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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Molecular basis of reovirus virulence: Role of the S1 gene</title><author><name sortKey="Weiner, Howard L" sort="Weiner, Howard L" uniqKey="Weiner H" first="Howard L." last="Weiner">Howard L. Weiner</name><affiliation><nlm:aff id="af1">Department of Microbiology and Molecular Genetics, Harvard Medical School, Boston, Massachusetts 02115</nlm:aff></affiliation><affiliation><nlm:aff id="af2">Department of Medicine, Sections of Neurology and Infectious Diseases, Peter Bent Brigham Hospital, Boston, Massachusetts 02115</nlm:aff></affiliation></author><author><name sortKey="Drayna, Dennis" sort="Drayna, Dennis" uniqKey="Drayna D" first="Dennis" last="Drayna">Dennis Drayna</name><affiliation><nlm:aff id="af1">Department of Microbiology and Molecular Genetics, Harvard Medical School, Boston, Massachusetts 02115</nlm:aff></affiliation></author><author><name sortKey="Averill, Damon R" sort="Averill, Damon R" uniqKey="Averill D" first="Damon R." last="Averill">Damon R. Averill</name><affiliation><nlm:aff id="af3">Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115</nlm:aff></affiliation></author><author><name sortKey="Fields, Bernard N" sort="Fields, Bernard N" uniqKey="Fields B" first="Bernard N." last="Fields">Bernard N. Fields</name><affiliation><nlm:aff id="af1">Department of Microbiology and Molecular Genetics, Harvard Medical School, Boston, Massachusetts 02115</nlm:aff></affiliation><affiliation><nlm:aff id="af2">Department of Medicine, Sections of Neurology and Infectious Diseases, Peter Bent Brigham Hospital, Boston, Massachusetts 02115</nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">271999</idno><idno type="pmc">431870</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC431870</idno><idno type="RBID">PMC:431870</idno><date when="1977">1977</date><idno type="wicri:Area/Pmc/Corpus">000440</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000440</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Molecular basis of reovirus virulence: Role of the S1 gene</title><author><name sortKey="Weiner, Howard L" sort="Weiner, Howard L" uniqKey="Weiner H" first="Howard L." last="Weiner">Howard L. Weiner</name><affiliation><nlm:aff id="af1">Department of Microbiology and Molecular Genetics, Harvard Medical School, Boston, Massachusetts 02115</nlm:aff></affiliation><affiliation><nlm:aff id="af2">Department of Medicine, Sections of Neurology and Infectious Diseases, Peter Bent Brigham Hospital, Boston, Massachusetts 02115</nlm:aff></affiliation></author><author><name sortKey="Drayna, Dennis" sort="Drayna, Dennis" uniqKey="Drayna D" first="Dennis" last="Drayna">Dennis Drayna</name><affiliation><nlm:aff id="af1">Department of Microbiology and Molecular Genetics, Harvard Medical School, Boston, Massachusetts 02115</nlm:aff></affiliation></author><author><name sortKey="Averill, Damon R" sort="Averill, Damon R" uniqKey="Averill D" first="Damon R." last="Averill">Damon R. Averill</name><affiliation><nlm:aff id="af3">Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115</nlm:aff></affiliation></author><author><name sortKey="Fields, Bernard N" sort="Fields, Bernard N" uniqKey="Fields B" first="Bernard N." last="Fields">Bernard N. Fields</name><affiliation><nlm:aff id="af1">Department of Microbiology and Molecular Genetics, Harvard Medical School, Boston, Massachusetts 02115</nlm:aff></affiliation><affiliation><nlm:aff id="af2">Department of Medicine, Sections of Neurology and Infectious Diseases, Peter Bent Brigham Hospital, Boston, Massachusetts 02115</nlm:aff></affiliation></author></analytic><series><title level="j">Proceedings of the National Academy of Sciences of the United States of America</title><idno type="ISSN">0027-8424</idno><idno type="eISSN">1091-6490</idno><imprint><date when="1977">1977</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>A genetic approach has been used to define the molecular basis for the different patterns of virulence and central nervous system cell tropism exhibited by reovirus types 1 and 3. Intracerebral inoculation of reovirus type 3 into newborn mice causes a necrotizing encephalitis (without ependymal damage) that is uniformly fatal. Animal inoculated with reovirus type 1 generally survive and may develop epedymal cell damage (without neuronal necrosis) and hydrocephalus. Using recombinant clones derived from crosses between reovirus types 1 and 3, we have been able to determine that the S1 genome segment is responsible for the differing cell tropism of reovirus serotypes and is the major determinant of neurovirulence. The type 1 S1 genome segment is responsible for ependymal damage with subsequent hydrocephalus; the type 3 S1 genome segment is responsible for neuronal necrosis and neurovirulence. We postulate that these differences are due to the specific interaction of the σ1 outer capsid polypeptide (the protein coded for by the S1 genome segment) with receptors on the surface of either ependymal cells or neuronal cells.