Inhibition, escape, and attenuated growth of severe acute respiratory syndrome coronavirus treated with antisense morpholino oligomers.
Identifieur interne : 001056 ( Ncbi/Merge ); précédent : 001055; suivant : 001057Inhibition, escape, and attenuated growth of severe acute respiratory syndrome coronavirus treated with antisense morpholino oligomers.
Auteurs : Benjamin W. Neuman [États-Unis] ; David A. Stein ; Andrew D. Kroeker ; Michael J. Churchill ; Alice M. Kim ; Peter Kuhn ; Philip Dawson ; Hong M. Moulton ; Richard K. Bestwick ; Patrick L. Iversen ; Michael J. BuchmeierSource :
- Journal of virology [ 0022-538X ] ; 2005.
Descripteurs français
- KwdFr :
- Animaux, Antiviraux (pharmacologie), Cellules Vero, Conception de médicament, Conformation d'acide nucléique, Données de séquences moléculaires, Effet cytopathogène viral, Morpholines (pharmacologie), Morpholinos, Mutation, Passage en série, Peptides, Régions 5' non traduites, Résistance virale aux médicaments, Syndrome respiratoire aigu sévère, Séquence nucléotidique, Transcription génétique (), Virus du SRAS (), Virus du SRAS (croissance et développement), Virus du SRAS (génétique).
- MESH :
- croissance et développement : Virus du SRAS.
- génétique : Virus du SRAS.
- pharmacologie : Antiviraux, Morpholines.
- Animaux, Cellules Vero, Conception de médicament, Conformation d'acide nucléique, Données de séquences moléculaires, Effet cytopathogène viral, Morpholinos, Mutation, Passage en série, Peptides, Régions 5' non traduites, Résistance virale aux médicaments, Syndrome respiratoire aigu sévère, Séquence nucléotidique, Transcription génétique, Virus du SRAS.
English descriptors
- KwdEn :
- 5' Untranslated Regions, Animals, Antiviral Agents (pharmacology), Base Sequence, Chlorocebus aethiops, Cytopathogenic Effect, Viral, Drug Design, Drug Resistance, Viral, Molecular Sequence Data, Morpholines (pharmacology), Morpholinos, Mutation, Nucleic Acid Conformation, Peptides, SARS Virus (drug effects), SARS Virus (genetics), SARS Virus (growth & development), Serial Passage, Severe Acute Respiratory Syndrome, Transcription, Genetic (drug effects), Vero Cells.
- MESH :
- chemical , pharmacology : Antiviral Agents, Morpholines.
- chemical : 5' Untranslated Regions, Morpholinos, Peptides.
- drug effects : SARS Virus, Transcription, Genetic.
- genetics : SARS Virus.
- growth & development : SARS Virus.
- Animals, Base Sequence, Chlorocebus aethiops, Cytopathogenic Effect, Viral, Drug Design, Drug Resistance, Viral, Molecular Sequence Data, Mutation, Nucleic Acid Conformation, Serial Passage, Severe Acute Respiratory Syndrome, Vero Cells.
Abstract
The recently emerged severe acute respiratory syndrome coronavirus (SARS-CoV) is a potent pathogen of humans and is capable of rapid global spread. Peptide-conjugated antisense morpholino oligomers (P-PMO) were designed to bind by base pairing to specific sequences in the SARS-CoV (Tor2 strain) genome. The P-PMO were tested for their capacity to inhibit production of infectious virus as well as to probe the function of conserved viral RNA motifs and secondary structures. Several virus-targeted P-PMO and a random-sequence control P-PMO showed low inhibitory activity against SARS coronavirus. Certain other virus-targeted P-PMO reduced virus-induced cytopathology and cell-to-cell spread as a consequence of decreasing viral amplification. Active P-PMO were effective when administered at any time prior to peak viral synthesis and exerted sustained antiviral effects while present in culture medium. P-PMO showed low nonspecific inhibitory activity against translation of nontargeted RNA or growth of the arenavirus lymphocytic choriomeningitis virus. Two P-PMO targeting the viral transcription-regulatory sequence (TRS) region in the 5' untranslated region were the most effective inhibitors tested. After several viral passages in the presence of a TRS-targeted P-PMO, partially drug-resistant SARS-CoV mutants arose which contained three contiguous base point mutations at the binding site of a TRS-targeted P-PMO. Those partially resistant viruses grew more slowly and formed smaller plaques than wild-type SARS-CoV. These results suggest PMO compounds have powerful therapeutic and investigative potential toward coronavirus infection.
