Interferon alfacon1 is an inhibitor of SARS-corona virus in cell-based models.
Identifieur interne : 000F66 ( Ncbi/Merge ); précédent : 000F65; suivant : 000F67Interferon alfacon1 is an inhibitor of SARS-corona virus in cell-based models.
Auteurs : Jason Paragas [États-Unis] ; Lawrence M. Blatt ; Chris Hartmann ; John W. Huggins ; Tim P. EndySource :
- Antiviral research [ 0166-3542 ] ; 2005.
Descripteurs français
- KwdFr :
- MESH :
- pharmacocinétique : Interféron de type I.
- pharmacologie : Antiviraux, Interféron de type I.
- Effet cytopathogène viral, Humains, Interféron alpha, Modèles biologiques, Protéines recombinantes, Tests de sensibilité microbienne, Virus du SRAS.
English descriptors
- KwdEn :
- MESH :
- chemical , pharmacokinetics : Interferon Type I.
- chemical , pharmacology : Antiviral Agents, Interferon Type I.
- drug effects : SARS Virus.
- Cytopathogenic Effect, Viral, Humans, Interferon-alpha, Microbial Sensitivity Tests, Models, Biological, Recombinant Proteins.
Abstract
Preliminary data examining interferon alfacon1 treatment of SARS-CoV (severe acute respiratory syndrome-corona virus)-infected patients suggests this therapy is well tolerated and of therapeutic benefit. We report herein that interferon alfacon1, has potent in vitro antiviral activity against SARS-CoV. In a cytopathic effect protection (CPE) assay, interferon alfacon1 inhibited the generation of CPE in a dose-dependent manner with an IC50 of 0.001 microg/ml, a clinically achievable level. Furthermore, interferon alfacon1 also demonstrated significant antiviral activity in yield reduction and plaque reduction assays. The in vitro antiviral activity of interferon alfacon1 against SARS-CoV suggests continued evaluation of interferon alfacon1 as a therapeutic treatment for patients infected with SARS-CoV.
DOI: 10.1016/j.antiviral.2005.01.002
PubMed: 15911026
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pubmed:15911026Le document en format XML
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We report herein that interferon alfacon1, has potent in vitro antiviral activity against SARS-CoV. In a cytopathic effect protection (CPE) assay, interferon alfacon1 inhibited the generation of CPE in a dose-dependent manner with an IC50 of 0.001 microg/ml, a clinically achievable level. Furthermore, interferon alfacon1 also demonstrated significant antiviral activity in yield reduction and plaque reduction assays. The in vitro antiviral activity of interferon alfacon1 against SARS-CoV suggests continued evaluation of interferon alfacon1 as a therapeutic treatment for patients infected with SARS-CoV.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">15911026</PMID><DateCompleted><Year>2005</Year><Month>09</Month><Day>19</Day></DateCompleted><DateRevised><Year>2020</Year><Month>04</Month><Day>07</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Print">0166-3542</ISSN><JournalIssue CitedMedium="Print"><Volume>66</Volume><Issue>2-3</Issue><PubDate><Year>2005</Year><Month>Jun</Month></PubDate></JournalIssue><Title>Antiviral research</Title><ISOAbbreviation>Antiviral Res.</ISOAbbreviation></Journal><ArticleTitle>Interferon alfacon1 is an inhibitor of SARS-corona virus in cell-based models.</ArticleTitle><Pagination><MedlinePgn>99-102</MedlinePgn></Pagination><Abstract><AbstractText>Preliminary data examining interferon alfacon1 treatment of SARS-CoV (severe acute respiratory syndrome-corona virus)-infected patients suggests this therapy is well tolerated and of therapeutic benefit. We report herein that interferon alfacon1, has potent in vitro antiviral activity against SARS-CoV. In a cytopathic effect protection (CPE) assay, interferon alfacon1 inhibited the generation of CPE in a dose-dependent manner with an IC50 of 0.001 microg/ml, a clinically achievable level. Furthermore, interferon alfacon1 also demonstrated significant antiviral activity in yield reduction and plaque reduction assays. The in vitro antiviral activity of interferon alfacon1 against SARS-CoV suggests continued evaluation of interferon alfacon1 as a therapeutic treatment for patients infected with SARS-CoV.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Paragas</LastName><ForeName>Jason</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Virology Division, United States Army Medical Research Institute of Infectious Diseases (USAMRIID), 1425 Porter Street, Fort Detrick, MD 21702-5011, USA. 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Blatt</name><name sortKey="Endy, Tim P" sort="Endy, Tim P" uniqKey="Endy T" first="Tim P" last="Endy">Tim P. Endy</name><name sortKey="Hartmann, Chris" sort="Hartmann, Chris" uniqKey="Hartmann C" first="Chris" last="Hartmann">Chris Hartmann</name><name sortKey="Huggins, John W" sort="Huggins, John W" uniqKey="Huggins J" first="John W" last="Huggins">John W. Huggins</name></noCountry><country name="États-Unis"><region name="Maryland"><name sortKey="Paragas, Jason" sort="Paragas, Jason" uniqKey="Paragas J" first="Jason" last="Paragas">Jason Paragas</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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