Abstract
The 90% human cytomegalovirus inhibitory concentration of 17-allylamino-17-(demethoxy)geldanamycin (17-AAG) was 0.1nM and 50% cytotoxicity required at least a 10μM concentration. Three molecular targets may explain the antiviral activities of this compound. These are (1) heat shock protein maturation complexes, (2) host cell cycle progression and (3) phosphatidylinositol 3-kinase signaling. However, the data suggested a mechanism of action where 17-AAG blocked immediate-early protein transactivation.
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