The nsp2 replicase proteins of murine hepatitis virus and severe acute respiratory syndrome coronavirus are dispensable for viral replication
Identifieur interne : 000580 ( PascalFrancis/Corpus ); précédent : 000579; suivant : 000581The nsp2 replicase proteins of murine hepatitis virus and severe acute respiratory syndrome coronavirus are dispensable for viral replication
Auteurs : Rachel L. Graham ; Amy C. Sims ; Sarah M. Brockway ; Ralph S. Baric ; Mark R. DenisonSource :
- Journal of virology [ 0022-538X ] ; 2005.
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- Pascal (Inist)
English descriptors
- KwdEn :
Abstract
The positive-stranded RNA genome of the coronaviruses is translated from ORF1 to yield polyproteins that are proteolytically processed into intermediate and mature nonstructural proteins (nsps). Murine hepatitis virus (MHV) and severe acute respiratory syndrome coronavirus (SARS-CoV) polyproteins incorporate 16 protein domains (nsps), with nspl and nsp2 being the most variable among the coronaviruses and having no experimentally confirmed or predicted functions in replication. To determine if nsp2 is essential for viral replication, MHV and SARS-CoV genome RNA was generated with deletions of the nsp2 coding sequence (MHVAnsp2 and SARSAnsp2, respectively). Infectious MHVAnsp2 and SARSAnsp2 viruses recovered from electroporated cells had 0.5 to 1 logic reductions in peak titers in single-cycle growth assays, as well as a reduction in viral RNA synthesis that was not specific for any positive-stranded RNA species. The Ansp2 mutant viruses lacked expression of both nsp2 and an nsp2-nsp3 precursor, but cleaved the engineered chimeric nspl-nsp3 cleavage site as efficiently as the native nsp1-nsp2 cleavage site. Replication complexes in MHVAnsp2-infected cells lacked nsp2 but were morphologically indistinguishable from those of wild-type MHV by immunofluorescence. nsp2 expressed in cells by stable retroviral transduction was specifically recruited to viral replication complexes upon infection with MHVAnsp2. These results demonstrate that while nsp2 of MHV and SARS-CoV is dispensable for viral replication in cell culture, deletion of the nsp2 coding sequence attenuates viral growth and RNA synthesis. These findings also provide a system for the study of determinants of nsp targeting and function.
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Format Inist (serveur)
NO : | PASCAL 05-0485339 INIST |
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ET : | The nsp2 replicase proteins of murine hepatitis virus and severe acute respiratory syndrome coronavirus are dispensable for viral replication |
AU : | GRAHAM (Rachel L.); SIMS (Amy C.); BROCKWAY (Sarah M.); BARIC (Ralph S.); DENISON (Mark R.) |
AF : | Department of Microbiology and Immunology, Vanderbilt University Medical Center/Nashville, Tennessee/Etats-Unis (1 aut., 3 aut., 5 aut.); Elizabeth B. Lamb Center for Pediatric Research, Vanderbilt University Medical Center/Nashville, Tennessee/Etats-Unis (1 aut., 3 aut., 5 aut.); Department of Epidemiology, School of Public Health, University of North Carolina/Chapel Hill, North Carolina/Etats-Unis (2 aut., 4 aut.); Department of Pediatrics, Vanderbilt University Medical Center/Nashville, Tennessee/Etats-Unis (5 aut.) |
DT : | Publication en série; Niveau analytique |
SO : | Journal of virology; ISSN 0022-538X; Etats-Unis; Da. 2005; Vol. 79; No. 21; Pp. 13399-13411; Bibl. 54 ref. |
LA : | Anglais |
EA : | The positive-stranded RNA genome of the coronaviruses is translated from ORF1 to yield polyproteins that are proteolytically processed into intermediate and mature nonstructural proteins (nsps). Murine hepatitis virus (MHV) and severe acute respiratory syndrome coronavirus (SARS-CoV) polyproteins incorporate 16 protein domains (nsps), with nspl and nsp2 being the most variable among the coronaviruses and having no experimentally confirmed or predicted functions in replication. To determine if nsp2 is essential for viral replication, MHV and SARS-CoV genome RNA was generated with deletions of the nsp2 coding sequence (MHVAnsp2 and