In vitro anti-influenza A activity of interferon (IFN)-λ1 combined with IFN-β or oseltamivir carboxylate
Identifieur interne : 000025 ( PascalFrancis/Corpus ); précédent : 000024; suivant : 000026In vitro anti-influenza A activity of interferon (IFN)-λ1 combined with IFN-β or oseltamivir carboxylate
Auteurs : Natalia A. Ilyushina ; Raymond P. DonnellySource :
- Antiviral research [ 0166-3542 ] ; 2014.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
Abstract
Influenza viruses, which can cross species barriers and adapt to new hosts, pose a constant potential threat to human health. The influenza pandemic of 2009 highlighted the rapidity with which an influenza virus can spread worldwide. Currently available antivirals have a number of limitations against influenza, and novel antiviral strategies, including novel drugs and drug combinations, are urgently needed. Here, we evaluated the in vitro effects of interferon (IFN)-β, IFN-λ1, oseltamivir carboxylate (a neuraminidase (NA) inhibitor), and combinations of these agents against two seasonal (i.e., H1N1 and H3N2) influenza A viruses. We observed that A/California/04/09 (H1N1) and A/Panama/2007/99 (H3N2) isolates were equally sensitive to the antiviral activity of IFN-β and oseltamivir carboxylate in A549 and Calu-3 cells. In contrast, IFN-λ1 exhibited substantially lower protective potential against the H1N1 strain (64-1030-fold ↓, P < 0.05), and was ineffective against H3N2 virus in both cell lines. Three dimensional analysis of drug-drug interactions revealed that IFN-λ1 interacted with IFN-β and oseltamivir carboxylate in an additive or synergistic manner, respectively, to inhibit influenza A virus replication in human airway epithelial cells. Overall, the present study demonstrated that anti-influenza agents with different mechanisms of action (e.g., a NA inhibitor combined with IFN-λ1) exerted a significantly greater (P < 0.05) synergistic effect compared to co-treatment with drugs that target the same signaling pathway (i.e., IFN-β plus IFN-λ1) in vitro. Our findings provide support for the combined use of interferon plus oseltamivir as a potential means for treating influenza infections.
Notice en format standard (ISO 2709)
Pour connaître la documentation sur le format Inist Standard.
pA |
|
---|
Format Inist (serveur)
NO : | PASCAL 14-0273479 INIST |
---|---|
ET : | In vitro anti-influenza A activity of interferon (IFN)-λ1 combined with IFN-β or oseltamivir carboxylate |
AU : | ILYUSHINA (Natalia A.); DONNELLY (Raymond P.) |
AF : | Division of Therapeutic Proteins, Center for Drug Evaluation and Research, Food and Drug Administration/Silver Spring, MD 20993/Etats-Unis (1 aut., 2 aut.) |
DT : | Publication en série; Niveau analytique |
SO : | Antiviral research; ISSN 0166-3542; Coden ARSRDR; Royaume-Uni; Da. 2014; Vol. 111; Pp. 112-120; Bibl. 3/4 p. |
LA : | Anglais |
EA : | Influenza viruses, which can cross species barriers and adapt to new hosts, pose a constant potential threat to human health. The influenza pandemic of 2009 highlighted the rapidity with which an influenza virus can spread worldwide. Currently available antivirals have a number of limitations against influenza, and novel antiviral strategies, including novel drugs and drug combinations, are urgently needed. Here, we evaluated the in vitro effects of interferon (IFN)-β, IFN-λ1, oseltamivir carboxylate (a neuraminidase (NA) inhibitor), and combinations of these agents against two seasonal (i.e., H1N1 and H3N2) influenza A viruses. We observed that A/California/04/09 (H1N1) and A/Panama/2007/99 (H3N2) isolates were equally sensitive to the antiviral activity of IFN-β and oseltamivir carboxylate in A549 and Calu-3 cells. In contrast, IFN-λ1 exhibited substantially lower protective potential against the H1N1 strain (64-1030-fold ↓, P < 0.05), and was ineffective against H3N2 virus in both cell lines. Three dimensional analysis of drug-drug interactions revealed that IFN-λ1 interacted with IFN-β and oseltamivir carboxylate in an additive or synergistic manner, respectively, to inhibit influenza A virus replication in human airway epithelial cells. Overall, the present study demonstrated that anti-influenza agents with different mechanisms of action (e.g., a NA inhibitor combined with IFN-λ1) exerted a significantly greater (P < 0.05) synergistic effect compared to co-treatment with drugs that target the same signaling pathway (i.e., IFN-β plus IFN-λ1) in vitro. Our findings provide support for the combined use of interferon plus oseltamivir as a potential means for treating influenza infections. |
