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,
* Microbiology and Tumorbiology Center and
Department of Immunology, Microbiology, Pathology, and Infectious Diseases, Karolinska Institutet, Stockholm, Sweden;
Department of Veterinary Microbiology, Swedish University of Agriculture Sciences, and
Department of Virology, National Veterinary Institute, Uppsala, Sweden;
¶ Units for Morphological Phenotype Analysis and Embryology and Genetics Clinical Research Center, Huddinge University Hospital, Stockholm, Sweden; and
|| Department of Vaccine Research, Swedish Institute for Infectious Disease Control, Solna, Sweden
Respiratory syncytial virus (RSV) causes severe respiratory
diseases in infants and young children. Inappropriate immunity to the
virus can lead to disease enhancement upon subsequent infection. In
this study, we have characterized the antiviral immunity elicited by
the recombinant Semliki Forest virus (SFV) encoding the RSV fusion (F)
and attachment (G) protein, and compared with that induced by the
immune-stimulating complex (ISCOM)-incorporated FG proteins. Antiviral
immunity against RSV elicited nasally or parentally by either of the
immunogen having divergent profiles could reduce lung RSV titers upon
challenge. However, resistance to RSV without disease enhancement was
only observed in those vaccinated with SFV recombinants via nasal
route. Presence of postvaccination pulmonary IFN-
response to the
H-2Kd-restricted T cell epitope (F85–93;
KYKNAVTEL) was found to be associated with absence of enhanced
pulmonary disease and goblet cell hyperplasia as well as reduced
Th2-cytokine expression. This result demonstrates that the SFV
recombinants can result in enhanced clearance of RSV without enhancing
the RSV-associated disease, and underlines the importance in priming
pulmonary MHC class I-restricted T cells when RSV FG-based vaccines are
used.
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