SARSAnsp2, respectively). Infectious MHVAnsp2 and SARSAnsp2 viruses recovered from electroporated cells had 0.5 to 1 logic reductions in peak titers in single-cycle growth assays, as well as a reduction in viral RNA synthesis that was not specific for any positive-stranded RNA species. The Ansp2 mutant viruses lacked expression of both nsp2 and an nsp2-nsp3 precursor, but cleaved the engineered chimeric nspl-nsp3 cleavage site as efficiently as the native nsp1-nsp2 cleavage site. Replication complexes in MHVAnsp2-infected cells lacked nsp2 but were morphologically indistinguishable from those of wild-type MHV by immunofluorescence. nsp2 expressed in cells by stable retroviral transduction was specifically recruited to viral replication complexes upon infection with MHVAnsp2. These results demonstrate that while nsp2 of MHV and SARS-CoV is dispensable for viral replication in cell culture, deletion of the nsp2 coding sequence attenuates viral growth and RNA synthesis. These findings also provide a system for the study of determinants of nsp targeting and function. |
CC : | 002A05C10 |
FD : | Virus hépatite murine; Virus syndrome respiratoire aigu sévère; RNA-directed RNA polymerase; Protéine; Réplication; Microbiologie; Virologie |
FG : | Coronavirus; Coronaviridae; Nidovirales; Virus; Nucleotidyltransferases; Transferases; Enzyme |
ED : | Murine hepatitis virus; Severe acute respiratory syndrome virus; RNA-directed RNA polymerase; Protein; Replication; Microbiology; Virology |
EG : | Coronavirus; Coronaviridae; Nidovirales; Virus; Nucleotidyltransferases; Transferases; Enzyme |
SD : | Murine hepatitis virus; Severe acute respiratory syndrome virus; RNA-directed RNA polymerase; Proteína; Replicación; Microbiología; Virología |
LO : | INIST-13592.354000131986280190 |
ID : | 05-0485339 |
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Pascal:05-0485339Le document en format XML
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<series><title level="j" type="main">Journal of virology</title>
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<front><div type="abstract" xml:lang="en">The positive-stranded RNA genome of the coronaviruses is translated from ORF1 to yield polyproteins that are proteolytically processed into intermediate and mature nonstructural proteins (nsps). Murine hepatitis virus (MHV) and severe acute respiratory syndrome coronavirus (SARS-CoV) polyproteins incorporate 16 protein domains (nsps), with nspl and nsp2 being the most variable among the coronaviruses and having no experimentally confirmed or predicted functions in replication. To determine if nsp2 is essential for viral replication, MHV and SARS-CoV genome RNA was generated with deletions of the nsp2 coding sequence (MHVAnsp2 and SARSAnsp2, respectively). Infectious MHVAnsp2 and SARSAnsp2 viruses recovered from electroporated cells had 0.5 to 1 logic reductions in peak titers in single-cycle growth assays, as well as a reduction in viral RNA synthesis that was not specific for any positive-stranded RNA species. The Ansp2 mutant viruses lacked expression of both nsp2 and an nsp2-nsp3 precursor, but cleaved the engineered chimeric nspl-nsp3 cleavage site as efficiently as the native nsp1-nsp2 cleavage site. Replication complexes in MHVAnsp2-infected cells lacked nsp2 but were morphologically indistinguishable from those of wild-type MHV by immunofluorescence. nsp2 expressed in cells by stable retroviral transduction was specifically recruited to viral replication complexes upon infection with MHVAnsp2. These results demonstrate that while nsp2 of MHV and SARS-CoV is dispensable for viral replication in cell culture, deletion of the nsp2 coding sequence attenuates viral growth and RNA synthesis. These findings also provide a system for the study of determinants of nsp targeting and function.</div>
