spleen were apparent. Flow cytometric analysis showed that abnormally large numbers of mature neutrophils and natural killer cells caused the splenomegaly. The hSLAM transgenic mouse constitutes an improved rodent model for studying the interaction of MV with immune cells that more accurately reflects the infection pattern found in humans.</description><identifier>ISSN: 0027-8424</identifier><identifier>EISSN: 1091-6490</identifier><identifier>DOI: 10.1073/pnas.0505945102</identifier><identifier>PMID: 16260741</identifier><language>eng</language><publisher>United States: National Academy of Sciences</publisher><subject>Animals ; Antigens, CD ; B lymphocytes ; Biological Sciences ; Dendritic cells ; Genes ; Glycoproteins - genetics ; Glycoproteins - physiology ; Immunoglobulins - genetics ; Immunoglobulins - physiology ; Infections ; Lymph nodes ; Lymphatic system ; Lymphocytes - virology ; Measles ; Measles virus ; Measles virus - immunology ; Measles virus - physiology ; Membrane Cofactor Protein - physiology ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Microbiology ; Receptors ; Receptors, Cell Surface ; Signaling Lymphocytic Activation Molecule Family Member 1 ; Spleen ; STAT1 Transcription Factor - physiology ; T lymphocytes ; Transgenic animals ; Virus Replication ; Viruses</subject><ispartof>Proceedings of the National Academy of Sciences - PNAS, 2005-11, Vol.102 (45), p.16415-16420</ispartof><rights>Copyright 2005 National Academy of Sciences of the United States of America</rights><rights>Copyright National Academy of Sciences Nov 8, 2005</rights><rights>Copyright © 2005, The National Academy of Sciences 2005</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c595t-5c0894b4d51b16cac2e1fa065e6699ec03a43b5e2e12a9121b26b08bc8d2aec23</citedby><cites>FETCH-LOGICAL-c595t-5c0894b4d51b16cac2e1fa065e6699ec03a43b5e2e12a9121b26b08bc8d2aec23</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://www.pnas.org/content/102/45.cover.gif</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/4152440$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/4152440$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>230,314,723,776,780,799,881,27901,27902,53766,53768,57992,58225</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16260741$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>G. Grant Welstead</creatorcontrib><creatorcontrib>Caterina Iorio</creatorcontrib><creatorcontrib>Ryan Draker</creatorcontrib><creatorcontrib>Jane Bayani</creatorcontrib><creatorcontrib>Squire, Jeremy</creatorcontrib><creatorcontrib>Sompong Vongpunsawad</creatorcontrib><creatorcontrib>Cattaneo, Roberto</creatorcontrib><creatorcontrib>Richardson, Christopher D.</creatorcontrib><title>Measles Virus Replication in Lymphatic Cells and Organs of CD150 (SLAM) Transgenic Mice</title><title>Proceedings of the National Academy of Sciences - PNAS</title><addtitle>Proc Natl Acad Sci U S A</addtitle><description>A transgenic mouse containing the complete human SLAM (hSLAM/CD150) gene, including its endogenous promoter for transcription, was generated by using human genomic DNA cloned into a bacterial artificial chromosome. hSLAM, the primary receptor for measles viruses (MV), was expressed on activated B, T, and dendritic cells with an expression profile equivalent to that of humans. We demonstrated that$hSLAM^+$cells obtained from the transgenic mouse, including activated B, T, and dendritic cells, were susceptible to MV infection in a receptor-dependent manner. Evidence was provided for transient infection in the nasal lymph nodes of$hSLAM^+$mice after intranasal inoculation. Virus was rapidly cleared without signs of secondary replication. To improve the efficiency of MV production, the$hSLAM^+$mice were bred with mice having a Stat7-deficient background. These mice were more susceptible to MV infection and produced more virus particles. After intranasal and intraperitoneal inoculation of these mice with MV, infections of the thymus, spleen, nasal, mesenteric, and leg lymph nodes were detected. Upon necropsy, enlarged lymph nodes and spleen were apparent. Flow cytometric analysis showed that abnormally large numbers of mature neutrophils and natural killer cells caused the splenomegaly. The hSLAM transgenic mouse constitutes an improved rodent model for studying the interaction of MV with immune cells that more accurately reflects the infection pattern found in humans.