DOI: 10.1128/JVI.79.15.9665-9676.2005
PubMed: 16014928
Links toward previous steps (curation, corpus...)
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- to stream PubMed, to step Curation: 002644
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pubmed:16014928Le document en format XML
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Peptide-conjugated antisense morpholino oligomers (P-PMO) were designed to bind by base pairing to specific sequences in the SARS-CoV (Tor2 strain) genome. The P-PMO were tested for their capacity to inhibit production of infectious virus as well as to probe the function of conserved viral RNA motifs and secondary structures. Several virus-targeted P-PMO and a random-sequence control P-PMO showed low inhibitory activity against SARS coronavirus. Certain other virus-targeted P-PMO reduced virus-induced cytopathology and cell-to-cell spread as a consequence of decreasing viral amplification. Active P-PMO were effective when administered at any time prior to peak viral synthesis and exerted sustained antiviral effects while present in culture medium. P-PMO showed low nonspecific inhibitory activity against translation of nontargeted RNA or growth of the arenavirus lymphocytic choriomeningitis virus. Two P-PMO targeting the viral transcription-regulatory sequence (TRS) region in the 5' untranslated region were the most effective inhibitors tested. After several viral passages in the presence of a TRS-targeted P-PMO, partially drug-resistant SARS-CoV mutants arose which contained three contiguous base point mutations at the binding site of a TRS-targeted P-PMO. Those partially resistant viruses grew more slowly and formed smaller plaques than wild-type SARS-CoV. These results suggest PMO compounds have powerful therapeutic and investigative potential toward coronavirus infection.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">16014928</PMID><DateCompleted><Year>2005</Year><Month>08</Month><Day>18</Day></DateCompleted><DateRevised><Year>2019</Year><Month>12</Month><Day>10</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0022-538X</ISSN><JournalIssue CitedMedium="Print"><Volume>79</Volume><Issue>15</Issue><PubDate><Year>2005</Year><Month>Aug</Month></PubDate></JournalIssue><Title>Journal of virology</Title><ISOAbbreviation>J. Virol.</ISOAbbreviation></Journal><ArticleTitle>Inhibition, escape, and attenuated growth of severe acute respiratory syndrome coronavirus treated with antisense morpholino oligomers.</ArticleTitle><Pagination><MedlinePgn>9665-76</MedlinePgn></Pagination><Abstract><AbstractText>The recently emerged severe acute respiratory syndrome coronavirus (SARS-CoV) is a potent pathogen of humans and is capable of rapid global spread. Peptide-conjugated antisense morpholino oligomers (P-PMO) were designed to bind by base pairing to specific sequences in the SARS-CoV (Tor2 strain) genome. The P-PMO were tested for their capacity to inhibit production of infectious virus as well as to probe the function of conserved viral RNA motifs and secondary structures. Several virus-targeted P-PMO and a random-sequence control P-PMO showed low inhibitory activity against SARS coronavirus. Certain other virus-targeted P-PMO reduced virus-induced cytopathology and cell-to-cell spread as a consequence of decreasing viral amplification. Active P-PMO were effective when administered at any time prior to peak viral synthesis and exerted sustained antiviral effects while present in culture medium. P-PMO showed low nonspecific inhibitory activity against translation of nontargeted RNA or growth of the arenavirus lymphocytic choriomeningitis virus. Two P-PMO targeting the viral transcription-regulatory sequence (TRS) region in the 5' untranslated region were the most effective inhibitors tested. After several viral passages in the presence of a TRS-targeted P-PMO, partially drug-resistant SARS-CoV mutants arose which contained three contiguous base point mutations at the binding site of a TRS-targeted P-PMO. Those partially resistant viruses grew more slowly and formed smaller plaques than wild-type SARS-CoV. These results suggest PMO compounds have powerful therapeutic and investigative potential toward coronavirus infection.