Lack of quantitative correlation between inhibition of replication of rhinoviruses by an antiviral drug and their stabilization.

Abstract:

:R 61,837, a new antirhinovirus compound, was able to protect several susceptible rhinoviruses against inactivation by mild acidification or heat. This observation strengthens the hypothesis that the drug exerts antiviral activity by a direct interaction with the viral protein capsid to stabilize the particle. However, the minimal concentrations necessary to inhibit either acetate or citrate or heat inactivation were different for each of five tested serotypes and we therefore conclude that stabilization and inhibition of replication are not causally linked but parallel events, both independently resulting from the binding of the drug to the viral capsid. Studies using drug resistant mutants of HRV51 and HRV9 confirmed this lack of quantitative correlation. The mutants were also shown to be cross resistant to a panel of seven different reference antirhinoviral drugs including SDS, WIN51711, chalcone, dichloroflavan and MDL20,610. This indicates that all these compounds bind to the same site corresponding to the hydrophobic pocket within the viral protein VP 1 beta-barrel structure of HRV14.

journal_name

Arch Virol

journal_title

Archives of virology

authors

Andries K,Dewindt B,Snoeks J,Willebrords R

doi

10.1007/BF01311037

subject

Has Abstract

pub_date

1989-01-01 00:00:00

pages

51-61

issue

1-2

eissn

0304-8608

issn

1432-8798

journal_volume

106

pub_type

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