</p><sec sec-type="scanned-figures"><title>Images</title><fig id="F1"><graphic xlink:href="pnas00043-0553-a" xlink:role="5745"></graphic></fig><fig id="F2"><graphic xlink:href="pnas00043-0556-a" xlink:role="5748"></graphic></fig></sec></div></front></TEI><pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Proc Natl Acad Sci U S A</journal-id><journal-title>Proceedings of the National Academy of Sciences of the United States of America</journal-title><issn pub-type="ppub">0027-8424</issn><issn pub-type="epub">1091-6490</issn></journal-meta><article-meta><article-id pub-id-type="pmid">271999</article-id><article-id pub-id-type="pmc">431870</article-id><article-categories><subj-group subj-group-type="heading"><subject>Biological Sciences: Microbiology</subject></subj-group></article-categories><title-group><article-title>Molecular basis of reovirus virulence: Role of the S1 gene</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Weiner</surname><given-names>Howard L.</given-names></name><xref ref-type="aff" rid="af1">*</xref><xref ref-type="aff" rid="af2">†</xref></contrib><contrib contrib-type="author"><name><surname>Drayna</surname><given-names>Dennis</given-names></name><xref ref-type="aff" rid="af1">*</xref></contrib><contrib contrib-type="author"><name><surname>Averill</surname><given-names>Damon R.</given-names><suffix>Jr.</suffix></name><xref ref-type="aff" rid="af3">‡</xref></contrib><contrib contrib-type="author"><name><surname>Fields</surname><given-names>Bernard N.</given-names></name><xref ref-type="aff" rid="af1">*</xref><xref ref-type="aff" rid="af2">†</xref></contrib></contrib-group><aff id="af1"><label>*</label>Department of Microbiology and Molecular Genetics, Harvard Medical School, Boston, Massachusetts 02115</aff><aff id="af2"><label>†</label>Department of Medicine, Sections of Neurology and Infectious Diseases, Peter Bent Brigham Hospital, Boston, Massachusetts 02115</aff><aff id="af3"><label>‡</label>Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115</aff><aff id="af4">Department of Neuropathology, Children's Hospital Medical Center, Boston, Massachusetts 02115</aff><pub-date pub-type="ppub"><month>12</month><year>1977</year></pub-date><volume>74</volume><issue>12</issue><fpage>5744</fpage><lpage>5748</lpage><abstract><p>A genetic approach has been used to define the molecular basis for the different patterns of virulence and central nervous system cell tropism exhibited by reovirus types 1 and 3. Intracerebral inoculation of reovirus type 3 into newborn mice causes a necrotizing encephalitis (without ependymal damage) that is uniformly fatal. Animal inoculated with reovirus type 1 generally survive and may develop epedymal cell damage (without neuronal necrosis) and hydrocephalus. Using recombinant clones derived from crosses between reovirus types 1 and 3, we have been able to determine that the S1 genome segment is responsible for the differing cell tropism of reovirus serotypes and is the major determinant of neurovirulence. The type 1 S1 genome segment is responsible for ependymal damage with subsequent hydrocephalus; the type 3 S1 genome segment is responsible for neuronal necrosis and neurovirulence. We postulate that these differences are due to the specific interaction of the σ1 outer capsid polypeptide (the protein coded for by the S1 genome segment) with receptors on the surface of either ependymal cells or neuronal cells.</p><sec sec-type="scanned-figures"><title>Images</title><fig id="F1"><graphic xlink:href="pnas00043-0553-a" xlink:role="5745"></graphic></fig><fig id="F2"><graphic xlink:href="pnas00043-0556-a" xlink:role="5748"></graphic></fig></sec></abstract><kwd-group><kwd>cell tropism</kwd><kwd>neurovirulence</kwd><kwd>ependyma and neurons</kwd><kwd>reovirus recombinants</kwd></kwd-group></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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