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

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About: Enhancement of the infectivity of SARS-CoV in BALB/c mice by IMP dehydrogenase inhibitors, including ribavirin Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

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type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Enhancement of the infectivity of SARS-CoV in BALB/c mice by IMP dehydrogenase inhibitors, including ribavirin
Creator	Tatti, K Murphy, B Fahle, G Fischer, S Mcauliffe, J Packard, M Shieh, W Vogel, L Zaki, S
Source	Elsevier; Medline; PMC
abstract	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 75mg/kg 4h 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.
has issue date	2006-08-31(xsd:dateTime)
bibo:doi	10.1016/j.antiviral.2006.03.001
bibo:pmid	16621037
has license	els-covid
sha1sum (hex)	24874af5c599f668e87df044bd03bb2743839af2
schema:url	https://doi.org/10.1016/j.antiviral.2006.03.001
resource representing a document's title	Enhancement of the infectivity of SARS-CoV in BALB/c mice by IMP dehydrogenase inhibitors, including ribavirin
has PubMed Central identifier	PMC7114261
has PubMed identifier	16621037
schema:publication	Antiviral Research
resource representing a document's body	covid:24874af5c599f668e87df044bd03bb2743839af2#body_text
is schema:about of	named entity 'PASSIVE' named entity 'PROLONGING' named entity 'PRO-' named entity 'PRIOR TO' named entity 'DEHYDROGENASE INHIBITOR' named entity 'CONFLICTING' named entity 'HUMANS' named entity 'SEVERE ACUTE RESPIRATORY SYNDROME' named entity 'LEVELS' named entity 'SUGGEST' named entity 'FOUND' named entity 'SARS' named entity 'LUNG' named entity 'SEVERE ACUTE RESPIRATORY SYNDROME CORONAVIRUS' named entity 'CONTINUAL' named entity 'SARS-COV' named entity 'PREVENTING' named entity 'SOURCE' covid:arg/24874af5c599f668e87df044bd03bb2743839af2 named entity 'PRIOR' named entity 'INFECTIONS' named entity 'RESPIRATORY TRACT' named entity 'NEUTRALIZING ANTIBODY' named entity 'INOSINE MONOPHOSPHATE' named entity 'PREVENT' named entity 'MYCOPHENOLIC ACID' named entity 'CESSATION' named entity 'DO NOT' named entity 'EFFICACY' named entity 'TREATING' named entity 'DAY' named entity 'REGIMEN' named entity 'TIME' named entity 'VIROL' named entity 'INTERLEUKIN-5 ' named entity 'STUDIES' named entity 'PRO-INFLAMMATORY CYTOKINE' named entity 'VIRUS' named entity '90%' named entity 'EVALUATE' named entity 'INHIBITING' named entity 'TO INCREASE' named entity 'CYTOKINE PRODUCTION' named entity 'GIVEN' named entity 'INFLAMMATORY RESPONSE' named entity 'DAYS' named entity 'ENHANCE' named entity 'LENGTH' named entity 'INFECTION' named entity 'REPLICATION' named entity 'VIRAL REPLICATION' named entity 'REDUCING' named entity 'PROVIDED' named entity 'MAXIMUM' named entity 'COULD BE' named entity 'DOSING' named entity 'ADDITION' named entity 'MG%' named entity 'DETECTED' named entity 'DATA' named entity 'PROMOTE' named entity 'INHIBITORY' named entity 'TRANSFER' named entity 'IMP DEHYDROGENASE INHIBITORS' named entity 'CSF' named entity 'INFECTION' named entity 'INFLAMMATORY' named entity 'INHIBITED' named entity 'EXPOSURE' named entity 'CARBOXAMIDE' named entity 'VIRUS REPLICATION' named entity 'MODEL' named entity 'THESE'

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