SrasV1, PascalFrancis, Corpus, bibRecord, 000472

Enhancement of the infectivity of SARS-CoV in BALB/c mice by IMP dehydrogenase inhibitors, including ribavirin

Identifieur interne : 000472 ( PascalFrancis/Corpus ); précédent : 000471; suivant : 000473

Enhancement of the infectivity of SARS-CoV in BALB/c mice by IMP dehydrogenase inhibitors, including ribavirin

Auteurs : Dale L. Barnard ; Craig W. Day ; Kevin Bailey ; Matthew Heiner ; Robert Montgomery ; Larry Lauridsen ; Scott Winslow ; Justin Hoopes ; Joseph K.-K. Li ; Jongdae Lee ; Dennis A. Carson ; Howard B. Cottam ; Robert W. Sidwell

Source :

Antiviral research [ 0166-3542 ] ; 2006.

RBID : Pascal:06-0398673

Descripteurs français

Pascal (Inist)
- Pouvoir infectant, Antiviral, Syndrome respiratoire aigu sévère, Animal, Souris, IMP dehydrogenase, Inhibiteur, Ribavirine, Coronavirus.

English descriptors

KwdEn :
- Animal, Antiviral, Coronavirus, IMP dehydrogenase, Infectivity, Inhibitor, Mouse, Ribavirin, Severe acute respiratory syndrome.

Abstract

Because of the conflicting data concerning the SARS-CoV inhibitory efficacy of ribavirin, an inosine monophosphate (IMP) dehydrogenase inhibitor, studies were done to evaluate the efficacy of ribavirin and other IMP dehydrogenase inhibitors (5-ethynyl- 1-β-D-ribofuranosylimidazole-4-carboxamide (EICAR), mizoribine, and mycophenolic acid) in preventing viral replication in the lungs of BALB/c mice, a replication model for severe acute respiratory syndrome (SARS) infections (Subbarao, K., McAuliffe, J., Vogel, L., Fahle, G., Fischer, S., Tatti, K., Packard, M., Shieh, W.J., Zaki, S., Murphy, B., 2004. Prior infection and passive transfer of neutralizing antibody prevent replication of severe acute respiratory syndrome coronavirus (SARS-CoV) in the respiratory tract of mice. J. Virol. 78, 3572-3577). Ribavirin given at 75 mg/kg 4 h prior to virus exposure and then given twice daily for 3 days beginning at day 0 was found to increase virus lung titers and extend the length of time that virus could be detected in the lungs of mice. Other IMP dehydrogenase inhibitors administered near maximum tolerated doses using the same dosing regimen as for ribavirin were found to slightly enhance virus replication in the lungs. In addition, ribavirin treatment seemed also to promote the production of pro-inflammatory cytokines 4 days after cessation of treatment, although after 3 days of treatment ribavirin inhibited pro-inflammatory cytokine production in infected mice, significantly reducing the levels of the cytokines IL-1α, interleukin-5 (IL-5), monocyte chemotactic protein-1 (MCP-1), and granulocyte-macrophage colony stimulating factor (GM-CSF). These findings suggest that ribavirin may actually contribute to the pathogenesis of SARS-CoV by prolonging and/or enhancing viral replication in the lungs. By not inhibiting viral replication in the lungs of infected mice, ribavirin treatment may have provided a continual source of stimulation for the inflammatory response thought to contribute to the pathogenesis of the infection. Our data do not support the use of ribavirin or other IMP dehydrogenase inhibitors for treating SARS infections in humans.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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Format Inist (serveur)

