Evaluation of immunomodulators, interferons and known in vitro SARS-CoV inhibitors for inhibition of SARS-CoV replication in BALB/c mice
Identifieur interne : 001D99 ( Main/Exploration ); précédent : 001D98; suivant : 001E00Evaluation of immunomodulators, interferons and known in vitro SARS-CoV inhibitors for inhibition of SARS-CoV replication in BALB/c mice
Auteurs : Dale L. Barnard [États-Unis] ; Craig W. Day [États-Unis] ; Kevin Bailey [États-Unis] ; Matthew Heiner [États-Unis] ; Robert Montgomery [États-Unis] ; Larry Lauridsen [États-Unis] ; Paul K. S. Chan [Hong Kong] ; Robert W. Sidwell [États-Unis]Source :
- Antiviral chemistry & chemotherapy [ 0956-3202 ] ; 2006.
Descripteurs français
- KwdFr :
- Administration par voie nasale, Animaux, Antiviraux (administration et posologie), Antiviraux (pharmacologie), Cellules Vero, Effet cytopathogène viral (), Facteurs immunologiques (administration et posologie), Facteurs immunologiques (pharmacologie), Femelle, Interférons (administration et posologie), Interférons (pharmacologie), Modèles animaux de maladie humaine, Perfusions parentérales, Poumon (), Poumon (virologie), Relation structure-activité, Réplication virale (), Souris, Souris de lignée BALB C, Virus du SRAS ().
- MESH :
- administration et posologie : Antiviraux, Facteurs immunologiques, Interférons.
- pharmacologie : Antiviraux, Facteurs immunologiques, Interférons.
- virologie : Poumon.
- Pascal (Inist)
- Administration par voie nasale, Animaux, Cellules Vero, Effet cytopathogène viral, Evaluation, Femelle, Immunomodulateur, Cytokine, Interféron, In vitro, Coronavirus, Modèles animaux de maladie humaine, Perfusions parentérales, Poumon, Relation structure-activité, Réplication virale, Souris, Souris de lignée BALB C, Syndrome respiratoire aigu sévère, Réplication, Animal, Souris, Chloroquine, Nelfinavir, Virus du SRAS, Virus syndrome respiratoire aigu sévère, Antipaludique, Antiparasitaire, Antirhumatismal, Antiviral, Antirétroviral.
English descriptors
- KwdEn :
- Administration, Intranasal, Animal, Animals, Antimalarial, Antiretroviral agent, Antirheumatic agent, Antiviral, Antiviral Agents (administration & dosage), Antiviral Agents (pharmacology), Chlorocebus aethiops, Chloroquine, Coronavirus, Cytokine, Cytopathogenic Effect, Viral (drug effects), Disease Models, Animal, Evaluation, Female, Immunologic Factors (administration & dosage), Immunologic Factors (pharmacology), Immunomodulator, In vitro, Infusions, Parenteral, Interferon, Interferons (administration & dosage), Interferons (pharmacology), Lung (drug effects), Lung (virology), Mice, Mice, Inbred BALB C, Mouse, Nelfinavir, Parasiticide, Replication, SARS Virus (drug effects), Severe acute respiratory syndrome, Severe acute respiratory syndrome virus, Structure-Activity Relationship, Vero Cells, Virus Replication (drug effects).
- MESH :
- chemical , administration & dosage : Antiviral Agents, Immunologic Factors, Interferons.
- chemical , pharmacology : Antiviral Agents, Immunologic Factors, Interferons.
- drug effects : Cytopathogenic Effect, Viral, Lung, SARS Virus, Virus Replication.
- virology : Lung.
- Administration, Intranasal, Animals, Chlorocebus aethiops, Disease Models, Animal, Female, Infusions, Parenteral, Mice, Mice, Inbred BALB C, Structure-Activity Relationship, Vero Cells.
