The antiviral effect of interferon-beta against SARS-coronavirus is not mediated by MxA protein.
Identifieur interne : 000802 ( Ncbi/Merge ); précédent : 000801; suivant : 000803The antiviral effect of interferon-beta against SARS-coronavirus is not mediated by MxA protein.
Auteurs : Martin Spiegel [Allemagne] ; Andreas Pichlmair ; Elke Mühlberger ; Otto Haller ; Friedemann WeberSource :
- Journal of clinical virology : the official publication of the Pan American Society for Clinical Virology [ 1386-6532 ] ; 2004.
Descripteurs français
- KwdFr :
- MESH :
- métabolisme : Protéines G.
- pharmacologie : Interféron bêta.
- physiologie : Virus du SRAS.
- virologie : Syndrome respiratoire aigu sévère.
- Animaux, Cellules Vero, Humains, Protéines de résistance aux myxovirus, Réplication virale, Virus du SRAS.
English descriptors
- KwdEn :
- MESH :
- chemical , metabolism : GTP-Binding Proteins.
- chemical , pharmacology : Interferon-beta.
- drug effects : SARS Virus, Virus Replication.
- physiology : SARS Virus.
- virology : Severe Acute Respiratory Syndrome.
- Animals, Chlorocebus aethiops, Humans, Myxovirus Resistance Proteins, Vero Cells.
Abstract
Severe acute respiratory syndrome (SARS) is caused by a novel coronavirus termed SARS-CoV. No antiviral treatment has been established so far. Interferons are cytokines which induce the synthesis of several antivirally active proteins in the cell. In this study, we demonstrated that multiplication of SARS-CoV in cell culture can be strongly inhibited by pretreatment with interferon-beta. Interferon-alpha and interferon-gamma, by contrast, were less effective. The human MxA protein is one of the most prominent proteins induced by interferon-beta. Nevertheless, no interference with SARS-CoV replication was observed in Vero cells stably expressing MxA. Therefore, other interferon-induced proteins must be responsible for the strong inhibitory effect of interferon-beta against SARS-CoV.
DOI: 10.1016/j.jcv.2003.11.013
PubMed: 15135736
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type="chemical" qualifier="metabolism" xml:lang="en"><term>GTP-Binding Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Interferon-beta</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>SARS Virus</term><term>Virus Replication</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Protéines G</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Interféron bêta</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Virus du SRAS</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>SARS Virus</term></keywords><keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Syndrome respiratoire aigu sévère</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" 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No antiviral treatment has been established so far. Interferons are cytokines which induce the synthesis of several antivirally active proteins in the cell. In this study, we demonstrated that multiplication of SARS-CoV in cell culture can be strongly inhibited by pretreatment with interferon-beta. Interferon-alpha and interferon-gamma, by contrast, were less effective. The human MxA protein is one of the most prominent proteins induced by interferon-beta. Nevertheless, no interference with SARS-CoV replication was observed in Vero cells stably expressing MxA. Therefore, other interferon-induced proteins must be responsible for the strong inhibitory effect of interferon-beta against SARS-CoV.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">15135736</PMID><DateCompleted><Year>2004</Year><Month>07</Month><Day>15</Day></DateCompleted><DateRevised><Year>2020</Year><Month>04</Month><Day>09</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">1386-6532</ISSN><JournalIssue CitedMedium="Print"><Volume>30</Volume><Issue>3</Issue><PubDate><Year>2004</Year><Month>Jul</Month></PubDate></JournalIssue><Title>Journal of clinical virology : the official publication of the Pan American Society for Clinical Virology</Title><ISOAbbreviation>J. Clin. Virol.</ISOAbbreviation></Journal><ArticleTitle>The antiviral effect of interferon-beta against SARS-coronavirus is not mediated by MxA protein.</ArticleTitle><Pagination><MedlinePgn>211-3</MedlinePgn></Pagination><Abstract><AbstractText>Severe acute respiratory syndrome (SARS) is caused by a novel coronavirus termed SARS-CoV. No antiviral treatment has been established so far. Interferons are cytokines which induce the synthesis of several antivirally active proteins in the cell. In this study, we demonstrated that multiplication of SARS-CoV in cell culture can be strongly inhibited by pretreatment with interferon-beta. Interferon-alpha and interferon-gamma, by contrast, were less effective. The human MxA protein is one of the most prominent proteins induced by interferon-beta. Nevertheless, no interference with SARS-CoV replication was observed in Vero cells stably expressing MxA. 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