CC : | 002B02S05; 002B05C02C |
FD : | In vitro; Grippe A; Cytokine; Interféron bêta; Oséltamivir; Virus grippal A; Traitement associé; Association médicamenteuse; Antiviral |
FG : | Virose; Infection; Influenzavirus A; Orthomyxoviridae; Virus; Exo-α-sialidase; Glycosidases; Glycosylases; Hydrolases; Enzyme; Inhibiteur enzyme; Inhibiteur neuraminidase |
ED : | In vitro; Influenza A; Cytokine; Beta interferon; Oseltamivir; Influenza A virus; Combined treatment; Drug combination; Antiviral |
EG : | Viral disease; Infection; Influenzavirus A; Orthomyxoviridae; Virus; Exo-α-sialidase; Glycosidases; Glycosylases; Hydrolases; Enzyme; Enzyme inhibitor; Neuraminidase inhibitor |
SD : | In vitro; Gripe A; Citoquina; Interferón beta; Oseltamivir; Influenza A virus; Tratamiento asociado; Asociación medicamentosa; Antiviral |
LO : | INIST-18839.354000502689950160 |
ID : | 14-0273479 |
Links to Exploration step
Pascal:14-0273479Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en" level="a">In vitro anti-influenza A activity of interferon (IFN)-λ1 combined with IFN-β or oseltamivir carboxylate</title>
<author><name sortKey="Ilyushina, Natalia A" sort="Ilyushina, Natalia A" uniqKey="Ilyushina N" first="Natalia A." last="Ilyushina">Natalia A. Ilyushina</name>
<affiliation><inist:fA14 i1="01"><s1>Division of Therapeutic Proteins, Center for Drug Evaluation and Research, Food and Drug Administration</s1>
<s2>Silver Spring, MD 20993</s2>
<s3>USA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Donnelly, Raymond P" sort="Donnelly, Raymond P" uniqKey="Donnelly R" first="Raymond P." last="Donnelly">Raymond P. Donnelly</name>
<affiliation><inist:fA14 i1="01"><s1>Division of Therapeutic Proteins, Center for Drug Evaluation and Research, Food and Drug Administration</s1>
<s2>Silver Spring, MD 20993</s2>
<s3>USA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
</titleStmt>
<publicationStmt><idno type="wicri:source">INIST</idno>
<idno type="inist">14-0273479</idno>
<date when="2014">2014</date>
<idno type="stanalyst">PASCAL 14-0273479 INIST</idno>
<idno type="RBID">Pascal:14-0273479</idno>
<idno type="wicri:Area/PascalFrancis/Corpus">000025</idno>
</publicationStmt>
<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">In vitro anti-influenza A activity of interferon (IFN)-λ1 combined with IFN-β or oseltamivir carboxylate</title>
<author><name sortKey="Ilyushina, Natalia A" sort="Ilyushina, Natalia A" uniqKey="Ilyushina N" first="Natalia A." last="Ilyushina">Natalia A. Ilyushina</name>
<affiliation><inist:fA14 i1="01"><s1>Division of Therapeutic Proteins, Center for Drug Evaluation and Research, Food and Drug Administration</s1>
<s2>Silver Spring, MD 20993</s2>
<s3>USA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Donnelly, Raymond P" sort="Donnelly, Raymond P" uniqKey="Donnelly R" first="Raymond P." last="Donnelly">Raymond P. Donnelly</name>
<affiliation><inist:fA14 i1="01"><s1>Division of Therapeutic Proteins, Center for Drug Evaluation and Research, Food and Drug Administration</s1>
<s2>Silver Spring, MD 20993</s2>
<s3>USA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
</analytic>
<series><title level="j" type="main">Antiviral research</title>
<title level="j" type="abbreviated">Antivir. res.</title>
<idno type="ISSN">0166-3542</idno>
<imprint><date when="2014">2014</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
<seriesStmt><title level="j" type="main">Antiviral research</title>
<title level="j" type="abbreviated">Antivir. res.</title>
<idno type="ISSN">0166-3542</idno>
</seriesStmt>
</fileDesc>
<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Antiviral</term>
<term>Beta interferon</term>
<term>Combined treatment</term>
<term>Cytokine</term>
<term>Drug combination</term>
<term>In vitro</term>
<term>Influenza A</term>
<term>Influenza A virus</term>
<term>Oseltamivir</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr"><term>In vitro</term>
<term>Grippe A</term>
<term>Cytokine</term>
<term>Interféron bêta</term>
<term>Oséltamivir</term>
<term>Virus grippal A</term>
<term>Traitement associé</term>
<term>Association médicamenteuse</term>
