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Thujaplicin-copper chelates inhibit replication of human influenza viruses

Identifieur interne : 000076 ( PascalFrancis/Corpus ); précédent : 000075; suivant : 000077

Thujaplicin-copper chelates inhibit replication of human influenza viruses

Auteurs : D. Miyamoto ; Y. Kusagaya ; N. Endo ; A. Sometani ; S. Takeo ; T. Suzuki ; Y. Arima ; K. Nakajima ; Y. Suzuki

Source :

RBID : Pascal:99-0041725

Descripteurs français

English descriptors

Abstract

The effects of α-, β- and γ-thujaplicins and six of their metal chelates on human influenza virus-induced apoptosis in Madin-Darby canine kidney (MDCK) cells were examined by DNA fragmentation and flow cytometry. Among the compounds tested, thujaplicin-copper chelates inhibited apoptosis induced in the infected MDCK cells with influenza A/PR/8/34(H1N1), A/Shingapol/1/57(H2N2), A/Aichi/2/68(H3N2) and B/Lee/40 viruses, at concentrations of more than 5 μM. These results indicate that the copper chelates inhibit influenza virus-induced apoptosis and that the inhibitory effects may be independent of influenza virus subtype or types. Furthermore, the copper chelates also inhibited the release of the viruses from the infected MDCK cells during apoptosis. The anti-apoptotic effects of the copper chelates may occur 2-4 h postinfection, suggesting that the copper chelates affect MDCK cells directly in the early stage of influenza virus-induced apoptosis. In this study, we demonstrated that thujaplicin-copper chelates inhibit influenza virus-induced apoptosis of MDCK cells and also inhibit virus replication and release from the infected cells.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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A03   1    @0 Antivir. res.
A05       @2 39
A06       @2 2
A08 01  1  ENG  @1 Thujaplicin-copper chelates inhibit replication of human influenza viruses
A11 01  1    @1 MIYAMOTO (D.)
A11 02  1    @1 KUSAGAYA (Y.)
A11 03  1    @1 ENDO (N.)
A11 04  1    @1 SOMETANI (A.)
A11 05  1    @1 TAKEO (S.)
A11 06  1    @1 SUZUKI (T.)
A11 07  1    @1 ARIMA (Y.)
A11 08  1    @1 NAKAJIMA (K.)
A11 09  1    @1 SUZUKI (Y.)
A14 01      @1 Department of Biochemistry, University of Shizuoka, School of Pharmaceutical Sciences, 52-1 Yada @2 Shizuoka-shi, Shizuoka 422-8526 @3 JPN @Z 1 aut. @Z 2 aut. @Z 3 aut. @Z 4 aut. @Z 5 aut. @Z 6 aut. @Z 9 aut.
A14 02      @1 Department of Analytical and Bioinorganic Chemistry, Kyoto Pharmaceutical University, 5 Nakauti-cho, Misasagi @2 Yamasina-ku, Kyoto 607 @3 JPN @Z 7 aut.
A14 03      @1 Otsuka America Pharmaceutical, Inc., 2440, Research Boulourd @2 Lock Ville, MD 20850 @3 USA @Z 8 aut.
A20       @1 89-100
A21       @1 1998
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A43 01      @1 INIST @2 18839 @5 354000071279630030
A44       @0 0000 @1 © 1999 INIST-CNRS. All rights reserved.
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A60       @1 P
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C01 01    ENG  @0 The effects of α-, β- and γ-thujaplicins and six of their metal chelates on human influenza virus-induced apoptosis in Madin-Darby canine kidney (MDCK) cells were examined by DNA fragmentation and flow cytometry. Among the compounds tested, thujaplicin-copper chelates inhibited apoptosis induced in the infected MDCK cells with influenza A/PR/8/34(H1N1), A/Shingapol/1/57(H2N2), A/Aichi/2/68(H3N2) and B/Lee/40 viruses, at concentrations of more than 5 μM. These results indicate that the copper chelates inhibit influenza virus-induced apoptosis and that the inhibitory effects may be independent of influenza virus subtype or types. Furthermore, the copper chelates also inhibited the release of the viruses from the infected MDCK cells during apoptosis. The anti-apoptotic effects of the copper chelates may occur 2-4 h postinfection, suggesting that the copper chelates affect MDCK cells directly in the early stage of influenza virus-induced apoptosis. In this study, we demonstrated that thujaplicin-copper chelates inhibit influenza virus-induced apoptosis of MDCK cells and also inhibit virus replication and release from the infected cells.
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Format Inist (serveur)

