Mechanism of Action of N-Butyl Deoxynojirimycin in Inhibiting HIV-1 Infection and Activity in Combination with Nucleoside Analogs

Lee Ratner, Nancy Vander Heyden

Research output: Contribution to journalArticlepeer-review

21 Scopus citations

Abstract

The effects on HIV-1 infection of a glucosidase inhibitor, N-butyl deoxynojirimycin (N-buDNJ), were examined. The combinations of N-buDNJ and nucleoside analogs dideoxyinosine (DDI), dideoxycytidine (DDC), or azidothymidine (AZT) were examined in an acute infection assay. The combination of N-buDNJ and nucleoside analog reduced the yield of reverse transcriptase activity more than did either agent alone, and the effects on the number of infectious virus particles were additive or synergistic. In studies of the mechanism whereby N-buDNJ alters HIV-1 envelope fusion activity, no effects on CD4 binding were detected. However, cleavage within the V3 loop of gp120 was reduced by N-buDNJ treatment, possibly reflecting an altered conformation of this region of the envelope protein.

Original languageEnglish
Pages (from-to)291-297
Number of pages7
JournalAIDS research and human retroviruses
Volume9
Issue number4
DOIs
StatePublished - Apr 1993

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