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Combined knock down of chaperones or AR\u201012 treatment acted to reduce the expression of virus receptors and essential glucosidase proteins. Combined knock down of chaperones or AR\u201012 treatment inactivated mTOR and elevated ATG13 S318 phosphorylation concomitant with inducing an endoplasmic reticulum stress response that in an eIF2\u03b1\u2014dependent fashion increased Beclin1 and LC3 expression and autophagosome formation. Over\u2010expression of chaperones prevented the reduction in receptor\/glucosidase expression, mTOR inactivation, the ER stress response, and autophagosome formation. AR\u201012 reduced the reproduction of viruses including Mumps, Influenza, Measles, Jun\u00edn, Rubella, HIV (wild type and protease resistant), and Ebola, an effect replicated by knock down of multiple chaperone proteins. AR\u201012\u2014stimulated the co\u2010localization of Influenza, EBV and HIV virus proteins with LC3 in autophagosomes and reduced viral protein association with the chaperones HSP90, HSP70, and GRP78. Knock down of Beclin1 suppressed drug\u2010induced autophagosome formation and reduced the anti\u2010viral protection afforded by AR\u201012. In an animal model of hemorrhagic fever virus, a transient exposure of animals to low doses of AR\u201012 doubled animal survival from \u223c30% to \u223c60% and suppressed liver damage as measured by ATL, GGT and LDH release. Thus through inhibition of chaperone protein functions; reducing the production, stability and processing of viral proteins; and stimulating autophagosome formation\/viral protein degradation, AR\u201012 acts as a broad\u2010specificity anti\u2010viral drug in vitro and in vivo. We argue future patient studies with AR\u201012 are warranted. J. Cell. 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