NO : PASCAL 99-0041725 INIST
ET : Thujaplicin-copper chelates inhibit replication of human influenza viruses
AU : MIYAMOTO (D.); KUSAGAYA (Y.); ENDO (N.); SOMETANI (A.); TAKEO (S.); SUZUKI (T.); ARIMA (Y.); NAKAJIMA (K.); SUZUKI (Y.)
AF : Department of Biochemistry, University of Shizuoka, School of Pharmaceutical Sciences, 52-1 Yada/Shizuoka-shi, Shizuoka 422-8526/Japon (1 aut., 2 aut., 3 aut., 4 aut., 5 aut., 6 aut., 9 aut.); Department of Analytical and Bioinorganic Chemistry, Kyoto Pharmaceutical University, 5 Nakauti-cho, Misasagi/Yamasina-ku, Kyoto 607/Japon (7 aut.); Otsuka America Pharmaceutical, Inc., 2440, Research Boulourd/Lock Ville, MD 20850/Etats-Unis (8 aut.)
DT : Publication en série; Niveau analytique
SO : Antiviral research; ISSN 0166-3542; Coden ARSRDR; Pays-Bas; Da. 1998; Vol. 39; No. 2; Pp. 89-100; Bibl. 25 ref.
LA : Anglais
EA : The effects of α-, β- and γ-thujaplicins and six of their metal chelates on human influenza virus-induced apoptosis in Madin-Darby canine kidney (MDCK) cells were examined by DNA fragmentation and flow cytometry. Among the compounds tested, thujaplicin-copper chelates inhibited apoptosis induced in the infected MDCK cells with influenza A/PR/8/34(H1N1), A/Shingapol/1/57(H2N2), A/Aichi/2/68(H3N2) and B/Lee/40 viruses, at concentrations of more than 5 μM. These results indicate that the copper chelates inhibit influenza virus-induced apoptosis and that the inhibitory effects may be independent of influenza virus subtype or types. Furthermore, the copper chelates also inhibited the release of the viruses from the infected MDCK cells during apoptosis. The anti-apoptotic effects of the copper chelates may occur 2-4 h postinfection, suggesting that the copper chelates affect MDCK cells directly in the early stage of influenza virus-induced apoptosis. In this study, we demonstrated that thujaplicin-copper chelates inhibit influenza virus-induced apoptosis of MDCK cells and also inhibit virus replication and release from the infected cells.
CC : 002B02S05
FD : Antiviral; Activité biologique; Influenzavirus; Apoptose; Mort cellulaire; In vitro; Chélateur; Cuivre Métal; Thuja; Origine végétale; Plante médicinale; Pharmacognosie; Lignée cellulaire établie; Chien; Réplication; Infection; Thujaplicine; Lignée MDCK
FG : Orthomyxoviridae; Virus; Coniferales; Gymnospermae; Spermatophyta; Fissipedia; Carnivora; Mammalia; Vertebrata
ED : Antiviral; Biological activity; Influenzavirus; Apoptosis; Cell death; In vitro; Chelating agent; Copper Metal; Thuja; Plant origin; Medicinal plant; Pharmacognosy; Established cell line; Dog; Replication; Infection
EG : Orthomyxoviridae; Virus; Coniferales; Gymnospermae; Spermatophyta; Fissipedia; Carnivora; Mammalia; Vertebrata
SD : Antiviral; Actividad biológica; Influenzavirus; Apoptosis; Muerte celular; In vitro; Quelante; Cobre Metal; Thuja; Origen vegetal; Planta medicinal; Farmacognosia; Línea celular establecida; Perro; Replicación; Infección
LO : INIST-18839.354000071279630030
ID : 99-0041725