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</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Nucleotidyltransferases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Nucleotidyltransferases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Nucleotidyltransferases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="06" i2="X" l="FRE"><s0>Transferases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="06" i2="X" l="ENG"><s0>Transferases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="06" i2="X" l="SPA"><s0>Transferases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="07" i2="X" l="FRE"><s0>Enzyme</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="07" i2="X" l="ENG"><s0>Enzyme</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="07" i2="X" l="SPA"><s0>Enzima</s0>
<s2>FE</s2>
</fC07>
<fN21><s1>339</s1>
</fN21>
<fN44 i1="01"><s1>OTO</s1>
</fN44>
<fN82><s1>OTO</s1>
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<ET>The nsp2 replicase proteins of murine hepatitis virus and severe acute respiratory syndrome coronavirus are dispensable for viral replication</ET>
<AU>GRAHAM (Rachel L.); SIMS (Amy C.); BROCKWAY (Sarah M.); BARIC (Ralph S.); DENISON (Mark R.)</AU>
<AF>Department of Microbiology and Immunology, Vanderbilt University Medical Center/Nashville, Tennessee/Etats-Unis (1 aut., 3 aut., 5 aut.); Elizabeth B. Lamb Center for Pediatric Research, Vanderbilt University Medical Center/Nashville, Tennessee/Etats-Unis (1 aut., 3 aut., 5 aut.); Department of Epidemiology, School of Public Health, University of North Carolina/Chapel Hill, North Carolina/Etats-Unis (2 aut., 4 aut.); Department of Pediatrics, Vanderbilt University Medical Center/Nashville, Tennessee/Etats-Unis (5 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Journal of virology; ISSN 0022-538X; Etats-Unis; Da. 2005; Vol. 79; No. 21; Pp. 13399-13411; Bibl. 54 ref.</SO>
<LA>Anglais</LA>
<EA>The positive-stranded RNA genome of the coronaviruses is translated from ORF1 to yield polyproteins that are proteolytically processed into intermediate and mature nonstructural proteins (nsps). Murine hepatitis virus (MHV) and severe acute respiratory syndrome coronavirus (SARS-CoV) polyproteins incorporate 16 protein domains (nsps), with nspl and nsp2 being the most variable among the coronaviruses and having no experimentally confirmed or predicted functions in replication. To determine if nsp2 is essential for viral replication, MHV and SARS-CoV genome RNA was generated with deletions of the nsp2 coding sequence (MHVAnsp2 and SARSAnsp2, respectively). Infectious MHVAnsp2 and SARSAnsp2 viruses recovered from electroporated cells had 0.5 to 1 logic reductions in peak titers in single-cycle growth assays, as well as a reduction in viral RNA synthesis that was not specific for any positive-stranded RNA species. The Ansp2 mutant viruses lacked expression of both nsp2 and an nsp2-nsp3 precursor, but cleaved the engineered chimeric nspl-nsp3 cleavage site as efficiently as the native nsp1-nsp2 cleavage site. Replication complexes in MHVAnsp2-infected cells lacked nsp2 but were morphologically indistinguishable from those of wild-type MHV by immunofluorescence. nsp2 expressed in cells by stable retroviral transduction was specifically recruited to viral replication complexes upon infection with MHVAnsp2. These results demonstrate that while nsp2 of MHV and SARS-CoV is dispensable for viral replication in cell culture, deletion of the nsp2 coding sequence attenuates viral growth and RNA synthesis. These findings also provide a system for the study of determinants of nsp targeting and function.</EA>
<CC>002A05C10</CC>
<FD>Virus hépatite murine; Virus syndrome respiratoire aigu sévère; RNA-directed RNA polymerase; Protéine; Réplication; Microbiologie; Virologie</FD>
<FG>Coronavirus; Coronaviridae; Nidovirales; Virus; Nucleotidyltransferases; Transferases; Enzyme</FG>
<ED>Murine hepatitis virus; Severe acute respiratory syndrome virus; RNA-directed RNA polymerase; Protein; Replication; Microbiology; Virology</ED>
<EG>Coronavirus; Coronaviridae; Nidovirales; Virus; Nucleotidyltransferases; Transferases; Enzyme</EG>
<SD>Murine hepatitis virus; Severe acute respiratory syndrome virus; RNA-directed RNA polymerase; Proteína; Replicación; Microbiología; Virología</SD>
<LO>INIST-13592.354000131986280190</LO>
<ID>05-0485339</ID>
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