<term>Antiviral</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">Influenza viruses, which can cross species barriers and adapt to new hosts, pose a constant potential threat to human health. The influenza pandemic of 2009 highlighted the rapidity with which an influenza virus can spread worldwide. Currently available antivirals have a number of limitations against influenza, and novel antiviral strategies, including novel drugs and drug combinations, are urgently needed. Here, we evaluated the in vitro effects of interferon (IFN)-β, IFN-λ1, oseltamivir carboxylate (a neuraminidase (NA) inhibitor), and combinations of these agents against two seasonal (i.e., H1N1 and H3N2) influenza A viruses. We observed that A/California/04/09 (H1N1) and A/Panama/2007/99 (H3N2) isolates were equally sensitive to the antiviral activity of IFN-β and oseltamivir carboxylate in A549 and Calu-3 cells. In contrast, IFN-λ1 exhibited substantially lower protective potential against the H1N1 strain (64-1030-fold ↓, P < 0.05), and was ineffective against H3N2 virus in both cell lines. Three dimensional analysis of drug-drug interactions revealed that IFN-λ1 interacted with IFN-β and oseltamivir carboxylate in an additive or synergistic manner, respectively, to inhibit influenza A virus replication in human airway epithelial cells. Overall, the present study demonstrated that anti-influenza agents with different mechanisms of action (e.g., a NA inhibitor combined with IFN-λ1) exerted a significantly greater (P < 0.05) synergistic effect compared to co-treatment with drugs that target the same signaling pathway (i.e., IFN-β plus IFN-λ1) in vitro. Our findings provide support for the combined use of interferon plus oseltamivir as a potential means for treating influenza infections.</div>
</front>
</TEI>
<inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0166-3542</s0>
</fA01>
<fA02 i1="01"><s0>ARSRDR</s0>
</fA02>
<fA03 i2="1"><s0>Antivir. res.</s0>
</fA03>
<fA05><s2>111</s2>
</fA05>
<fA08 i1="01" i2="1" l="ENG"><s1>In vitro anti-influenza A activity of interferon (IFN)-λ1 combined with IFN-β or oseltamivir carboxylate</s1>
</fA08>
<fA11 i1="01" i2="1"><s1>ILYUSHINA (Natalia A.)</s1>
</fA11>
<fA11 i1="02" i2="1"><s1>DONNELLY (Raymond P.)</s1>
</fA11>
<fA14 i1="01"><s1>Division of Therapeutic Proteins, Center for Drug Evaluation and Research, Food and Drug Administration</s1>
<s2>Silver Spring, MD 20993</s2>
<s3>USA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
</fA14>
<fA20><s1>112-120</s1>
</fA20>
<fA21><s1>2014</s1>
</fA21>
<fA23 i1="01"><s0>ENG</s0>
</fA23>
<fA43 i1="01"><s1>INIST</s1>
<s2>18839</s2>
<s5>354000502689950160</s5>
</fA43>
<fA44><s0>0000</s0>
<s1>© 2014 INIST-CNRS. All rights reserved.</s1>
</fA44>
<fA45><s0>3/4 p.</s0>
</fA45>
<fA47 i1="01" i2="1"><s0>14-0273479</s0>
</fA47>
<fA60><s1>P</s1>
</fA60>
<fA61><s0>A</s0>
</fA61>
<fA64 i1="01" i2="1"><s0>Antiviral research</s0>
</fA64>
<fA66 i1="01"><s0>GBR</s0>
</fA66>
<fC01 i1="01" l="ENG"><s0>Influenza viruses, which can cross species barriers and adapt to new hosts, pose a constant potential threat to human health. The influenza pandemic of 2009 highlighted the rapidity with which an influenza virus can spread worldwide. Currently available antivirals have a number of limitations against influenza, and novel antiviral strategies, including novel drugs and drug combinations, are urgently needed. Here, we evaluated the in vitro effects of interferon (IFN)-β, IFN-λ1, oseltamivir carboxylate (a neuraminidase (NA) inhibitor), and combinations of these agents against two seasonal (i.e., H1N1 and H3N2) influenza A viruses. We observed that A/California/04/09 (H1N1) and A/Panama/2007/99 (H3N2) isolates were equally sensitive to the antiviral activity of IFN-β and oseltamivir carboxylate in A549 and Calu-3 cells. In contrast, IFN-λ1 exhibited substantially lower protective potential against the H1N1 strain (64-1030-fold ↓, P < 0.05), and was ineffective against H3N2 virus in both cell lines. Three dimensional analysis of drug-drug interactions revealed that IFN-λ1 interacted with IFN-β and oseltamivir carboxylate in an additive or synergistic manner, respectively, to inhibit influenza A virus replication in human airway epithelial cells. Overall, the present study demonstrated that anti-influenza agents with different mechanisms of action (e.g., a NA inhibitor combined with IFN-λ1) exerted a significantly greater (P < 0.05) synergistic effect compared to co-treatment with drugs that target the same signaling pathway (i.e., IFN-β plus IFN-λ1) in vitro. Our findings provide support for the combined use of interferon plus oseltamivir as a potential means for treating influenza infections.</s0>
</fC01>
<fC02 i1="01" i2="X"><s0>002B02S05</s0>
</fC02>
