Isolation and Preliminary Characterization of Chalcone Ro 09-0410-Resistant Human Rhinovirus Type 2

Yasin, S. R.; Al‐Nakib, W.; Tyrrell, D. A. J.

doi:10.1177/095632029000100210

Cited by 5 publications

(4 citation statements)

References 16 publications

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“…Of 53 rhinovirus serotypes tested, 46 were inhibited by Ro 09-0410. Mutant rhinoviruses resistant to chalcone were also cross-resistant to dichloroflavan [73]. These results indicate that the three compounds had a similar mode of action based on their binding to virion particles.…”

Section: Antiviral Drugs Interacting With Virus Structural Proteinsmentioning

confidence: 79%

“…In a wider virological context the selection of drug-resistant viruses is expected and, indeed, acknowledged to confirm the specific antiviral activity of a drug, thus indicating that the compound is not inhibiting viral replication indirectly via an effect on the host cell. In all other virus-drug combinations including HIV and zidovudine [39,44], herpes simplex viruses and Zovirax [50] and rhinoviruses [73], drug-resistant viruses can be detected but, to date, they usually have had little clinical impact. Influenza viruses resistant to amantadine or rimantadine have been detected at low frequency in the field, even in countries such as Germany, which have not utilized amantadine-like drugs [33] and also have been specifically isolated from ill patients undergoing prophylactic or therapeutic treatment with rimantadine [29,31,32] or amantadine [17].…”

Section: Emergence Of Drug-resistant Virusesmentioning

confidence: 99%

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Specific Antiviral Therapy of Respiratory Viruses

Oxford¹,

Al-Jabri²

1996

Viral and Other Infections of the Human Respiratory Tract

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Introduction 21.2 The Medical Research Council Common Cold Unit 21.3 Clinical need for antivirals 21.3.1 Epidemic influenza 21.3.2 Serious lower respiratory tract infections caused by respiratory syncytial virus 21.3.3 Viruses causing upper respiratory tract infection 21.3.4 The chemistry of inhibitors of respiratory viruses 21.4 Influenza 21.4.1 Amantadinethe first antiinfluenza A virus drug 21.4.2 General recommendations for the clinical use of amantadine 21.4.3 'Designed' anti-neuraminidase drugs 21.5 Respiratory syncytial (RS) virus 21.5.1 Inhibition by ribavirin 21.6 Rhinoviruses 21.6.1 Antiviral drugs interacting with virus structural proteins 21.6.2 Virion-binding drugs acting against rhinovirus infections 21.7 Conclusions 21.8 References Viral and Other Infections of the Human Respiratory Tract. Edited by S. Myint and D. Taylor-Robinson.

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Section: Antiviral Drugs Interacting With Virus Structural Proteinsmentioning

confidence: 79%

Section: Emergence Of Drug-resistant Virusesmentioning

confidence: 99%

Specific Antiviral Therapy of Respiratory Viruses

Oxford¹,

Al-Jabri²

1996

Viral and Other Infections of the Human Respiratory Tract

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“…This has now been confirmed by sequencing the nucleic acid of drug resistant mutants (Heinz et al, 1989). It is noteworthy that resistant mutants prepared against any one of these capsid binding compounds show a great deal of cross-resistance to the others suggesting that this class of compounds may all bind to the same area within the hydrophobic pocket (Yasin, Al-Nakib & Tyrrell, 1990).…”

mentioning

confidence: 79%

Drugs against rhinoviruses

Al‐Nakib

Tyrrell

1992

J Antimicrob Chemother

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“…Of note, poliovirus variants selected for resistance to soluble poliovirus cell receptors, despite their reduced binding to HeLa cells, did not differ significantly from the wild-type virus with regard to the kinetics of viral replication in vitro or neurovirulence for mice (12). Although there are conflicting data on the ability of HRVs selected for resistance to a capsid-binding agent, chalcone Ro 09-0410, to grow in cell cultures (1,21), one resistant HRV-2 variant was found to have significantly reduced infectivity for humans (20). Further characterization of the sICAM-1-resistant phenotype, including its ability to replicate in human cell lines and respiratory cell epithelium, is warranted.…”