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Neuman</LastName><ForeName>Benjamin W</ForeName><Initials>BW</Initials><AffiliationInfo><Affiliation>The Scripps Research Institute, Division of Virology, Department of Neuropharmacology, La Jolla, CA 92037, USA. bneuman@scripps.edu</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Stein</LastName><ForeName>David A</ForeName><Initials>DA</Initials></Author><Author ValidYN="Y"><LastName>Kroeker</LastName><ForeName>Andrew D</ForeName><Initials>AD</Initials></Author><Author ValidYN="Y"><LastName>Churchill</LastName><ForeName>Michael J</ForeName><Initials>MJ</Initials></Author><Author ValidYN="Y"><LastName>Kim</LastName><ForeName>Alice M</ForeName><Initials>AM</Initials></Author><Author ValidYN="Y"><LastName>Kuhn</LastName><ForeName>Peter</ForeName><Initials>P</Initials></Author><Author ValidYN="Y"><LastName>Dawson</LastName><ForeName>Philip</ForeName><Initials>P</Initials></Author><Author ValidYN="Y"><LastName>Moulton</LastName><ForeName>Hong M</ForeName><Initials>HM</Initials></Author><Author ValidYN="Y"><LastName>Bestwick</LastName><ForeName>Richard K</ForeName><Initials>RK</Initials></Author><Author ValidYN="Y"><LastName>Iversen</LastName><ForeName>Patrick L</ForeName><Initials>PL</Initials></Author><Author ValidYN="Y"><LastName>Buchmeier</LastName><ForeName>Michael J</ForeName><Initials>MJ</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>AI25913</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>NS41219</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 AI025913</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>AI43103</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>T32 NS041219</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType><PublicationType UI="D013487">Research Support, U.S. Gov't, P.H.S.</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Virol</MedlineTA><NlmUniqueID>0113724</NlmUniqueID><ISSNLinking>0022-538X</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D020121">5' Untranslated Regions</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000998">Antiviral Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D009025">Morpholines</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D060172">Morpholinos</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D010455">Peptides</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D020121" MajorTopicYN="N">5' Untranslated Regions</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000998" MajorTopicYN="N">Antiviral Agents</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001483" MajorTopicYN="N">Base Sequence</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002522" MajorTopicYN="N">Chlorocebus aethiops</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003588" MajorTopicYN="N">Cytopathogenic Effect, Viral</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015195" MajorTopicYN="N">Drug Design</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D024882" MajorTopicYN="N">Drug Resistance, Viral</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008969" MajorTopicYN="N">Molecular Sequence Data</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009025" MajorTopicYN="N">Morpholines</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D060172" MajorTopicYN="N">Morpholinos</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009154" MajorTopicYN="N">Mutation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009690" MajorTopicYN="N">Nucleic Acid Conformation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010455" MajorTopicYN="N">Peptides</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D045473" MajorTopicYN="N">SARS Virus</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000254" MajorTopicYN="N">growth & development</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012692" MajorTopicYN="N">Serial Passage</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D045169" MajorTopicYN="N">Severe Acute Respiratory Syndrome</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014158" MajorTopicYN="N">Transcription, Genetic</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug 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Bestwick</name><name sortKey="Buchmeier, Michael J" sort="Buchmeier, Michael J" uniqKey="Buchmeier M" first="Michael J" last="Buchmeier">Michael J. Buchmeier</name><name sortKey="Churchill, Michael J" sort="Churchill, Michael J" uniqKey="Churchill M" first="Michael J" last="Churchill">Michael J. Churchill</name><name sortKey="Dawson, Philip" sort="Dawson, Philip" uniqKey="Dawson P" first="Philip" last="Dawson">Philip Dawson</name><name sortKey="Iversen, Patrick L" sort="Iversen, Patrick L" uniqKey="Iversen P" first="Patrick L" last="Iversen">Patrick L. Iversen</name><name sortKey="Kim, Alice M" sort="Kim, Alice M" uniqKey="Kim A" first="Alice M" last="Kim">Alice M. Kim</name><name sortKey="Kroeker, Andrew D" sort="Kroeker, Andrew D" uniqKey="Kroeker A" first="Andrew D" last="Kroeker">Andrew D. Kroeker</name><name sortKey="Kuhn, Peter" sort="Kuhn, Peter" uniqKey="Kuhn P" first="Peter" last="Kuhn">Peter Kuhn</name><name sortKey="Moulton, Hong M" sort="Moulton, Hong M" uniqKey="Moulton H" first="Hong M" last="Moulton">Hong M. Moulton</name><name sortKey="Stein, David A" sort="Stein, David A" uniqKey="Stein D" first="David A" last="Stein">David A. Stein</name></noCountry><country name="États-Unis"><region name="Californie"><name sortKey="Neuman, Benjamin W" sort="Neuman, Benjamin W" uniqKey="Neuman B" first="Benjamin W" last="Neuman">Benjamin W. Neuman</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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