Abstract
Compounds approved for therapeutic use and in vitro inhibitors of severe acute respiratory syndrome coronavirus (SARS-CoV) were evaluated for inhibition in the mouse SARS-CoV replication model. A hybrid interferon, interferon alpha (IFN-a) B/D, and a mismatched double-stranded (ds) RNA interferon (IFN) inducer, Ampligen® (poly I:poly C124), were the only compounds that potently inhibited virus titres in the lungs of infected mice as assessed by CPE titration assays. When mice were dosed intraperitoneally (i.p.) with IFN-α B/D once daily for 3 days beginning 4 h after virus exposure, SARS-CoV replication in the lungs of infected mice was reduced by 1 log10 at 10,000 and 32,000 IU; at the highest dose of 100,000 IU, virus lung titres were below detectable limits. Ampligen® used i.p. at 10 mg/kg 4 h prior to virus exposure also reduced virus lung titres to below detectable limits. Nelfinavir, β-D-N4-hydroxycytidine, calpain inhibitor VI, 3-deazaneplanocin A and Alferon® (human leukocyte IFN-α-n3) did not significantly reduce lung virus titres in mice. Anti-inflammatory agents, chloroquine, amodiaquin and pentoxifylline, were also inactive in vivo, suggesting that although they may be useful in ameliorating the hyperinflammatory response induced by the virus infection, they will not significantly reduce the replication of the virus, the inducer of inflammatory response. Thus, anti-inflammatory agents may only be useful in treating virus lung infections if used in combination with agents that inhibit virus replication. In , the data suggest that induction of IFN by mismatched dsRNA or actual treatment with exogenous IFN-a can inhibit SARS-CoV replication in the lungs of mice.
Affiliations:
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S." last="Chan">Paul K. S. Chan</name><affiliation wicri:level="4"><inist:fA14 i1="02"><s1>Department of Microbiology and Centre for Emerging Infectious Diseases, The Chinese University of Hong Kong, Prince of Wales Hospital</s1><s2>Shatin, New Territories</s2><s3>HKG</s3><sZ>7 aut.</sZ></inist:fA14><country>Hong Kong</country><wicri:noRegion>Shatin, New Territories</wicri:noRegion><orgName type="university">Université chinoise de Hong Kong</orgName><placeName><settlement type="city">Sha Tin</settlement></placeName></affiliation></author><author><name sortKey="Sidwell, Robert W" sort="Sidwell, Robert W" uniqKey="Sidwell R" first="Robert W." last="Sidwell">Robert W. 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Barnard</name><affiliation wicri:level="2"><inist:fA14 i1="01"><s1>Institute for Antiviral Research, Utah State University</s1><s2>Logan, UT</s2><s3>USA</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><sZ>8 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Utah</region></placeName></affiliation></author><author><name sortKey="Day, Craig W" sort="Day, Craig W" uniqKey="Day C" first="Craig W." last="Day">Craig W. Day</name><affiliation wicri:level="2"><inist:fA14 i1="01"><s1>Institute for Antiviral Research, Utah State University</s1><s2>Logan, UT</s2><s3>USA</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><sZ>8 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Utah</region></placeName></affiliation></author><author><name sortKey="Bailey, Kevin" sort="Bailey, Kevin" uniqKey="Bailey K" first="Kevin" last="Bailey">Kevin Bailey</name><affiliation wicri:level="2"><inist:fA14 i1="01"><s1>Institute for Antiviral Research, Utah State University</s1><s2>Logan, UT</s2><s3>USA</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><sZ>8 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Utah</region></placeName></affiliation></author><author><name sortKey="Heiner, Matthew" sort="Heiner, Matthew" uniqKey="Heiner M" first="Matthew" last="Heiner">Matthew Heiner</name><affiliation wicri:level="2"><inist:fA14 i1="01"><s1>Institute for Antiviral Research, Utah State University</s1><s2>Logan, UT</s2><s3>USA</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><sZ>8 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Utah</region></placeName></affiliation></author><author><name sortKey="Montgomery, Robert" sort="Montgomery, Robert" uniqKey="Montgomery R" first="Robert" last="Montgomery">Robert Montgomery</name><affiliation wicri:level="2"><inist:fA14 i1="01"><s1>Institute for Antiviral Research, Utah State University</s1><s2>Logan, UT</s2><s3>USA</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><sZ>8 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Utah</region></placeName></affiliation></author><author><name sortKey="Lauridsen, Larry" sort="Lauridsen, Larry" uniqKey="Lauridsen L" first="Larry" last="Lauridsen">Larry