{
   "source_x": "PMC",
   "title": "The alpha-glucosidase inhibitor N-butyldeoxynojirimycin inhibits human immunodeficiency virus entry at the level of post-CD4 binding.",
   "pmcid": "PMC189444",
   "abstract": "The alpha-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.",
   "authors": [
      "['Fischer, P B', 'Collin, M', 'Karlsson, G B', 'James, W', 'Butters, T D', 'Davis, S J', 'Gordon, S', 'Dwek, R A', 'Platt, F M']"
   ],
   "id": "https://www.ncbi.nlm.nih.gov/pmc/articles/PMC189444"
}