Molecular basis of reovirus virulence: Role of the S1 gene
Identifieur interne : 000E10 ( Pmc/Checkpoint ); précédent : 000E09; suivant : 000E11Molecular basis of reovirus virulence: Role of the S1 gene
Auteurs : Howard L. Weiner [États-Unis] ; Dennis Drayna [États-Unis] ; Damon R. Averill [États-Unis] ; Bernard N. Fields [États-Unis]Source :
- Proceedings of the National Academy of Sciences of the United States of America [ 0027-8424 ] ; 1977.
Abstract
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.
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PubMed: 271999
PubMed Central: 431870
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<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>
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<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>
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<title-group><article-title>Molecular basis of reovirus virulence: Role of the S1 gene</article-title>
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<contrib-group><contrib contrib-type="author"><name><surname>Weiner</surname>
<given-names>Howard L.</given-names>
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<xref ref-type="aff" rid="af1">*</xref>
<xref ref-type="aff" rid="af2">†</xref>
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<contrib contrib-type="author"><name><surname>Drayna</surname>
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<contrib contrib-type="author"><name><surname>Fields</surname>
<given-names>Bernard N.</given-names>
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<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>
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<kwd-group><kwd>cell tropism</kwd>
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