(RSV) has changed very little over the years, the leitmotif being that RSV is a major cause of serious respiratory illnesses such as bronchiolitis and pneumonia worldwide, yet no safe, effective vaccine or good antiviral therapy is available. In this issue of the European Respiratory Journal, OLSZEWSKA et al.[1] report an exciting advance that could well be a key step toward pulling the field of anti-RSV interventions out of its doldrums. TMC353121, a remarkable ‘‘designer’’molecule with a rather unremarkable name, is a potent pharmacological inhibitor of the RSV fusion (F) protein, a viral protein crucial to initial entry of RSV into cells and in subsequent cell-to-cell spread of infection. In contrast to many other F inhibitors that have been developed as promising pharmaceuticals and then abandoned, OLSZEWSKA et al.[1] used a mouse model to provide compelling evidence that TMC353121 can be used either prophylactically or therapeutically to decrease RSV lung infection and virusassociated lung inflammation and histopathology. This work extends the previous success of palivizumab (Synagis®; Med-Immune, Gaithersburg, MD, USA), a humanised monoclonal antibody directed against the RSV F protein, an effective prophylactic that is used in children considered at high risk for serious RSV infections [2]. TMC353121 appears to have a suitable pharmacokinetic and safety profile and is amenable to a variety of dosing regimens. Importantly, and if TMC353121 administration is started within 48 h of RSV infection, the drug is an effective therapeutic agent. The 48-h time window between onset of infection and onset of treatment has bona fide practical utility for human RSV infections in the clinical setting. Administration of TMC353121 decreased RSV load by 1–2 logs at the peak of infection (day 4 post-RSV inoculation in the mouse model). Decreases in viral load were associated with a significantly attenuated host immune and inflammatory response, as assessed by lung histopathological examination, and measurement of inflammatory cells and chemical mediators in bronchoalveolar lavage fluids. RSV-induced weight loss, a characteristic of the mouse model, was also inhibited by TMC353121. As a compound effective for both prophylaxis and therapy in vivo, TMC353121 has true potential for successful translation into clinical use.