Abstract 1023 Poster Session IV, Tuesday, 5/4 (poster 92)

Although animal models of RSV infection have helped elucidate the immunopathogenesis of disease, existing animal models have limitations. High titers [107 plaque forming units (pfu)] of virus are required and are difficult to achieve, and quantification of the severity of infection has been somewhat limited. Our objectives were to develop a lower inoculum model of RSV infection and a novel method by which to quantify the severity of disease. 9-10 mo. old female retired breeder BALB/c mice were anesthetized by halothane inhalation, inoculated twice intranasally (IN) with varied titers of RSV on day 0 and day 1, and sacrificed day 7 for assessment of lung pathology and pulmonary cytokine expression. Lung histopathology was quantified by dividing perivascular spaces (PVS) into those with no to slight cellular infiltrate (0-3 layers, Grade I) or those PVS with moderate to abundant cellular infiltrate (> 3 layers, Grade II). Quantified pathology was then calculated by dividing the number of Grade II PVS by the number of Grade I plus Grade II PVS and is reported as percent. Interferon-gamma (IFN-γ) and interleukin-5 (IL-5) were measured in lungs by quantitative competitive RT-PCR. Results of a dose-response to IN RSV challenge are shown in the following table: This novel model of RSV disease using low inoculum (105.5-106 pfu) IN challenge produced quantifiable pulmonary pathology and measurable cytokine expression. This model will aid in the evaluation of new RSV vaccines, pathogenicity of vaccine challenge strains, and new treatment strategies for RSV infection.

Table 1 No caption
Full size table