New Antiviral Drugs, Vaccines and Classic Public Health Interventions against SARS Coronavirus

Oxford, John; Balasingam, Shobana; Chan, Charlotte; Catchpole, Andrew; Lambkin, Robert

doi:10.1177/095632020501600102

Cited by 10 publications

(11 citation statements)

References 71 publications

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“…Visual assay NR assay Virus yield reduction assay Oxford et al, 2005;Hui and Wong, 2004;Morgenstern et al, 2005;Chen et al, 2004). In other studies in which ribavirin was evaluated for efficacy in cells less likely to phosphorylate the compound, ribavirin was not efficacious against SARS-CoV ( Barnard et al, 2004b;Ströher et al, 2004;Chen et al, 2004;Tan et al, 2004).…”

Section: Compoundmentioning

confidence: 99%

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

et al. 2006

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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-beta-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-1alpha, 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.

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Section: Compoundmentioning

confidence: 99%

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

et al. 2006

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“…Anti-inflammatory agents have also been used for clinical treatment (Fujii et al, 2004;Groneberg et al, 2005;Lai, 2005;So et al, 2003;Tsang and Seto, 2004;Tsang and Zhong, 2003;van Vonderen et al, 2003). SARS vaccines are currently under development and evaluation (Bai et al, 2008;Cheung et al, 2007;Groneberg et al, 2005;Jiang et al, 2005b;Lin et al, 2007;Marshall and Enserink, 2004;Martin et al, 2008;Okada et al, 2007;Oxford et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

Annexin A2 on lung epithelial cell surface is recognized by severe acute respiratory syndrome-associated coronavirus spike domain 2 antibodies

Fang

Lin

Liao

et al. 2010

Molecular Immunology

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Severe acute respiratory syndrome-associated coronavirus (SARS-CoV) infection causes lung failure characterized by atypical pneumonia. We previously showed that antibodies against SARS-CoV spike domain 2 (S2) in the patient sera can cross-react with human lung epithelial cells; however, the autoantigen is not yet identified. In this study, we performed proteomic studies and identified several candidate autoantigens recognized by SARS patient sera in human lung type II epithelial cell A549. Among the candidate proteins, annexin A2, which was identified by mass spectrometry analysis and had the highest score by Mascot data search, was further characterized and investigated for its role as an autoantigen. By confocal microscopic observation, SARS patient sera and anti-S2 antibodies were co-localized on A549 cells and both of them were co-localized with anti-annexin A2 antibodies. Anti-annexin A2 antibodies bound to purified S2 proteins, and anti-S2 bound to immunoprecipitated annexin A2 from A549 cell lysate in a dose-dependent manner. Furthermore, an increased surface expression and raft-structure distribution of annexin A2 was present in A549 cells after stimulation with SARS-induced cytokines interleukin-6 and interferon-gamma. Cytokine stimulation increased the binding capability of anti-S2 antibodies to human lung epithelial cells. Together, the upregulated expression of annexin A2 by SARS-associated cytokines and the cross-reactivity of anti-SARS-CoV S2 antibodies to annexin A2 may have implications in SARS disease pathogenesis.

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“…The spread of SARS-CoV and the severity of the highly contagious disease it causes have aroused scientific interest in coronaviruses. In order to prevent the circle of infection from widening, antiviral chemotherapy and prophylaxis have been developed (Oxford et al, 2005;Shigeta and Yamase, 2005;Tan et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

Canine coronavirus inactivation with physical and chemical agents

Pratelli¹

2008

The Veterinary Journal

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Canine coronavirus (CCoV) is responsible for mild or moderate enteritis in puppies. The virus is highly contagious and avoiding contact with infected dogs and their excretions is the only way to ensure disease prevention. Since no studies have yet focused on the sensitivity of CCoV to chemical biocides the present investigation examined the efficiency of physical and chemical methods of viral inactivation. CCoV infectivity was stable at +56 degrees C for up to 30 min, but tended to decrease rapidly at +65 degrees C and +75 degrees C. Germicidal ultra-violet (UV-C) light exposure demonstrated no significant effects on virus inactivation for up to 3 days. CCoV was observed to be more stable at pH 6.0-6.5 while extreme acidic conditions inactivated the virus. Two tested aldehydes inactivated the virus but their action was temperature- and time-dependent. The methods for CCoV inactivation could be applied as animal models to study human coronavirus infection, reducing the risk of accidental exposure of researchers to pathogens during routine laboratory procedures.

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New Antiviral Drugs, Vaccines and Classic Public Health Interventions against SARS Coronavirus

Cited by 10 publications

References 71 publications

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

Annexin A2 on lung epithelial cell surface is recognized by severe acute respiratory syndrome-associated coronavirus spike domain 2 antibodies

Canine coronavirus inactivation with physical and chemical agents

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