Lauridsen</name><affiliation wicri:level="2"><inist:fA14 i1="01"><s1>Institute for Antiviral Research, Utah State University</s1><s2>Logan, UT</s2><s3>USA</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><sZ>8 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Utah</region></placeName></affiliation></author><author><name sortKey="Chan, Paul K S" sort="Chan, Paul K S" uniqKey="Chan P" first="Paul K. S." last="Chan">Paul K. S. Chan</name><affiliation wicri:level="4"><inist:fA14 i1="02"><s1>Department of Microbiology and Centre for Emerging Infectious Diseases, The Chinese University of Hong Kong, Prince of Wales Hospital</s1><s2>Shatin, New Territories</s2><s3>HKG</s3><sZ>7 aut.</sZ></inist:fA14><country>Hong Kong</country><wicri:noRegion>Shatin, New Territories</wicri:noRegion><orgName type="university">Université chinoise de Hong Kong</orgName><placeName><settlement type="city">Sha Tin</settlement></placeName></affiliation></author><author><name sortKey="Sidwell, Robert W" sort="Sidwell, Robert W" uniqKey="Sidwell R" first="Robert W." last="Sidwell">Robert W. Sidwell</name><affiliation wicri:level="2"><inist:fA14 i1="01"><s1>Institute for Antiviral Research, Utah State University</s1><s2>Logan, UT</s2><s3>USA</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><sZ>8 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Utah</region></placeName></affiliation></author></analytic><series><title level="j" type="main">Antiviral chemistry & chemotherapy</title><title level="j" type="abbreviated">Antivir. chem. chemother.</title><idno type="ISSN">0956-3202</idno><imprint><date when="2006">2006</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Antiviral chemistry & chemotherapy</title><title level="j" type="abbreviated">Antivir. chem. chemother.</title><idno type="ISSN">0956-3202</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Administration, Intranasal</term><term>Animal</term><term>Animals</term><term>Antimalarial</term><term>Antiretroviral agent</term><term>Antirheumatic agent</term><term>Antiviral</term><term>Antiviral Agents (administration & dosage)</term><term>Antiviral Agents (pharmacology)</term><term>Chlorocebus aethiops</term><term>Chloroquine</term><term>Coronavirus</term><term>Cytokine</term><term>Cytopathogenic Effect, Viral (drug effects)</term><term>Disease Models, Animal</term><term>Evaluation</term><term>Female</term><term>Immunologic Factors (administration & dosage)</term><term>Immunologic Factors (pharmacology)</term><term>Immunomodulator</term><term>In vitro</term><term>Infusions, Parenteral</term><term>Interferon</term><term>Interferons (administration & dosage)</term><term>Interferons (pharmacology)</term><term>Lung (drug effects)</term><term>Lung (virology)</term><term>Mice</term><term>Mice, Inbred BALB C</term><term>Mouse</term><term>Nelfinavir</term><term>Parasiticide</term><term>Replication</term><term>SARS Virus (drug effects)</term><term>Severe acute respiratory syndrome</term><term>Severe acute respiratory syndrome virus</term><term>Structure-Activity Relationship</term><term>Vero Cells</term><term>Virus Replication (drug effects)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Administration par voie nasale</term><term>Animaux</term><term>Antiviraux (administration et posologie)</term><term>Antiviraux (pharmacologie)</term><term>Cellules Vero</term><term>Effet cytopathogène viral ()</term><term>Facteurs immunologiques (administration et posologie)</term><term>Facteurs immunologiques (pharmacologie)</term><term>Femelle</term><term>Interférons (administration et posologie)</term><term>Interférons (pharmacologie)</term><term>Modèles animaux de maladie humaine</term><term>Perfusions parentérales</term><term>Poumon ()</term><term>Poumon (virologie)</term><term>Relation structure-activité</term><term>Réplication virale ()</term><term>Souris</term><term>Souris de lignée BALB C</term><term>Virus du SRAS ()</term></keywords><keywords scheme="MESH" type="chemical" qualifier="administration & dosage" xml:lang="en"><term>Antiviral Agents</term><term>Immunologic Factors</term><term>Interferons</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Antiviral Agents</term><term>Immunologic Factors</term><term>Interferons</term></keywords><keywords scheme="MESH" qualifier="administration et posologie" xml:lang="fr"><term>Antiviraux</term><term>Facteurs immunologiques</term><term>Interférons</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Cytopathogenic Effect, Viral</term><term>Lung</term><term>SARS Virus</term><term>Virus Replication</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Antiviraux</term><term>Facteurs