Abstract
Vpr, an accessory gene of human immunodeficiency virus, encodes a virion-associated nuclear protein of 15 KDa in size. Vpr is supposed to have an important role for the AIDS development. It induces cell cycle abnormality and enhances virus production. We have established a stable transfectant (MIT-23) in which Vpr expression is highly regulated. Using MIT-23 cells, we found that quercetin, a f lavonoid, inhibited Vpr function, and that Vpr expression induced genomic instability. We discuss the feasibility of using Vpr as a target molecule for the development of a novel anti-HIV therapy.
