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 : 000093 ( Ncbi/Checkpoint ); précédent : 000092; suivant : 000094Antiviral 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 : G. Civitico [Australie] ; Y Y Wang ; C. Luscombe ; N. Bishop ; G. Tachedjian ; I. Gust ; S. LocarniniSource :
- Journal of medical virology [ 0146-6615 ] ; 1990.
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.
- Animals, Cells, Cultured, DNA Damage, Disease Models, Animal, Ducks, Humans, Reverse Transcriptase Inhibitors.
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.
DOI: 10.1002/jmv.1890310205
PubMed: 1696959
Affiliations:
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pubmed:1696959Le document en format XML
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Civitico</name><affiliation wicri:level="1"><nlm:affiliation>Hepatitis Research Unit, Macfarlane Burnet Centre for Medical Research, Fairfield Hospital, Victoria, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>Hepatitis Research Unit, Macfarlane Burnet Centre for Medical Research, Fairfield Hospital, Victoria</wicri:regionArea><wicri:noRegion>Victoria</wicri:noRegion></affiliation></author><author><name sortKey="Wang, Y Y" sort="Wang, Y Y" uniqKey="Wang Y" first="Y Y" last="Wang">Y Y Wang</name></author><author><name sortKey="Luscombe, C" sort="Luscombe, C" uniqKey="Luscombe C" first="C" last="Luscombe">C. Luscombe</name></author><author><name sortKey="Bishop, N" sort="Bishop, N" uniqKey="Bishop N" first="N" last="Bishop">N. Bishop</name></author><author><name sortKey="Tachedjian, G" sort="Tachedjian, G" uniqKey="Tachedjian G" first="G" last="Tachedjian">G. Tachedjian</name></author><author><name sortKey="Gust, I" sort="Gust, I" uniqKey="Gust I" first="I" last="Gust">I. Gust</name></author><author><name sortKey="Locarnini, S" sort="Locarnini, S" uniqKey="Locarnini S" first="S" last="Locarnini">S. 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Inhibition of duck hepatitis B virus in vitro using conventional antiviral agents and supercoiled-DNA active compounds.</title><author><name sortKey="Civitico, G" sort="Civitico, G" uniqKey="Civitico G" first="G" last="Civitico">G. Civitico</name><affiliation wicri:level="1"><nlm:affiliation>Hepatitis Research Unit, Macfarlane Burnet Centre for Medical Research, Fairfield Hospital, Victoria, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>Hepatitis Research Unit, Macfarlane Burnet Centre for Medical Research, Fairfield Hospital, Victoria</wicri:regionArea><wicri:noRegion>Victoria</wicri:noRegion></affiliation></author><author><name sortKey="Wang, Y Y" sort="Wang, Y Y" uniqKey="Wang Y" first="Y Y" last="Wang">Y Y Wang</name></author><author><name sortKey="Luscombe, C" sort="Luscombe, C" uniqKey="Luscombe C" first="C" last="Luscombe">C. Luscombe</name></author><author><name sortKey="Bishop, N" sort="Bishop, N" uniqKey="Bishop N" first="N" last="Bishop">N. Bishop</name></author><author><name sortKey="Tachedjian, G" sort="Tachedjian, G" uniqKey="Tachedjian G" first="G" last="Tachedjian">G. Tachedjian</name></author><author><name sortKey="Gust, I" sort="Gust, I" uniqKey="Gust I" first="I" last="Gust">I. Gust</name></author><author><name sortKey="Locarnini, S" sort="Locarnini, S" uniqKey="Locarnini S" first="S" last="Locarnini">S. Locarnini</name></author></analytic><series><title level="j">Journal of medical virology</title><idno type="ISSN">0146-6615</idno><imprint><date when="1990" type="published">1990</date></imprint></series></biblStruct></sourceDesc></fileDesc><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="MESH" xml:lang="en"><term>Animals</term><term>Cells, Cultured</term><term>DNA Damage</term><term>Disease Models, Animal</term><term>Ducks</term><term>Humans</term><term>Reverse Transcriptase Inhibitors</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></textClass></profileDesc></teiHeader><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></TEI><affiliations><list><country><li>Australie</li></country></list><tree><noCountry><name sortKey="Bishop, N" sort="Bishop, N" uniqKey="Bishop N" first="N" last="Bishop">N. Bishop</name><name sortKey="Gust, I" sort="Gust, I" uniqKey="Gust I" first="I" last="Gust">I. Gust</name><name sortKey="Locarnini, S" sort="Locarnini, S" uniqKey="Locarnini S" first="S" last="Locarnini">S. Locarnini</name><name sortKey="Luscombe, C" sort="Luscombe, C" uniqKey="Luscombe C" first="C" last="Luscombe">C. Luscombe</name><name sortKey="Tachedjian, G" sort="Tachedjian, G" uniqKey="Tachedjian G" first="G" last="Tachedjian">G. Tachedjian</name><name sortKey="Wang, Y Y" sort="Wang, Y Y" uniqKey="Wang Y" first="Y Y" last="Wang">Y Y Wang</name></noCountry><country name="Australie"><noRegion><name sortKey="Civitico, G" sort="Civitico, G" uniqKey="Civitico G" first="G" last="Civitico">G. Civitico</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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