immunologiques</term><term>Interférons</term></keywords><keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Poumon</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Lung</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Administration, Intranasal</term><term>Animals</term><term>Chlorocebus aethiops</term><term>Disease Models, Animal</term><term>Female</term><term>Infusions, Parenteral</term><term>Mice</term><term>Mice, Inbred BALB C</term><term>Structure-Activity Relationship</term><term>Vero Cells</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Administration par voie nasale</term><term>Animaux</term><term>Cellules Vero</term><term>Effet cytopathogène viral</term><term>Evaluation</term><term>Femelle</term><term>Immunomodulateur</term><term>Cytokine</term><term>Interféron</term><term>In vitro</term><term>Coronavirus</term><term>Modèles animaux de maladie humaine</term><term>Perfusions parentérales</term><term>Poumon</term><term>Relation structure-activité</term><term>Réplication virale</term><term>Souris</term><term>Souris de lignée BALB C</term><term>Syndrome respiratoire aigu sévère</term><term>Réplication</term><term>Animal</term><term>Souris</term><term>Chloroquine</term><term>Nelfinavir</term><term>Virus du SRAS</term><term>Virus syndrome respiratoire aigu sévère</term><term>Antipaludique</term><term>Antiparasitaire</term><term>Antirhumatismal</term><term>Antiviral</term><term>Antirétroviral</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Compounds approved for therapeutic use and in vitro inhibitors of severe acute respiratory syndrome coronavirus (SARS-CoV) were evaluated for inhibition in the mouse SARS-CoV replication model. A hybrid interferon, interferon alpha (IFN-a) B/D, and a mismatched double-stranded (ds) RNA interferon (IFN) inducer, Ampligen® (poly I:poly C<sub>124</sub>), were the only compounds that potently inhibited virus titres in the lungs of infected mice as assessed by CPE titration assays. When mice were dosed intraperitoneally (i.p.) with IFN-α B/D once daily for 3 days beginning 4 h after virus exposure, SARS-CoV replication in the lungs of infected mice was reduced by 1 log<sub>10</sub> at 10,000 and 32,000 IU; at the highest dose of 100,000 IU, virus lung titres were below detectable limits. Ampligen® used i.p. at 10 mg/kg 4 h prior to virus exposure also reduced virus lung titres to below detectable limits. Nelfinavir, β-D-N<sup>4</sup>-hydroxycytidine, calpain inhibitor VI, 3-deazaneplanocin A and Alferon® (human leukocyte IFN-α-n3) did not significantly reduce lung virus titres in mice. Anti-inflammatory agents, chloroquine, amodiaquin and pentoxifylline, were also inactive in vivo, suggesting that although they may be useful in ameliorating the hyperinflammatory response induced by the virus infection, they will not significantly reduce the replication of the virus, the inducer of inflammatory response. Thus, anti-inflammatory agents may only be useful in treating virus lung infections if used in combination with agents that inhibit virus replication. In , the data suggest that induction of IFN by mismatched dsRNA or actual treatment with exogenous IFN-a can inhibit SARS-CoV replication in the lungs of mice.</div></front></TEI><affiliations><list><country><li>Hong Kong</li><li>États-Unis</li></country><region><li>Utah</li></region><settlement><li>Sha Tin</li></settlement><orgName><li>Université chinoise de Hong Kong</li></orgName></list><tree><country name="États-Unis"><region name="Utah"><name sortKey="Barnard, Dale L" sort="Barnard, Dale L" uniqKey="Barnard D" first="Dale L." last="Barnard">Dale L. Barnard</name></region><name sortKey="Bailey, Kevin" sort="Bailey, Kevin" uniqKey="Bailey K" first="Kevin" last="Bailey">Kevin Bailey</name><name sortKey="Day, Craig W" sort="Day, Craig W" uniqKey="Day C" first="Craig W." last="Day">Craig W. Day</name><name sortKey="Heiner, Matthew" sort="Heiner, Matthew" uniqKey="Heiner M" first="Matthew" last="Heiner">Matthew Heiner</name><name sortKey="Lauridsen, Larry" sort="Lauridsen, Larry" uniqKey="Lauridsen L" first="Larry" last="Lauridsen">Larry Lauridsen</name><name sortKey="Montgomery, Robert" sort="Montgomery, Robert" uniqKey="Montgomery R" first="Robert" last="Montgomery">Robert Montgomery</name><name sortKey="Sidwell, Robert W" sort="Sidwell, Robert W" uniqKey="Sidwell R" first="Robert W." last="Sidwell">Robert W. Sidwell</name></country><country name="Hong Kong"><noRegion><name sortKey="Chan, Paul K S" sort="Chan, Paul K S" uniqKey="Chan P" first="Paul K. S." last="Chan">Paul K. S. Chan</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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