Antiviral strategies in chronic hepatitis B virus infection: II. Inhibition of duck hepatitis B Virus in vitro using conventional antiviral agents and supercoiled‐DNA active compounds
Identifieur interne : 003090 ( Main/Exploration ); précédent : 003089; suivant : 003091Antiviral strategies in chronic hepatitis B virus infection: II. Inhibition of duck hepatitis B Virus in vitro using conventional antiviral agents and supercoiled‐DNA active compounds
Auteurs : Gilda Civitico [Australie] ; Yanyan Wang [Australie] ; Carolyn Luscombe [Australie] ; Naomi Bishop [Australie] ; Gilda Tachedjian [Australie] ; Ian Gust [Australie] ; Stephen Locarnini [Australie]Source :
- Journal of Medical Virology [ 0146-6615 ] ; 1990-06.
Descripteurs français
- KwdFr :
- ADN superhélicoïdal (), ADN viral (), Altération de l'ADN, Animaux, Antiviraux (), Antiviraux (pharmacologie), Canards, Cellules cultivées, Foie (anatomopathologie), Humains, Hépatite virale animale (anatomopathologie), Inhibiteurs de la transcriptase inverse, Intercalants (pharmacologie), Modèles animaux de maladie humaine, Protéines de liaison à l'ADN (antagonistes et inhibiteurs), Réplication de l'ADN (), Réplication virale (), Virus de l'hépatite B du canard (), Virus de l'hépatite B du canard (génétique), Virus de l'hépatite B du canard (physiologie).
- MESH :
- anatomopathologie : Foie, Hépatite virale animale.
- antagonistes et inhibiteurs : Protéines de liaison à l'ADN.
- génétique : Virus de l'hépatite B du canard.
- pharmacologie : Antiviraux, Intercalants.
- physiologie : Virus de l'hépatite B du canard.
- ADN superhélicoïdal, ADN viral, Altération de l'ADN, Animaux, Antiviraux, Canards, Cellules cultivées, Humains, Inhibiteurs de la transcriptase inverse, Modèles animaux de maladie humaine, Réplication de l'ADN, Réplication virale, Virus de l'hépatite B du canard.
English descriptors
- KwdEn :
- Animals, Antiviral Agents (classification), Antiviral Agents (pharmacology), Cells, Cultured, DNA Damage, DNA Replication (drug effects), DNA, Superhelical (drug effects), DNA, Viral (drug effects), DNA-Binding Proteins (antagonists & inhibitors), Disease Models, Animal, Ducks, Hepatitis B Virus, Duck (drug effects), Hepatitis B Virus, Duck (genetics), Hepatitis B Virus, Duck (physiology), Hepatitis, Viral, Animal (pathology), Humans, Intercalating Agents (pharmacology), Liver (pathology), Reverse Transcriptase Inhibitors, Virus Replication (drug effects).
- MESH :
- chemical , antagonists & inhibitors : DNA-Binding Proteins.
- chemical , classification : Antiviral Agents.
- chemical , drug effects : DNA, Superhelical, DNA, Viral.
- chemical , pharmacology : Antiviral Agents, Intercalating Agents.
- drug effects : DNA Replication, Hepatitis B Virus, Duck, Virus Replication.
- genetics : Hepatitis B Virus, Duck.
- pathology : Hepatitis, Viral, Animal, Liver.
- physiology : Hepatitis B Virus, Duck.
- Teeft :
- Active compounds, Acyclovir, Adenine, Adenine arabinoside, Adriamycin, Amsacrine, Animals, Antimicrobial agents, Antiviral, Antiviral agents, Antiviral strategies, Arabinoside, Binding agents, Binding compounds, Bvdu, Camptothecin, Cells, Cultured, Chloroquine, Chronic hepatitis, Compound, Conventional agents, Coumermycin, DNA Damage, Days postplating, Densitometer analysis, Dhbsag, Dhbsag production, Dhbv, Dideoxyadenosine, Disease Models, Animal, Duck hepatitis, Ducks, Ellipticine, Etoposide, Fairfield hospital, Ganciclovir, Gyrase inhibitors, Hepatitis, Humans, Hybridization, Immunoblot analysis, Inhibitor, Macfarlane burnet centre, Medical research, Medical virology, Mitozantrone, Nalidixic, Nalidixic acid, Neocarzinostatin, Novobiocin, Phosphonoformate, Polymerase, Postplating, Replication, Replicative, Replicative intermediates, Reverse Transcriptase Inhibitors, Ribavirin, Southern hybridization, Supercoiled, Teniposide, Topoisomerase, Transcriptase, Transcriptase inhibitors, Tuttleman, Untreated, Viral, Virology, Virus infection, Virus replication.