NO :	PASCAL 06-0398673 INIST
ET :	Enhancement of the infectivity of SARS-CoV in BALB/c mice by IMP dehydrogenase inhibitors, including ribavirin
AU :	BARNARD (Dale L.); DAY (Craig W.); BAILEY (Kevin); HEINER (Matthew); MONTGOMERY (Robert); LAURIDSEN (Larry); WINSLOW (Scott); HOOPES (Justin); LI (Joseph K.-K.); LEE (Jongdae); CARSON (Dennis A.); COTTAM (Howard B.); SIDWELL (Robert W.)
AF :	Institute for Antiviral Research, Utah State University, 5600 Old Main Hill/Logan, UT 84322-5600/Etats-Unis (1 aut., 2 aut., 3 aut., 4 aut., 5 aut., 6 aut., 7 aut., 13 aut.); Department of Biology, Utah State University, 5305 Old Main Hill/Logan, UT 84322-5305/Etats-Unis (8 aut., 9 aut.); Moores Cancer Center 0820, University of California, San Diego, 3855 Health Sciences Drive/La Jolla, CA 92093-0820/Etats-Unis (10 aut., 11 aut., 12 aut.)
DT :	Publication en série; Niveau analytique
SO :	Antiviral research; ISSN 0166-3542; Coden ARSRDR; Pays-Bas; Da. 2006; Vol. 71; No. 1; Pp. 53-63; Bibl. 1 p.1/4
LA :	Anglais
EA :	Because of the conflicting data concerning the SARS-CoV inhibitory efficacy of ribavirin, an inosine monophosphate (IMP) dehydrogenase inhibitor, studies were done to evaluate the efficacy of ribavirin and other IMP dehydrogenase inhibitors (5-ethynyl- 1-β-D-ribofuranosylimidazole-4-carboxamide (EICAR), mizoribine, and mycophenolic acid) in preventing viral replication in the lungs of BALB/c mice, a replication model for severe acute respiratory syndrome (SARS) infections (Subbarao, K., McAuliffe, J., Vogel, L., Fahle, G., Fischer, S., Tatti, K., Packard, M., Shieh, W.J., Zaki, S., Murphy, B., 2004. Prior infection and passive transfer of neutralizing antibody prevent replication of severe acute respiratory syndrome coronavirus (SARS-CoV) in the respiratory tract of mice. J. Virol. 78, 3572-3577). Ribavirin given at 75 mg/kg 4 h prior to virus exposure and then given twice daily for 3 days beginning at day 0 was found to increase virus lung titers and extend the length of time that virus could be detected in the lungs of mice. Other IMP dehydrogenase inhibitors administered near maximum tolerated doses using the same dosing regimen as for ribavirin were found to slightly enhance virus replication in the lungs. In addition, ribavirin treatment seemed also to promote the production of pro-inflammatory cytokines 4 days after cessation of treatment, although after 3 days of treatment ribavirin inhibited pro-inflammatory cytokine production in infected mice, significantly reducing the levels of the cytokines IL-1α, interleukin-5 (IL-5), monocyte chemotactic protein-1 (MCP-1), and granulocyte-macrophage colony stimulating factor (GM-CSF). These findings suggest that ribavirin may actually contribute to the pathogenesis of SARS-CoV by prolonging and/or enhancing viral replication in the lungs. By not inhibiting viral replication in the lungs of infected mice, ribavirin treatment may have provided a continual source of stimulation for the inflammatory response thought to contribute to the pathogenesis of the infection. Our data do not support the use of ribavirin or other IMP dehydrogenase inhibitors for treating SARS infections in humans.
CC :	002B02S05
FD :	Pouvoir infectant; Antiviral; Syndrome respiratoire aigu sévère; Animal; Souris; IMP dehydrogenase; Inhibiteur; Ribavirine; Coronavirus
FG :	Virose; Infection; Rodentia; Mammalia; Vertebrata; Oxidoreductases; Enzyme; Coronaviridae; Nidovirales; Virus; Appareil respiratoire pathologie; Poumon pathologie; Analogue nucléoside
ED :	Infectivity; Antiviral; Severe acute respiratory syndrome; Animal; Mouse; IMP dehydrogenase; Inhibitor; Ribavirin; Coronavirus
EG :	Viral disease; Infection; Rodentia; Mammalia; Vertebrata; Oxidoreductases; Enzyme; Coronaviridae; Nidovirales; Virus; Respiratory disease; Lung disease; Nucleoside analog
SD :	Poder infectante; Antiviral; Síndrome respiratorio agudo severo; Animal; Ratón; IMP dehydrogenase; Inhibidor; Ribavirina; Coronavirus
LO :	INIST-18839.354000142413440070
ID :	06-0398673

