ALKALOIDAL GLYCOSIDASE INHIBITORS (AGIS) AS THE CAUSE OF SPORADIC SCRAPIE, AND THE POTENTIAL TREATMENT OF BOTH TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES (TSES) AND HUMAN-IMMUNODEFICIENCY-VIRUS (HIV) INFECTION

AGIs are produced by plants and microorganisms in the environment. The y are absorbed from the gut, distributed throughout the body and are c oncentrated inside cells. AGIs alter the glycan chains of cellular gly coproteins (CGP) during their formation so that the same CGP produced by different clones of cells (and hence with different glycan chains) becomes structurally the same. Prion protein (PrP), a CGP, is rendered indestructable to cellular mechanisms (as PrPi) by the TSE infective process; it is suggested that AGIs could both cause and prevent this b y altering the primary structure of PrP. HIV envelope protein, gp120, carries glycan chains that are decided by the clone of the cells by wh ich it is produced. Each cellular clone would be expected to add a spe cific group of glycan chains, making the gp120 antigenically separate. As HIV infection progresses, infected clone numbers rise, the antigen ic diversity of gp120 may rise as would antibody production, trying to keep pace. Antigenically stimulated CD4+ cells carrying HIV genes, in crease HIV production with gp120 antigenically different from its stim ulant. AGIs prevent the glycan diversity and may prevent the extension of HIV infection.