</description><subject>Animals</subject><subject>Antigens, CD</subject><subject>B lymphocytes</subject><subject>Biological Sciences</subject><subject>Dendritic cells</subject><subject>Genes</subject><subject>Glycoproteins - genetics</subject><subject>Glycoproteins - physiology</subject><subject>Immunoglobulins - genetics</subject><subject>Immunoglobulins - physiology</subject><subject>Infections</subject><subject>Lymph nodes</subject><subject>Lymphatic system</subject><subject>Lymphocytes - virology</subject><subject>Measles</subject><subject>Measles virus</subject><subject>Measles virus - immunology</subject><subject>Measles virus - physiology</subject><subject>Membrane Cofactor Protein - physiology</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Transgenic</subject><subject>Microbiology</subject><subject>Receptors</subject><subject>Receptors, Cell Surface</subject><subject>Signaling Lymphocytic Activation Molecule Family Member 1</subject><subject>Spleen</subject><subject>STAT1 Transcription Factor - physiology</subject><subject>T lymphocytes</subject><subject>Transgenic animals</subject><subject>Virus Replication</subject><subject>Viruses</subject><issn>0027-8424</issn><issn>1091-6490</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqF0c9v0zAUB3ALgVgZnLkgZO0wsUO29xzbiS9IUxk_pFaTYMDRclynS5U6wU4Q--_nqNUKXHaybH_eV35-hLxGOEco8ovem3gOAoTiAoE9ITMEhZnkCp6SGQArspIzfkRexLgBACVKeE6OUDIJBccZ-bl0JrYu0h9NGCP96vq2sWZoOk8bTxd32_427Sydu7aN1PgVvQ5r4yPtajr_gALou2-Ly-UZvQnpdO18ssvGupfkWW3a6F7t12Py_ePVzfxztrj-9GV-ucisUGLIhIVS8YqvBFYorbHMYW1ACielUs5CbnheCZeOmVHIsGKygrKy5YoZZ1l-TN7vcvux2rqVdX4IptV9aLYm3OnONPrfG9_c6nX3WyMrc55PAaf7gND9Gl0c9LaJNnVrvOvGqGVZFIIp9ShEVXLkChM8-Q9uujH49AuaAeaykGJKu9ghG7oYg6sfnoygp9HqabT6MNpU8fbvTg9-P8sE6B5MlYc4prlIiqNI5OwRouuxbQf3Z0j2zc5u4tCFB5wM4xzye8U3v8E</recordid><startdate>20051108</startdate><enddate>20051108</enddate><creator>G. 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Grant Welstead</au><au>Caterina Iorio</au><au>Ryan Draker</au><au>Jane Bayani</au><au>Squire, Jeremy</au><au>Sompong Vongpunsawad</au><au>Cattaneo, Roberto</au><au>Richardson, Christopher D.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Measles Virus Replication in Lymphatic Cells and Organs of CD150 (SLAM) Transgenic Mice</atitle><jtitle>Proceedings of the National Academy of Sciences - PNAS</jtitle><addtitle>Proc Natl Acad Sci U S A</addtitle><date>2005-11-08</date><risdate>2005</risdate><volume>102</volume><issue>45</issue><spage>16415</spage><epage>16420</epage><pages>16415-16420</pages><issn>0027-8424</issn><eissn>1091-6490</eissn><abstract>A transgenic mouse containing the complete human SLAM (hSLAM/CD150) gene, including its endogenous promoter for transcription, was generated by using human genomic DNA cloned into a bacterial artificial chromosome. hSLAM, the primary receptor for measles viruses (MV), was expressed on activated B, T, and dendritic cells with an expression profile equivalent to that of humans. We demonstrated that$hSLAM^+$cells obtained from the transgenic mouse, including activated B, T, and dendritic cells, were susceptible to MV infection in a receptor-dependent manner. Evidence was provided for transient infection in the nasal lymph nodes of$hSLAM^+$mice after intranasal inoculation. Virus was rapidly cleared without signs of secondary replication. To improve the efficiency of MV production, the$hSLAM^+$mice were bred with mice having a Stat7-deficient background. These mice were more susceptible to MV infection and produced more virus particles. After intranasal and intraperitoneal inoculation of these mice with MV, infections of the thymus, spleen, nasal, mesenteric, and leg lymph nodes were detected. Upon necropsy, enlarged lymph nodes and spleen were apparent. Flow cytometric analysis showed that abnormally large numbers of mature neutrophils and natural killer cells caused the splenomegaly. The hSLAM transgenic mouse constitutes an improved rodent model for studying the interaction of MV with immune cells that more accurately reflects the infection pattern found in humans.</abstract><cop>United States</cop><pub>National Academy of Sciences</pub><pmid>16260741</pmid><doi>10.1073/pnas.0505945102</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Antigens, CD B lymphocytes Biological Sciences Dendritic cells Genes Glycoproteins - genetics Glycoproteins - physiology Immunoglobulins - genetics Immunoglobulins - physiology Infections Lymph nodes Lymphatic system Lymphocytes - virology Measles Measles virus Measles virus - immunology Measles virus - physiology Membrane Cofactor Protein - physiology Mice Mice, Inbred C57BL Mice, Transgenic Microbiology Receptors Receptors, Cell Surface Signaling Lymphocytic Activation Molecule Family Member 1 Spleen STAT1 Transcription Factor - physiology T lymphocytes Transgenic animals Virus Replication Viruses |
| title | Measles Virus Replication in Lymphatic Cells and Organs of CD150 (SLAM) Transgenic Mice |
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