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Pascal:06-0398673

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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Enhancement of the infectivity of SARS-CoV in BALB/c mice by IMP dehydrogenase inhibitors, including ribavirin</title>
<author><name sortKey="Barnard, Dale L" sort="Barnard, Dale L" uniqKey="Barnard D" first="Dale L." last="Barnard">Dale L. Barnard</name>
<affiliation><inist:fA14 i1="01"><s1>Institute for Antiviral Research, Utah State University, 5600 Old Main Hill</s1>
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<author><name sortKey="Heiner, Matthew" sort="Heiner, Matthew" uniqKey="Heiner M" first="Matthew" last="Heiner">Matthew Heiner</name>
<affiliation><inist:fA14 i1="01"><s1>Institute for Antiviral Research, Utah State University, 5600 Old Main Hill</s1>
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<affiliation><inist:fA14 i1="01"><s1>Institute for Antiviral Research, Utah State University, 5600 Old Main Hill</s1>
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<affiliation><inist:fA14 i1="01"><s1>Institute for Antiviral Research, Utah State University, 5600 Old Main Hill</s1>
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<affiliation><inist:fA14 i1="01"><s1>Institute for Antiviral Research, Utah State University, 5600 Old Main Hill</s1>
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<affiliation><inist:fA14 i1="02"><s1>Department of Biology, Utah State University, 5305 Old Main Hill</s1>
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<author><name sortKey="Li, Joseph K K" sort="Li, Joseph K K" uniqKey="Li J" first="Joseph K.-K." last="Li">Joseph K.-K. Li</name>
<affiliation><inist:fA14 i1="02"><s1>Department of Biology, Utah State University, 5305 Old Main Hill</s1>
<s2>Logan, UT 84322-5305</s2>
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<sZ>8 aut.</sZ>
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<author><name sortKey="Lee, Jongdae" sort="Lee, Jongdae" uniqKey="Lee J" first="Jongdae" last="Lee">Jongdae Lee</name>
<affiliation><inist:fA14 i1="03"><s1>Moores Cancer Center 0820, University of California, San Diego, 3855 Health Sciences Drive</s1>
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<affiliation><inist:fA14 i1="03"><s1>Moores Cancer Center 0820, University of California, San Diego, 3855 Health Sciences Drive</s1>
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<affiliation><inist:fA14 i1="03"><s1>Moores Cancer Center 0820, University of California, San Diego, 3855 Health Sciences Drive</s1>
<s2>La Jolla, CA 92093-0820</s2>
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<affiliation><inist:fA14 i1="01"><s1>Institute for Antiviral Research, Utah State University, 5600 Old Main Hill</s1>
<s2>Logan, UT 84322-5600</s2>
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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="2006">2006</date>
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<seriesStmt><title level="j" type="main">Antiviral research</title>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animal</term>
<term>Antiviral</term>
<term>Coronavirus</term>
<term>IMP dehydrogenase</term>
<term>Infectivity</term>
<term>Inhibitor</term>
<term>Mouse</term>
<term>Ribavirin</term>
<term>Severe acute respiratory syndrome</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr"><term>Pouvoir infectant</term>
<term>Antiviral</term>
<term>Syndrome respiratoire aigu sévère</term>
<term>Animal</term>
<term>Souris</term>
<term>IMP dehydrogenase</term>
<term>Inhibiteur</term>
<term>Ribavirine</term>
<term>Coronavirus</term>
