Computational screening of 261 resveratrol-associated targets against 1,196 RSV-related targets yielded 67 shared candidates. Protein-protein interaction network analysis narrowed these to 10 core targets — prominently EGFR, SRC, and HSP90AA1 — with molecular docking confirming stable binding (all energies below −5 kcal/mol). KEGG enrichment implicated the Ras, PI3K-Akt, and MAPK signaling cascades as likely mechanistic conduits for resveratrol's known anti-RSV effect.
RSV remains a genuine unmet therapeutic need: despite recent maternal and older-adult vaccines and nirsevimab prophylaxis for infants, no orally available small-molecule antiviral has cleared regulatory approval. Resveratrol's antiviral credibility has grown through direct virucidal and entry-inhibition studies, but this paper shifts the frame toward host-directed pharmacology — a strategically attractive angle because host targets are harder for the virus to mutate around. The EGFR–PI3K–Akt axis in particular is biologically coherent; RSV exploits EGFR-mediated signaling to facilitate cellular entry and suppress innate immune responses.
However, the limitations here are substantial. This is entirely in-silico work — no cell culture, no animal model, no human data. Network pharmacology approaches are hypothesis-generating tools prone to false positives, and molecular docking scores do not predict biological potency. Resveratrol's notoriously poor oral bioavailability further clouds translational prospects. Treat this as a structured hypothesis, not a therapeutic claim — incremental scaffolding that must survive wet-lab scrutiny before clinical relevance can be assessed.
