Abstract
The Vpu protein of human immunodeficiency virus type 1 forms cation-selective ion channels and enhances the process of virion budding and release. Mutagenesis studies have shown that the N-terminal transmembrane domain primarily controls both of these activities. Here we report that the Vpu ion channel is inhibited by the amiloride derivatives 5-(N,N-hexamethylene)amiloride and 5-(N,N-dimethyl)amiloride but not by amiloride itself, nor by amantadine. Hexamethyleneamiloride also inhibits budding of virus-like particles from HeLa cells expressing HIV-1 Gag and Vpu proteins. These results confirm the link between Vpu ion channel activity and the budding process and also suggest that amiloride derivatives might have useful anti-HIV-1 properties.
Similar content being viewed by others
Author information
Authors and Affiliations
Additional information
Revised version: 19 July 2001
Electronic Publication
Rights and permissions
About this article
Cite this article
Ewart, G.D., Mills, K., Cox, G.B. et al. Amiloride derivatives block ion channel activity and enhancement of virus-like particle budding caused by HIV-1 protein Vpu. Eur Biophys J 31, 26–35 (2002). https://doi.org/10.1007/s002490100177
Received:
Accepted:
Published:
Issue Date:
DOI: https://doi.org/10.1007/s002490100177