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<front><div type="abstract" xml:lang="en">Because of the conflicting data concerning the SARS-CoV inhibitory efficacy of ribavirin, an inosine monophosphate (IMP) dehydrogenase inhibitor, studies were done to evaluate the efficacy of ribavirin and other IMP dehydrogenase inhibitors (5-ethynyl- 1-β-D-ribofuranosylimidazole-4-carboxamide (EICAR), mizoribine, and mycophenolic acid) in preventing viral replication in the lungs of BALB/c mice, a replication model for severe acute respiratory syndrome (SARS) infections (Subbarao, K., McAuliffe, J., Vogel, L., Fahle, G., Fischer, S., Tatti, K., Packard, M., Shieh, W.J., Zaki, S., Murphy, B., 2004. Prior infection and passive transfer of neutralizing antibody prevent replication of severe acute respiratory syndrome coronavirus (SARS-CoV) in the respiratory tract of mice. J. Virol. 78, 3572-3577). Ribavirin given at 75 mg/kg 4 h prior to virus exposure and then given twice daily for 3 days beginning at day 0 was found to increase virus lung titers and extend the length of time that virus could be detected in the lungs of mice. Other IMP dehydrogenase inhibitors administered near maximum tolerated doses using the same dosing regimen as for ribavirin were found to slightly enhance virus replication in the lungs. In addition, ribavirin treatment seemed also to promote the production of pro-inflammatory cytokines 4 days after cessation of treatment, although after 3 days of treatment ribavirin inhibited pro-inflammatory cytokine production in infected mice, significantly reducing the levels of the cytokines IL-1α, interleukin-5 (IL-5), monocyte chemotactic protein-1 (MCP-1), and granulocyte-macrophage colony stimulating factor (GM-CSF). These findings suggest that ribavirin may actually contribute to the pathogenesis of SARS-CoV by prolonging and/or enhancing viral replication in the lungs. By not inhibiting viral replication in the lungs of infected mice, ribavirin treatment may have provided a continual source of stimulation for the inflammatory response thought to contribute to the pathogenesis of the infection. Our data do not support the use of ribavirin or other IMP dehydrogenase inhibitors for treating SARS infections in humans.</div>
</front>
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<fC01 i1="01" l="ENG"><s0>Because of the conflicting data concerning the SARS-CoV inhibitory efficacy of ribavirin, an inosine monophosphate (IMP) dehydrogenase inhibitor, studies were done to evaluate the efficacy of ribavirin and other IMP dehydrogenase inhibitors (5-ethynyl- 1-β-D-ribofuranosylimidazole-4-carboxamide (EICAR), mizoribine, and mycophenolic acid) in preventing viral replication in the lungs of BALB/c mice, a replication model for severe acute respiratory syndrome (SARS) infections (Subbarao, K., McAuliffe, J., Vogel, L., Fahle, G., Fischer, S., Tatti, K., Packard, M., Shieh, W.J., Zaki, S., Murphy, B., 2004. Prior infection and passive transfer of neutralizing antibody prevent replication of severe acute respiratory syndrome coronavirus (SARS-CoV) in the respiratory tract of mice. J. Virol. 78, 3572-3577). Ribavirin given at 75 mg/kg 4 h prior to virus exposure and then given twice daily for 3 days beginning at day 0 was found to increase virus lung titers and extend the length of time that virus could be detected in the lungs of mice. Other IMP dehydrogenase inhibitors administered near maximum tolerated doses using the same dosing regimen as for ribavirin were found to slightly enhance virus replication in the lungs. In addition, ribavirin treatment seemed also to promote the production of pro-inflammatory cytokines 4 days after cessation of treatment, although after 3 days of treatment ribavirin inhibited pro-inflammatory cytokine production in infected mice, significantly reducing the levels of the cytokines IL-1α, interleukin-5 (IL-5), monocyte chemotactic protein-1 (MCP-1), and granulocyte-macrophage colony stimulating factor (GM-CSF). These findings suggest that ribavirin may actually contribute to the pathogenesis of SARS-CoV by prolonging and/or enhancing viral replication in the lungs. By not inhibiting viral replication in the lungs of infected mice, ribavirin treatment may have provided a continual source of stimulation for the inflammatory response thought to contribute to the pathogenesis of the infection. Our data do not support the use of ribavirin or other IMP dehydrogenase inhibitors for treating SARS infections in humans.</s0>
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<server><NO>PASCAL 06-0398673 INIST</NO>
<ET>Enhancement of the infectivity of SARS-CoV in BALB/c mice by IMP dehydrogenase inhibitors, including ribavirin</ET>