Abstract
Primary duck hepatocyte (PDH) cultures, congenitally infected with the duck hepatitis B virus (DHBV), were grown on feeder cell layers of irradiated human embryonic lung fibroblasts and then exposed to a number of compounds with recognized or potential antiviral activity. These compounds included conventional antiviral agents, reverse transcriptase inhibitors, compounds with activity to supercoiled‐DNA, and DNA‐binding agents. Twenty‐three compounds were evaluated, and 13 were found to inhibit significantly viral DNA replication. Seven of these compounds (ellipticine, amsacrine, coumermycin A1, Adriamycin, mitozantrone, chloroquine, and neocarzinostatin) acted at the level of viral SC DNA and significantly inhibited production of duck hepatitis B surface antigen (DHBsAg). Conventional agents that inhibited DHBV DNA replication included ganciclovir, acyclovir, bromovinyldeoxyuridine, ribavirin, phosphonoformate, and dideoxyadenosine. Except for dideoxyadenosine, these inhibitors of viral DNA synthesis did not significantly inhibit DHBsAg production. Two additional compounds, novobiocin and nalidixic acid, altered the pattern of viral DNA replication, especially the generation and processing of viral SC DNA, and also inhibited the production of DHBsAg. Several compounds acting at the level of viral SC DNA have now been identified and may offer potential for the management of chronic hepatitis B virus infection.
Url:
DOI: 10.1002/jmv.1890310205
Affiliations:
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Le document en format XML
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term>
<term>Antiviral Agents (classification)</term>
<term>Antiviral Agents (pharmacology)</term>
<term>Cells, Cultured</term>
<term>DNA Damage</term>
<term>DNA Replication (drug effects)</term>
<term>DNA, Superhelical (drug effects)</term>
<term>DNA, Viral (drug effects)</term>
<term>DNA-Binding Proteins (antagonists & inhibitors)</term>
<term>Disease Models, Animal</term>
<term>Ducks</term>
<term>Hepatitis B Virus, Duck (drug effects)</term>
<term>Hepatitis B Virus, Duck (genetics)</term>
<term>Hepatitis B Virus, Duck (physiology)</term>
<term>Hepatitis, Viral, Animal (pathology)</term>
<term>Humans</term>
<term>Intercalating Agents (pharmacology)</term>
<term>Liver (pathology)</term>
<term>Reverse Transcriptase Inhibitors</term>
<term>Virus Replication (drug effects)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>ADN superhélicoïdal ()</term>
<term>ADN viral ()</term>
<term>Altération de l'ADN</term>
<term>Animaux</term>
<term>Antiviraux ()</term>
<term>Antiviraux (pharmacologie)</term>
<term>Canards</term>
<term>Cellules cultivées</term>
<term>Foie (anatomopathologie)</term>
<term>Humains</term>
<term>Hépatite virale animale (anatomopathologie)</term>
<term>Inhibiteurs de la transcriptase inverse</term>
<term>Intercalants (pharmacologie)</term>
<term>Modèles animaux de maladie humaine</term>
<term>Protéines de liaison à l'ADN (antagonistes et inhibiteurs)</term>
<term>Réplication de l'ADN ()</term>
<term>Réplication virale ()</term>
<term>Virus de l'hépatite B du canard ()</term>
<term>Virus de l'hépatite B du canard (génétique)</term>
<term>Virus de l'hépatite B du canard (physiologie)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>DNA-Binding Proteins</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="classification" xml:lang="en"><term>Antiviral Agents</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="drug effects" xml:lang="en"><term>DNA, Superhelical</term>
<term>DNA, Viral</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Antiviral Agents</term>
<term>Intercalating Agents</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Foie</term>
<term>Hépatite virale animale</term>
</keywords>
<keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>Protéines de liaison à l'ADN</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>DNA Replication</term>
<term>Hepatitis B Virus, Duck</term>
<term>Virus Replication</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Hepatitis B Virus, Duck</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Virus de l'hépatite B du canard</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Hepatitis, Viral, Animal</term>
<term>Liver</term>
</keywords>
<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Antiviraux</term>
<term>Intercalants</term>
</keywords>
<keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Virus de l'hépatite B du canard</term>
</keywords>
<keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Hepatitis B Virus, Duck</term>
</keywords>
<keywords scheme="Teeft" xml:lang="en"><term>Active compounds</term>
<term>Acyclovir</term>
<term>Adenine</term>
<term>Adenine arabinoside</term>
<term>Adriamycin</term>
<term>Amsacrine</term>
<term>Animals</term>
<term>Antimicrobial agents</term>
<term>Antiviral</term>
<term>Antiviral agents</term>
<term>Antiviral strategies</term>
