Airway epithelium repair after infection consists of wound repair, re-synthesis of the extracellular matrix (ECM), and tight junction proteins. In humans, EPs®7630 obtained fromPelargonium sidoidesroots reduces the severity and duration of acute respiratory tract infections. The effect of EPs®7630 on tissue repair of rhinovirus-16 (RV-16) infected and control human airway epithelial cells was assessed for: (i) epithelial cell proliferation by manual cell counts, (ii) epithelial wound repair by “scratch assay”, (iii) ECM composition by Western-blotting and cell-based ELISA, and (iv) epithelial tight junction proteins by Western-blotting. EPs®7630 stimulated cell proliferation through cAMP, CREB, and p38 MAPK. EPs®7630 significantly improved wound repair. Pro-inflammatory collagen type-I expression was reduced by EPs®7630, while fibronectin was increased. Virus-binding tight junction proteins desmoglein2, desmocollin2, ZO-1, claudin1, and claudin4 were downregulated by EPs®7630. The RV16-induced shift of the ECM towards the pro-inflammatory type was prevented by EPs®7630. Most of the effects of EPs®7630 on tissue repair and regeneration were sensitive to inhibition of cAMP-induced signaling. The data suggest that EPs®7630-dependent modification of epithelial cell metabolism and function might underlie the faster recovery time from viral infections, as reported by others in clinical studies.