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To help address this Ebola crisis, as we were preparing this manuscript, we communicated our discoveries to Medecins Sans Frontieres (MSF, Doctors Without Borders) and encouraged them to explore whether the administration of AQ in West African countries hit by Ebola epidemic is associated with a reduced mortality due to Ebola infections. MSF conducted a study and observed that the administration of AQ provided a substantial protection against Ebola mortality and reduced the mortality risk by 31% and in this study MSF acknowledged the authors of this study (https://www. As seen in current Ebola epidemic, the human host can be co-exposed to numerous deadly pathogens and thus the infected individual will need to take numerous countermeasures (each with their own side-effects) to protect against multiple infectious organisms. Therefore, therapies capable of inhibiting multiple pathogens are needed. Broad-spectrum anti-pathogen drugs, capable of simultaneously inhibiting numerous unrelated pathogens, could be developed by targeting host proteins commonly exploited by those pathogens. In this work we show that AQ inhibits the host target rather than the pathogen, which makes AQ host-oriented broad-spectrum antimicrobial that is less likely to be circumvented by pathogen mutations that lead to microbial resistance to the countermeasure. AQ was discovered by Parke-Davis in the 1940s and was approved by the FDA as an anti-malarial in the late 1940s and early 1950s under the trade name Camoquine. AQ is currently on the WHO’s Model List of Essential Medicines. Today AQ is recommended as a frontline anti-malarial therapy in combination with artemisinin. AQ belongs to the ‘quinoline antimalarials’ (Reviewed in 42 ). AQ inhibits Plasmodium falciparum phosphoethanolamine methyltransferase, an enzyme found in malarial parasites but not in humans 43. Here we report that AQ also binds and blocks the function of host cathepsin B protein and thus entry of key pathogens into the cytoplasm. Since AQ has been used for the past 60 years, its safety and pharmacokinetic profiles are well known. For example, it has been determined that after oral administration in healthy subjects, AQ is quickly absorbed and biotransformed into its main active form, DEAQ, which in turn is slowly eliminated with a terminal half-life of 9’18 days. The availability of PK values for AQ allows us to compare it to our in vitro data. The EC50 values for all of the tested pathogens inhibited by AQ or by DEAQ were at low ?M range. Importantly, the known Cmax values (maximal amounts of drug in the blood after oral administration) of DEAQ in humans are in low ?M range 43,44,45 and are comparable to the DEAQ EC50 values found in vitro for tested pathogens. This suggests that it is possible to achieve anti-pathogen effective AQ doses in blood by orally administered AQ. 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