<fC02 i1="02" i2="X"><s0>002B05C02C</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE"><s0>In vitro</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG"><s0>In vitro</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA"><s0>In vitro</s0>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE"><s0>Grippe A</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG"><s0>Influenza A</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA"><s0>Gripe A</s0>
<s5>02</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE"><s0>Cytokine</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG"><s0>Cytokine</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA"><s0>Citoquina</s0>
<s5>03</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE"><s0>Interféron bêta</s0>
<s2>FR</s2>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG"><s0>Beta interferon</s0>
<s2>FR</s2>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA"><s0>Interferón beta</s0>
<s2>FR</s2>
<s5>04</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>Oséltamivir</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>05</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG"><s0>Oseltamivir</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>05</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA"><s0>Oseltamivir</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>05</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE"><s0>Virus grippal A</s0>
<s2>NW</s2>
<s5>06</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG"><s0>Influenza A virus</s0>
<s2>NW</s2>
<s5>06</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA"><s0>Influenza A virus</s0>
<s2>NW</s2>
<s5>06</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE"><s0>Traitement associé</s0>
<s5>07</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG"><s0>Combined treatment</s0>
<s5>07</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA"><s0>Tratamiento asociado</s0>
<s5>07</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE"><s0>Association médicamenteuse</s0>
<s5>08</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG"><s0>Drug combination</s0>
<s5>08</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA"><s0>Asociación medicamentosa</s0>
<s5>08</s5>
</fC03>
<fC03 i1="09" i2="X" l="FRE"><s0>Antiviral</s0>
<s5>23</s5>
</fC03>
<fC03 i1="09" i2="X" l="ENG"><s0>Antiviral</s0>
<s5>23</s5>
</fC03>
<fC03 i1="09" i2="X" l="SPA"><s0>Antiviral</s0>
<s5>23</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Virose</s0>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Viral disease</s0>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Virosis</s0>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Infection</s0>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Infection</s0>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Infección</s0>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Influenzavirus A</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Influenzavirus A</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Influenzavirus A</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Orthomyxoviridae</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Orthomyxoviridae</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Orthomyxoviridae</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="06" i2="X" l="FRE"><s0>Exo-α-sialidase</s0>
<s2>FE</s2>
<s5>37</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG"><s0>Exo-α-sialidase</s0>
<s2>FE</s2>
<s5>37</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA"><s0>Exo-α-sialidase</s0>
<s2>FE</s2>
<s5>37</s5>
</fC07>
<fC07 i1="07" i2="X" l="FRE"><s0>Glycosidases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="07" i2="X" l="ENG"><s0>Glycosidases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="07" i2="X" l="SPA"><s0>Glycosidases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="08" i2="X" l="FRE"><s0>Glycosylases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="08" i2="X" l="ENG"><s0>Glycosylases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="08" i2="X" l="SPA"><s0>Glycosylases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="09" i2="X" l="FRE"><s0>Hydrolases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="09" i2="X" l="ENG"><s0>Hydrolases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="09" i2="X" l="SPA"><s0>Hydrolases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="10" i2="X" l="FRE"><s0>Enzyme</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="10" i2="X" l="ENG"><s0>Enzyme</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="10" i2="X" l="SPA"><s0>Enzima</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="11" i2="X" l="FRE"><s0>Inhibiteur enzyme</s0>
