The α-glucosidase inhibitor N-butyldeoxynojirimycin inhibits human immunodeficiency virus entry at the level of post-CD4 binding

P. B. Fischer, M. Collin, G. B. Karlsson, W. James, T. D. Butters, S. J. Davis, S. Gordon, R. A. Dwek, F. M. Platt*

*Corresponding author for this work

Research output: Contribution to journalJournal Article peer-review

166 Scopus citations

Abstract

The α-glucosidase inhibitor N-butyldeoxynojirimycin (NB-DNJ) is a potent inhibitor of human immunodeficiency virus (HIV) replication and syncytium formation in vitro. However, the exact mechanism of action of NB-DNJ remains to be determined. In this study we have examined the impairment of HIV infectivity mediated by NB-DNJ. By two independent HIV entry assays [PCR- based HIV entry assay and entry of Cocal(HIV) pseudotypes], the reduction in infectivity was found to be due to an impairment of viral entry. No effect of NB-DNJ treatment was seen on the kinetics of the interaction between gp120 and CD4 (surface plasmon resonance; BIAcore) or on the binding of virus particles to H9 cells (using radiolabeled virions). We therefore conclude that a major mechanism of action of NB-DNJ as an inhibitor of HIV replication is the impairment of viral entry at the level of post-CD4 binding, due to an effect on viral envelope components.

Original languageEnglish
Pages (from-to)5791-5797
Number of pages7
JournalJournal of Virology
Volume69
Issue number9
DOIs
StatePublished - 09 1995
Externally publishedYes

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