Journal
VIRUS GENES
Volume 33, Issue 2, Pages 253-264Publisher
SPRINGER
DOI: 10.1007/s11262-006-0063-y
Keywords
respiratory syncytial virus(rsv); pathogenicity genes; sG glycoprotein; CX3C fractalkine domain; superantigen domain; allergy; eosinophilia; bronchiolitis; cytokines; antagonists
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Based on the hypothesis that respiratory syncytial virus (RSV) sG protein causes allergy in patients, it is suggested that treatment of RSV patients with antagonists of IL-4 and FKN early in infection will prevent the increased level of IL-4 in the serum. Together with CpG ODNs that induce Toll-like receptor 9(+) (TLR9(+)p) plasmacytoid dendritic cells to release type I IFN-alpha and -beta will reactivate the inhibited Th1 cells and the antiviral cytotoxic T leukocytes. In addition, binding of CpG ODNs to TLR9(+) B cells will stop IgE synthesis and antiviral IgG and IgA will continue. Together, the IL-4 and FKN antagonists and CpG ODNs reactivate the adaptive immune response to clear the virus and protect the patient from a second RSV infection. It is also suggested that the less-pathogenic RSV strain Long may be a candidate for vaccine development after deletion of the FKN and superantigen domains from the G gene.
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