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Journal of Virology, February 2006, p. 1130-1139, Vol. 80, No. 3
0022-538X/06/$08.00+0     doi:10.1128/JVI.80.3.1130-1139.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Protection against Respiratory Syncytial Virus by a Recombinant Newcastle Disease Virus Vector

Luis Martinez-Sobrido,1,{dagger} Negin Gitiban,2,{dagger} Ana Fernandez-Sesma,1 Jerome Cros,1 Sara E. Mertz,2 Nancy A. Jewell,2 Sue Hammond,2 Emilio Flano,2 Russell K. Durbin,2 Adolfo García-Sastre,1 and Joan E. Durbin2,3*

Department of Microbiology, Mount Sinai School of Medicine, New York, New York,1 Columbus Children's Research Institute,2 Department of Pediatrics, The Ohio State University College of Medicine and Public Health, Columbus, Ohio3

Received 27 September 2005/ Accepted 15 October 2005

Respiratory syncytial virus (RSV) is a major cause of severe lower respiratory tract disease in infants and the elderly, but no safe and effective RSV vaccine is yet available. For reasons that are not well understood, RSV is only weakly immunogenic, and reinfection occurs throughout life. This has complicated the search for an effective live attenuated viral vaccine, and past trials with inactivated virus preparations have led to enhanced immunopathology following natural infection. We have tested the hypothesis that weak stimulation of innate immunity by RSV correlates with ineffective adaptive responses by asking whether expression of the fusion glycoprotein of RSV by Newcastle disease virus (NDV) would stimulate a more robust immune response to RSV than primary RSV infection. NDV is a potent inducer of both alpha/beta interferon (IFN-{alpha}/ß) production and dendritic cell maturation, while RSV is not. When a recombinant NDV expressing the RSV fusion glycoprotein was administered to BALB/c mice, they were protected from RSV challenge, and this protection correlated with a robust anti-F CD8+ T-cell response. The effectiveness of this vaccine construct reflects the differential abilities of NDV and RSV to promote dendritic cell maturation and is retained even in the absence of a functional IFN-{alpha}/ß receptor.

* Corresponding author. Mailing address: Columbus Children's Research Institute, 700 Children's Drive, WA-4104, Columbus, OH 43205. Phone: (614) 722-2798. Fax: (614) 722-3680. E-mail: durbinj{at}pediatrics.ohio-state.edu.

{dagger} L.M.-S. and N.G. contributed equally to this work.

Journal of Virology, February 2006, p. 1130-1139, Vol. 80, No. 3
0022-538X/06/$08.00+0     doi:10.1128/JVI.80.3.1130-1139.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



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