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Pascal:99-0041725

Le document en format XML

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<name sortKey="Nakajima, K" sort="Nakajima, K" uniqKey="Nakajima K" first="K." last="Nakajima">K. Nakajima</name>
<affiliation>
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<s1>Otsuka America Pharmaceutical, Inc., 2440, Research Boulourd</s1>
<s2>Lock Ville, MD 20850</s2>
<s3>USA</s3>
<sZ>8 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Suzuki, Y" sort="Suzuki, Y" uniqKey="Suzuki Y" first="Y." last="Suzuki">Y. Suzuki</name>
<affiliation>
<inist:fA14 i1="01">
<s1>Department of Biochemistry, University of Shizuoka, School of Pharmaceutical Sciences, 52-1 Yada</s1>
<s2>Shizuoka-shi, Shizuoka 422-8526</s2>
<s3>JPN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
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<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="1998">1998</date>
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<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>Apoptosis</term>
<term>Biological activity</term>
<term>Cell death</term>
<term>Chelating agent</term>
<term>Copper Metal</term>
<term>Dog</term>
<term>Established cell line</term>
<term>In vitro</term>
<term>Infection</term>
<term>Influenzavirus</term>
<term>Medicinal plant</term>
<term>Pharmacognosy</term>
<term>Plant origin</term>
<term>Replication</term>
<term>Thuja</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr">
<term>Antiviral</term>
<term>Activité biologique</term>
<term>Influenzavirus</term>
<term>Apoptose</term>
<term>Mort cellulaire</term>
<term>In vitro</term>
<term>Chélateur</term>
<term>Cuivre Métal</term>
<term>Thuja</term>
<term>Origine végétale</term>
<term>Plante médicinale</term>
<term>Pharmacognosie</term>
<term>Lignée cellulaire établie</term>
<term>Chien</term>
<term>Réplication</term>
<term>Infection</term>
<term>Thujaplicine</term>
<term>Lignée MDCK</term>
</keywords>
</textClass>
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<front>
<div type="abstract" xml:lang="en">The effects of α-, β- and γ-thujaplicins and six of their metal chelates on human influenza virus-induced apoptosis in Madin-Darby canine kidney (MDCK) cells were examined by DNA fragmentation and flow cytometry. Among the compounds tested, thujaplicin-copper chelates inhibited apoptosis induced in the infected MDCK cells with influenza A/PR/8/34(H1N1), A/Shingapol/1/57(H2N2), A/Aichi/2/68(H3N2) and B/Lee/40 viruses, at concentrations of more than 5 μM. These results indicate that the copper chelates inhibit influenza virus-induced apoptosis and that the inhibitory effects may be independent of influenza virus subtype or types. Furthermore, the copper chelates also inhibited the release of the viruses from the infected MDCK cells during apoptosis. The anti-apoptotic effects of the copper chelates may occur 2-4 h postinfection, suggesting that the copper chelates affect MDCK cells directly in the early stage of influenza virus-induced apoptosis. In this study, we demonstrated that thujaplicin-copper chelates inhibit influenza virus-induced apoptosis of MDCK cells and also inhibit virus replication and release from the infected cells.</div>
</front>
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<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
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<fA14 i1="02">
<s1>Department of Analytical and Bioinorganic Chemistry, Kyoto Pharmaceutical University, 5 Nakauti-cho, Misasagi</s1>
<s2>Yamasina-ku, Kyoto 607</s2>
<s3>JPN</s3>
<sZ>7 aut.</sZ>
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<fA14 i1="03">
<s1>Otsuka America Pharmaceutical, Inc., 2440, Research Boulourd</s1>
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<s1>© 1999 INIST-CNRS. All rights reserved.</s1>
</fA44>