Section: Discussionmentioning

confidence: 99%

In vitro selection of human rhinovirus relatively resistant to soluble intercellular adhesion molecule-1

Arruda

Crump

Hayden

1994

Antimicrob Agents Chemother

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Variants of human rhinovirus serotype 39 (HRV-39) relatively resistant to inhibition by soluble intercellular adhesion molecule-1 (sICAM-1) were selected by serial passages in HeLa or WI-38 cells in the presence of sICAM-1. Moderate resistance (four-to fivefold increases in 50%v effective inhibitory concentrations [EC50s]) was observed after the second passage in HeLa cells and remained constant during six further passages in the presence of 10 ,ug of sICAM-1 per ml. A 7-to 17-fold increase in EC50s was observed in WI-38 cells during passage with 10 ,ug/ml, and reversion to a nonresistant phenotype was not observed after four passages in the absence of sICAM-1. Resistance of a higher degree was obtained by passaging HRV-39 in the presence of 100 pg of sICAM-1 per ml in HeLa cells (30-fold EC50 increase). The sICAM-1-resistant phenotype was estimated to constitute 1 in 104 to 1 in 105 PFU of a nonexposed HRV-39 population. Low to moderate levels of resistance to sICAM-1 inhibition emerge readily during in vitro passage in the presence of sICAM-1 and appear to be phenotypically stable.The cell receptor for human rhinoviruses (HRVs) of the major receptor group has been identified as intercellular adhesion molecule-i (ICAM-1) (8,18,19), and recombinant soluble forms of ICAM-1 (sICAM-1) have been shown to inhibit HRV replication in vitro (3,9,14). One form of sICAM-1 (14) inhibits the replication of 88 of the 90 numbered HRV serotypes of the major receptor group, with 50% effective inhibitory concentrations (EC50s) ranging from 0.1 to 41.1 ,ug/ml (5). Because the virus receptor binding site appears to be conserved, it has been postulated that a viral mutation which confers resistance to inhibition by a soluble cell receptor molecule might be lethal, unless attachment by an alternative receptor is possible (14). However, poliovirus mutants resistant to the antiviral effects of the poliovirus soluble cell receptor have been isolated (12). Furthermore, these resistant variants maintained the same receptor specificity as the original poliovirus, as determined by a receptor blockade with an antireceptor monoclonal antibody, and appeared to be as virulent as the wild-type virus following mouse inoculation (12).This report describes the selection of variants of HRV serotype 39 (HRV-39), a major receptor group HRV readily inhibited by sICAM-1 in cell cultures and human adenoid explants (3), that are moderately resistant to the antiviral action of sICAM-1 in vitro. We have also estimated the frequency with which such resistant variants occur in a native population of HRV-39. .). Growth and maintenance media were the same as those previously described (3). sICAM-1, prepared and purified as previously described (14, 16), was kindly furnished by Boehringer Ingelheim Pharmaceuticals (Ridgefield, Conn.). MATERIALS AND METHODSSelection of resistance to sICAM-1. Isolation of HRV-39 resistant to sICAM-1 was achieved by end-point titration in the presence of sICAM-1. In brief, serial log1o dilutions of HRV-39, 107 50% tissue culture ...

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Isolation and Preliminary Characterization of Chalcone Ro 09-0410-Resistant Human Rhinovirus Type 2

Cited by 5 publications

References 16 publications

Specific Antiviral Therapy of Respiratory Viruses

Specific Antiviral Therapy of Respiratory Viruses

Drugs against rhinoviruses

In vitro selection of human rhinovirus relatively resistant to soluble intercellular adhesion molecule-1

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