Respiratory syncytial virus infects the bonnet monkey, Macaca radiata

The Bonnet monkey model of respiratory syncytial virus (RSV) infection may be a useful nonhuman primate model for studying RSV disease in humans becau se Bonnet monkeys can predictably be infected to obtain an orderly sequence of morphologic, cytologic, virologic, serologic, and inflammatory changes related to time of infection. Young feral Bonnet monkeys, Macaca radiata, w ere infected endotracheally with 10(6) plaque-forming units (pfu) of the Lo ng strain of RSV. RSV was recovered from the animals' lungs at necropsy on days 3, 5, and 7 with the highest viral titer obtained on day 3 (1.1 and 5. 2 x 10(3) pfu/g of tissue in the upper and lower lobes, respectively). RSV antigen and F protein mRNA were detected 3-5 days after infection in alveol ar macrophages and in the epithelium of bronchi, terminal bronchioles, and alveoli. Histologic analysis of RSV-infected lungs at necropsy revealed pro gressive bronchiolar mucosal and submucosal inflammation, periarterial mono nuclear interstitial inflammation, and focal alveolitis, with a maximal res ponse at 7 days after infection. Cell counts in bronchoalveolar lavage (BAL ) increased with time with neutrophils and macrophages predominating on day 3 (6.47 and 5.85 x 10(5)/mm(3), respectively) and lymphocytes predominatin g on day 9 (4.18 x 10(5)/mm(3)). Serum-neutralizing antibody appeared on da y 5 and IgG antibody to RSV was detected on day 9. This sequence of morphol ogic, cytologic, virologic, serologic, and inflammatory change following RS V infection creates a useful model in the study ol: experimentally induced RSV disease with a potential for testing future vaccine-induced alterations in RSV disease response.