<term>Arabinoside</term>
<term>Binding agents</term>
<term>Binding compounds</term>
<term>Bvdu</term>
<term>Camptothecin</term>
<term>Cells, Cultured</term>
<term>Chloroquine</term>
<term>Chronic hepatitis</term>
<term>Compound</term>
<term>Conventional agents</term>
<term>Coumermycin</term>
<term>DNA Damage</term>
<term>Days postplating</term>
<term>Densitometer analysis</term>
<term>Dhbsag</term>
<term>Dhbsag production</term>
<term>Dhbv</term>
<term>Dideoxyadenosine</term>
<term>Disease Models, Animal</term>
<term>Duck hepatitis</term>
<term>Ducks</term>
<term>Ellipticine</term>
<term>Etoposide</term>
<term>Fairfield hospital</term>
<term>Ganciclovir</term>
<term>Gyrase inhibitors</term>
<term>Hepatitis</term>
<term>Humans</term>
<term>Hybridization</term>
<term>Immunoblot analysis</term>
<term>Inhibitor</term>
<term>Macfarlane burnet centre</term>
<term>Medical research</term>
<term>Medical virology</term>
<term>Mitozantrone</term>
<term>Nalidixic</term>
<term>Nalidixic acid</term>
<term>Neocarzinostatin</term>
<term>Novobiocin</term>
<term>Phosphonoformate</term>
<term>Polymerase</term>
<term>Postplating</term>
<term>Replication</term>
<term>Replicative</term>
<term>Replicative intermediates</term>
<term>Reverse Transcriptase Inhibitors</term>
<term>Ribavirin</term>
<term>Southern hybridization</term>
<term>Supercoiled</term>
<term>Teniposide</term>
<term>Topoisomerase</term>
<term>Transcriptase</term>
<term>Transcriptase inhibitors</term>
<term>Tuttleman</term>
<term>Untreated</term>
<term>Viral</term>
<term>Virology</term>
<term>Virus infection</term>
<term>Virus replication</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>ADN superhélicoïdal</term>
<term>ADN viral</term>
<term>Altération de l'ADN</term>
<term>Animaux</term>
<term>Antiviraux</term>
<term>Canards</term>
<term>Cellules cultivées</term>
<term>Humains</term>
<term>Inhibiteurs de la transcriptase inverse</term>
<term>Modèles animaux de maladie humaine</term>
<term>Réplication de l'ADN</term>
<term>Réplication virale</term>
<term>Virus de l'hépatite B du canard</term>
</keywords>
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<front><div type="abstract" xml:lang="en">Primary duck hepatocyte (PDH) cultures, congenitally infected with the duck hepatitis B virus (DHBV), were grown on feeder cell layers of irradiated human embryonic lung fibroblasts and then exposed to a number of compounds with recognized or potential antiviral activity. These compounds included conventional antiviral agents, reverse transcriptase inhibitors, compounds with activity to supercoiled‐DNA, and DNA‐binding agents. Twenty‐three compounds were evaluated, and 13 were found to inhibit significantly viral DNA replication. Seven of these compounds (ellipticine, amsacrine, coumermycin A1, Adriamycin, mitozantrone, chloroquine, and neocarzinostatin) acted at the level of viral SC DNA and significantly inhibited production of duck hepatitis B surface antigen (DHBsAg). Conventional agents that inhibited DHBV DNA replication included ganciclovir, acyclovir, bromovinyldeoxyuridine, ribavirin, phosphonoformate, and dideoxyadenosine. Except for dideoxyadenosine, these inhibitors of viral DNA synthesis did not significantly inhibit DHBsAg production. Two additional compounds, novobiocin and nalidixic acid, altered the pattern of viral DNA replication, especially the generation and processing of viral SC DNA, and also inhibited the production of DHBsAg. Several compounds acting at the level of viral SC DNA have now been identified and may offer potential for the management of chronic hepatitis B virus infection.</div>
</front>
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<affiliations><list><country><li>Australie</li>
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<tree><country name="Australie"><noRegion><name sortKey="Civitico, Gilda" sort="Civitico, Gilda" uniqKey="Civitico G" first="Gilda" last="Civitico">Gilda Civitico</name>
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<name sortKey="Bishop, Naomi" sort="Bishop, Naomi" uniqKey="Bishop N" first="Naomi" last="Bishop">Naomi Bishop</name>
<name sortKey="Gust, Ian" sort="Gust, Ian" uniqKey="Gust I" first="Ian" last="Gust">Ian Gust</name>
<name sortKey="Locarnini, Stephen" sort="Locarnini, Stephen" uniqKey="Locarnini S" first="Stephen" last="Locarnini">Stephen Locarnini</name>
<name sortKey="Locarnini, Stephen" sort="Locarnini, Stephen" uniqKey="Locarnini S" first="Stephen" last="Locarnini">Stephen Locarnini</name>
<name sortKey="Luscombe, Carolyn" sort="Luscombe, Carolyn" uniqKey="Luscombe C" first="Carolyn" last="Luscombe">Carolyn Luscombe</name>
<name sortKey="Tachedjian, Gilda" sort="Tachedjian, Gilda" uniqKey="Tachedjian G" first="Gilda" last="Tachedjian">Gilda Tachedjian</name>
<name sortKey="Wang, Yanyan" sort="Wang, Yanyan" uniqKey="Wang Y" first="Yanyan" last="Wang">Yanyan Wang</name>
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