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Journal of Virology, August 2004, p. 8753-8760, Vol. 78, No. 16
0022-538X/04/$08.00+0     DOI: 10.1128/JVI.78.16.8753-8760.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Vß14+ T Cells Mediate the Vaccine-Enhanced Disease Induced by Immunization with Respiratory Syncytial Virus (RSV) G Glycoprotein but Not with Formalin-Inactivated RSV

Teresa R. Johnson,1* Steven M. Varga,2,{dagger} Thomas J. Braciale,2 and Barney S. Graham1

Viral Pathogenesis Laboratory, Vaccine Research Center, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892,1 Bernie B. Carter Center for Immunology Research, University of Virginia Health Sciences Center, Charlottesville, Virginia 229082

Received 16 December 2003/ Accepted 12 April 2004

Mice immunized with respiratory syncytial virus (RSV) G glycoprotein or with formalin-inactivated RSV (FI-RSV) exhibit severe disease following RSV challenge. This results in type 2 cytokine production and pulmonary eosinophilia, both hallmarks of vaccine-enhanced disease. RSV G-induced T-cell responses were shown to be restricted to CD4+ T cells expressing Vß14 in the T-cell receptor (TCR), and the deletion of these T cells resulted in less severe disease. We therefore examined the role of Vß14+ T cells in FI-RSV-induced disease. BALB/c mice were immunized with vaccinia virus expressing secreted RSV G (vvGs) or with FI-RSV. At the time of challenge with live RSV, mice were injected with antibody to the Vß14 component of the TCR. vvGs-immunized mice treated with anti-Vß14 had reduced cytokine levels in the lung. Eosinophil recruitment to the lung was also significantly reduced. In contrast, depletion of Vß14+ T cells in FI-RSV-immunized mice had little impact on cytokine production or pulmonary eosinophilia. An analysis of TCR Vß chain usage confirmed a bias toward Vß14 expression on CD4+ T cells from vvGs-immunized mice, whereas the CD4+ T cells in FI-RSV-immunized mice expressed a diverse array of Vß chains. These data show that although FI-RSV and vvGs induce responses resulting in similar immunopathology, the T-cell repertoire mediating the response is different for each immunogen and suggest that the immune responses elicited by RSV G are not the basis for FI-RSV vaccine-enhanced disease.

* Corresponding author. Mailing address: VRC NIAID NIH, Bldg. 40, Room 2614, 40 Convent Dr., MSC 3017, Bethesda, MD 20892-3017. Phone: (301) 594-8570. Fax: (301) 480-2771. E-mail: teresaj{at}nih.gov.

{dagger} Present address: Department of Microbiology, University of Iowa, Iowa City, IA 52242.

Journal of Virology, August 2004, p. 8753-8760, Vol. 78, No. 16
0022-538X/04/$08.00+0     DOI: 10.1128/JVI.78.16.8753-8760.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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