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The respiratory syncytial virus (RSV) causes abundant annual fatalities on young children and elder adults by infecting human cells mediated by RSV fusion (F) surface homotrimeric proteins. Despite their RSV fusion in vitro inhibitors, anti-F therapeutic molecules are not yet clinically available because of emergent resistant mutations. Here, alternative therapeutic strategies are explored to dock mutated F protein models. For that thousands of trimeric drug-like candidates were computationally generated/selected by parent-children co-evolution. New top-children candidates may help experimental tests since they display 3-fold star-like molecules fitting similar trimeric F cavities than previous in vitro inhibitors but improved higher sub-nanoMolar affinities. Additionally, some top-children also successfully targeted F mutations previously implicated in RSV fusion drug-resistances
Julio Coll (Thu,) studied this question.