In comparison with other virus infections, such as HIV, HBV, HCV, influenza and herpes virus, dengue virus infections have received relatively little attention from a (chemo)therapeutic viewpoint, despite their global incidence (2.5 billion people estimated to be at risk) and absence of an effective prophylactic measure (i.e., vaccination). However, the replicative cycle of the dengue virus offers a wealth of potential target sites, including virus adsorption and fusion, RNA-dependent RNA polymerase (and the associated 2´-O-methyltransferase) and the N-glycosylation process. Numerous compounds have been identified that interfere with dengue virus infections (i.e., ribavirin, interferon, sulfated polysaccharides, 2´-C-methylnucleoside analogs and iminosugar derivatives). For other compounds found to be effective against the dengue virus, including geneticin (G418) and FGI-106, the mechanism of action still remains unresolved.
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