Abstract

Many proteins are difficult to target with drugs because their primary function is to participate in protein-protein interactions (PPIs) and protein-nucleic acid interactions (PNIs) through flat interfaces that are less conducive to small molecule binding. These interactions are found in many viral proteins that interact with host factors and viral nucleic acids in order to evade the host immune system. We focused our study on viral protein 35 (VP35), from the highly lethal Ebola virus. VP35 plays essential roles in Ebola's replication cycle, including binding the viral RNA genome to block a host's innate immunity.

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