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<s0>The effects of α-, β- and γ-thujaplicins and six of their metal chelates on human influenza virus-induced apoptosis in Madin-Darby canine kidney (MDCK) cells were examined by DNA fragmentation and flow cytometry. Among the compounds tested, thujaplicin-copper chelates inhibited apoptosis induced in the infected MDCK cells with influenza A/PR/8/34(H1N1), A/Shingapol/1/57(H2N2), A/Aichi/2/68(H3N2) and B/Lee/40 viruses, at concentrations of more than 5 μM. These results indicate that the copper chelates inhibit influenza virus-induced apoptosis and that the inhibitory effects may be independent of influenza virus subtype or types. Furthermore, the copper chelates also inhibited the release of the viruses from the infected MDCK cells during apoptosis. The anti-apoptotic effects of the copper chelates may occur 2-4 h postinfection, suggesting that the copper chelates affect MDCK cells directly in the early stage of influenza virus-induced apoptosis. In this study, we demonstrated that thujaplicin-copper chelates inhibit influenza virus-induced apoptosis of MDCK cells and also inhibit virus replication and release from the infected cells.</s0>
</fC01>
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<s0>002B02S05</s0>
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<s5>01</s5>
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<s5>07</s5>
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<fC03 i1="03" i2="X" l="SPA">
<s0>Influenzavirus</s0>
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<s5>10</s5>
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<s0>Apoptosis</s0>
<s5>10</s5>
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<s0>Apoptosis</s0>
<s5>10</s5>
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<s5>11</s5>
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<s2>NS</s2>
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<s0>Origine végétale</s0>
<s5>18</s5>
</fC03>
<fC03 i1="10" i2="X" l="ENG">
<s0>Plant origin</s0>
<s5>18</s5>
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<fC03 i1="10" i2="X" l="SPA">
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<s0>Chien</s0>
<s5>22</s5>
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<s0>Dog</s0>
<s5>22</s5>
</fC03>
<fC03 i1="14" i2="X" l="SPA">
<s0>Perro</s0>
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<s0>Réplication</s0>
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<s0>Replication</s0>
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<s0>Infección</s0>
<s5>79</s5>
</fC03>
<fC03 i1="17" i2="X" l="FRE">
<s0>Thujaplicine</s0>
<s2>FR</s2>
<s4>INC</s4>
<s5>86</s5>
</fC03>
<fC03 i1="18" i2="X" l="FRE">
<s0>Lignée MDCK</s0>
<s4>INC</s4>
<s5>89</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE">
<s0>Orthomyxoviridae</s0>
<s2>NW</s2>
</fC07>
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<s0>Orthomyxoviridae</s0>
<s2>NW</s2>
</fC07>
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<s0>Virus</s0>
<s2>NW</s2>
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<fC07 i1="02" i2="X" l="ENG">
<s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="02" i2="X" l="SPA">
<s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="03" i2="X" l="FRE">
<s0>Coniferales</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="03" i2="X" l="ENG">
<s0>Coniferales</s0>
<s2>NS</s2>
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<s0>Coniferales</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="04" i2="X" l="FRE">
<s0>Gymnospermae</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="04" i2="X" l="ENG">
<s0>Gymnospermae</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="04" i2="X" l="SPA">
<s0>Gymnospermae</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="05" i2="X" l="FRE">
<s0>Spermatophyta</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="05" i2="X" l="ENG">
<s0>Spermatophyta</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="05" i2="X" l="SPA">
<s0>Spermatophyta</s0>
<s2>NS</s2>
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<fC07 i1="06" i2="X" l="FRE">
<s0>Fissipedia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="06" i2="X" l="ENG">