<s5>38</s5>
</fC07>
<fC07 i1="11" i2="X" l="ENG"><s0>Enzyme inhibitor</s0>
<s5>38</s5>
</fC07>
<fC07 i1="11" i2="X" l="SPA"><s0>Inhibidor enzima</s0>
<s5>38</s5>
</fC07>
<fC07 i1="12" i2="X" l="FRE"><s0>Inhibiteur neuraminidase</s0>
<s2>FR</s2>
<s5>39</s5>
</fC07>
<fC07 i1="12" i2="X" l="ENG"><s0>Neuraminidase inhibitor</s0>
<s2>FR</s2>
<s5>39</s5>
</fC07>
<fC07 i1="12" i2="X" l="SPA"><s0>Inhibidor neuraminidas</s0>
<s2>FR</s2>
<s5>39</s5>
</fC07>
<fN21><s1>342</s1>
</fN21>
<fN44 i1="01"><s1>OTO</s1>
</fN44>
<fN82><s1>OTO</s1>
</fN82>
</pA>
</standard>
<server><NO>PASCAL 14-0273479 INIST</NO>
<ET>In vitro anti-influenza A activity of interferon (IFN)-λ1 combined with IFN-β or oseltamivir carboxylate</ET>
<AU>ILYUSHINA (Natalia A.); DONNELLY (Raymond P.)</AU>
<AF>Division of Therapeutic Proteins, Center for Drug Evaluation and Research, Food and Drug Administration/Silver Spring, MD 20993/Etats-Unis (1 aut., 2 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Antiviral research; ISSN 0166-3542; Coden ARSRDR; Royaume-Uni; Da. 2014; Vol. 111; Pp. 112-120; Bibl. 3/4 p.</SO>
<LA>Anglais</LA>
<EA>Influenza viruses, which can cross species barriers and adapt to new hosts, pose a constant potential threat to human health. The influenza pandemic of 2009 highlighted the rapidity with which an influenza virus can spread worldwide. Currently available antivirals have a number of limitations against influenza, and novel antiviral strategies, including novel drugs and drug combinations, are urgently needed. Here, we evaluated the in vitro effects of interferon (IFN)-β, IFN-λ1, oseltamivir carboxylate (a neuraminidase (NA) inhibitor), and combinations of these agents against two seasonal (i.e., H1N1 and H3N2) influenza A viruses. We observed that A/California/04/09 (H1N1) and A/Panama/2007/99 (H3N2) isolates were equally sensitive to the antiviral activity of IFN-β and oseltamivir carboxylate in A549 and Calu-3 cells. In contrast, IFN-λ1 exhibited substantially lower protective potential against the H1N1 strain (64-1030-fold ↓, P < 0.05), and was ineffective against H3N2 virus in both cell lines. Three dimensional analysis of drug-drug interactions revealed that IFN-λ1 interacted with IFN-β and oseltamivir carboxylate in an additive or synergistic manner, respectively, to inhibit influenza A virus replication in human airway epithelial cells. Overall, the present study demonstrated that anti-influenza agents with different mechanisms of action (e.g., a NA inhibitor combined with IFN-λ1) exerted a significantly greater (P < 0.05) synergistic effect compared to co-treatment with drugs that target the same signaling pathway (i.e., IFN-β plus IFN-λ1) in vitro. Our findings provide support for the combined use of interferon plus oseltamivir as a potential means for treating influenza infections.</EA>
<CC>002B02S05; 002B05C02C</CC>
<FD>In vitro; Grippe A; Cytokine; Interféron bêta; Oséltamivir; Virus grippal A; Traitement associé; Association médicamenteuse; Antiviral</FD>
<FG>Virose; Infection; Influenzavirus A; Orthomyxoviridae; Virus; Exo-α-sialidase; Glycosidases; Glycosylases; Hydrolases; Enzyme; Inhibiteur enzyme; Inhibiteur neuraminidase</FG>
<ED>In vitro; Influenza A; Cytokine; Beta interferon; Oseltamivir; Influenza A virus; Combined treatment; Drug combination; Antiviral</ED>
<EG>Viral disease; Infection; Influenzavirus A; Orthomyxoviridae; Virus; Exo-α-sialidase; Glycosidases; Glycosylases; Hydrolases; Enzyme; Enzyme inhibitor; Neuraminidase inhibitor</EG>
<SD>In vitro; Gripe A; Citoquina; Interferón beta; Oseltamivir; Influenza A virus; Tratamiento asociado; Asociación medicamentosa; Antiviral</SD>
<LO>INIST-18839.354000502689950160</LO>
<ID>14-0273479</ID>
</server>
</inist>
</record>
Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Sante/explor/PandemieGrippaleV1/Data/PascalFrancis/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000025 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/PascalFrancis/Corpus/biblio.hfd -nk 000025 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien |wiki= Sante |area= PandemieGrippaleV1 |flux= PascalFrancis |étape= Corpus |type= RBID |clé= Pascal:14-0273479 |texte= In vitro anti-influenza A activity of interferon (IFN)-λ1 combined with IFN-β or oseltamivir carboxylate }}
This area was generated with Dilib version V0.6.34. |