<AU>BARNARD (Dale L.); DAY (Craig W.); BAILEY (Kevin); HEINER (Matthew); MONTGOMERY (Robert); LAURIDSEN (Larry); WINSLOW (Scott); HOOPES (Justin); LI (Joseph K.-K.); LEE (Jongdae); CARSON (Dennis A.); COTTAM (Howard B.); SIDWELL (Robert W.)</AU>
<AF>Institute for Antiviral Research, Utah State University, 5600 Old Main Hill/Logan, UT 84322-5600/Etats-Unis (1 aut., 2 aut., 3 aut., 4 aut., 5 aut., 6 aut., 7 aut., 13 aut.); Department of Biology, Utah State University, 5305 Old Main Hill/Logan, UT 84322-5305/Etats-Unis (8 aut., 9 aut.); Moores Cancer Center 0820, University of California, San Diego, 3855 Health Sciences Drive/La Jolla, CA 92093-0820/Etats-Unis (10 aut., 11 aut., 12 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Antiviral research; ISSN 0166-3542; Coden ARSRDR; Pays-Bas; Da. 2006; Vol. 71; No. 1; Pp. 53-63; Bibl. 1 p.1/4</SO>
<LA>Anglais</LA>
<EA>Because of the conflicting data concerning the SARS-CoV inhibitory efficacy of ribavirin, an inosine monophosphate (IMP) dehydrogenase inhibitor, studies were done to evaluate the efficacy of ribavirin and other IMP dehydrogenase inhibitors (5-ethynyl- 1-β-D-ribofuranosylimidazole-4-carboxamide (EICAR), mizoribine, and mycophenolic acid) in preventing viral replication in the lungs of BALB/c mice, a replication model for severe acute respiratory syndrome (SARS) infections (Subbarao, K., McAuliffe, J., Vogel, L., Fahle, G., Fischer, S., Tatti, K., Packard, M., Shieh, W.J., Zaki, S., Murphy, B., 2004. Prior infection and passive transfer of neutralizing antibody prevent replication of severe acute respiratory syndrome coronavirus (SARS-CoV) in the respiratory tract of mice. J. Virol. 78, 3572-3577). Ribavirin given at 75 mg/kg 4 h prior to virus exposure and then given twice daily for 3 days beginning at day 0 was found to increase virus lung titers and extend the length of time that virus could be detected in the lungs of mice. Other IMP dehydrogenase inhibitors administered near maximum tolerated doses using the same dosing regimen as for ribavirin were found to slightly enhance virus replication in the lungs. In addition, ribavirin treatment seemed also to promote the production of pro-inflammatory cytokines 4 days after cessation of treatment, although after 3 days of treatment ribavirin inhibited pro-inflammatory cytokine production in infected mice, significantly reducing the levels of the cytokines IL-1α, interleukin-5 (IL-5), monocyte chemotactic protein-1 (MCP-1), and granulocyte-macrophage colony stimulating factor (GM-CSF). These findings suggest that ribavirin may actually contribute to the pathogenesis of SARS-CoV by prolonging and/or enhancing viral replication in the lungs. By not inhibiting viral replication in the lungs of infected mice, ribavirin treatment may have provided a continual source of stimulation for the inflammatory response thought to contribute to the pathogenesis of the infection. Our data do not support the use of ribavirin or other IMP dehydrogenase inhibitors for treating SARS infections in humans.</EA>
<CC>002B02S05</CC>
<FD>Pouvoir infectant; Antiviral; Syndrome respiratoire aigu sévère; Animal; Souris; IMP dehydrogenase; Inhibiteur; Ribavirine; Coronavirus</FD>
<FG>Virose; Infection; Rodentia; Mammalia; Vertebrata; Oxidoreductases; Enzyme; Coronaviridae; Nidovirales; Virus; Appareil respiratoire pathologie; Poumon pathologie; Analogue nucléoside</FG>
<ED>Infectivity; Antiviral; Severe acute respiratory syndrome; Animal; Mouse; IMP dehydrogenase; Inhibitor; Ribavirin; Coronavirus</ED>
<EG>Viral disease; Infection; Rodentia; Mammalia; Vertebrata; Oxidoreductases; Enzyme; Coronaviridae; Nidovirales; Virus; Respiratory disease; Lung disease; Nucleoside analog</EG>
<SD>Poder infectante; Antiviral; Síndrome respiratorio agudo severo; Animal; Ratón; IMP dehydrogenase; Inhibidor; Ribavirina; Coronavirus</SD>
<LO>INIST-18839.354000142413440070</LO>
<ID>06-0398673</ID>
</server>
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Enhancement of the infectivity of SARS-CoV in BALB/c mice by IMP dehydrogenase inhibitors, including ribavirin

Enhancement of the infectivity of SARS-CoV in BALB/c mice by IMP dehydrogenase inhibitors, including ribavirin

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