<s0>Fissipedia</s0>
<s2>NS</s2>
</fC07>
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<s0>Fissipedia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="07" i2="X" l="FRE">
<s0>Carnivora</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="07" i2="X" l="ENG">
<s0>Carnivora</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="07" i2="X" l="SPA">
<s0>Carnivora</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="08" i2="X" l="FRE">
<s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="08" i2="X" l="ENG">
<s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="08" i2="X" l="SPA">
<s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="09" i2="X" l="FRE">
<s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="09" i2="X" l="ENG">
<s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="09" i2="X" l="SPA">
<s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fN21>
<s1>025</s1>
</fN21>
</pA>
</standard>
<server>
<NO>PASCAL 99-0041725 INIST</NO>
<ET>Thujaplicin-copper chelates inhibit replication of human influenza viruses</ET>
<AU>MIYAMOTO (D.); KUSAGAYA (Y.); ENDO (N.); SOMETANI (A.); TAKEO (S.); SUZUKI (T.); ARIMA (Y.); NAKAJIMA (K.); SUZUKI (Y.)</AU>
<AF>Department of Biochemistry, University of Shizuoka, School of Pharmaceutical Sciences, 52-1 Yada/Shizuoka-shi, Shizuoka 422-8526/Japon (1 aut., 2 aut., 3 aut., 4 aut., 5 aut., 6 aut., 9 aut.); Department of Analytical and Bioinorganic Chemistry, Kyoto Pharmaceutical University, 5 Nakauti-cho, Misasagi/Yamasina-ku, Kyoto 607/Japon (7 aut.); Otsuka America Pharmaceutical, Inc., 2440, Research Boulourd/Lock Ville, MD 20850/Etats-Unis (8 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Antiviral research; ISSN 0166-3542; Coden ARSRDR; Pays-Bas; Da. 1998; Vol. 39; No. 2; Pp. 89-100; Bibl. 25 ref.</SO>
<LA>Anglais</LA>
<EA>The effects of α-, β- and γ-thujaplicins and six of their metal chelates on human influenza virus-induced apoptosis in Madin-Darby canine kidney (MDCK) cells were examined by DNA fragmentation and flow cytometry. Among the compounds tested, thujaplicin-copper chelates inhibited apoptosis induced in the infected MDCK cells with influenza A/PR/8/34(H1N1), A/Shingapol/1/57(H2N2), A/Aichi/2/68(H3N2) and B/Lee/40 viruses, at concentrations of more than 5 μM. These results indicate that the copper chelates inhibit influenza virus-induced apoptosis and that the inhibitory effects may be independent of influenza virus subtype or types. Furthermore, the copper chelates also inhibited the release of the viruses from the infected MDCK cells during apoptosis. The anti-apoptotic effects of the copper chelates may occur 2-4 h postinfection, suggesting that the copper chelates affect MDCK cells directly in the early stage of influenza virus-induced apoptosis. In this study, we demonstrated that thujaplicin-copper chelates inhibit influenza virus-induced apoptosis of MDCK cells and also inhibit virus replication and release from the infected cells.</EA>
<CC>002B02S05</CC>
<FD>Antiviral; Activité biologique; Influenzavirus; Apoptose; Mort cellulaire; In vitro; Chélateur; Cuivre Métal; Thuja; Origine végétale; Plante médicinale; Pharmacognosie; Lignée cellulaire établie; Chien; Réplication; Infection; Thujaplicine; Lignée MDCK</FD>
<FG>Orthomyxoviridae; Virus; Coniferales; Gymnospermae; Spermatophyta; Fissipedia; Carnivora; Mammalia; Vertebrata</FG>
<ED>Antiviral; Biological activity; Influenzavirus; Apoptosis; Cell death; In vitro; Chelating agent; Copper Metal; Thuja; Plant origin; Medicinal plant; Pharmacognosy; Established cell line; Dog; Replication; Infection</ED>
<EG>Orthomyxoviridae; Virus; Coniferales; Gymnospermae; Spermatophyta; Fissipedia; Carnivora; Mammalia; Vertebrata</EG>
<SD>Antiviral; Actividad biológica; Influenzavirus; Apoptosis; Muerte celular; In vitro; Quelante; Cobre Metal; Thuja; Origen vegetal; Planta medicinal; Farmacognosia; Línea celular establecida; Perro; Replicación; Infección</SD>
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