The protective immunity induced by intranasally inoculated serotype 63 chimpanzee adenovirus vector expressing human respiratory syncytial virus prefusion fusion glycoprotein in BALB/c mice.

Human respiratory syncytial virus (RSV) is a ubiquitous pediatric pathogen causing serious lower respiratory tract disease worldwide. No licensed vaccine is currently available. In this work, the coding gene for mDS-Dav1, the full-length and prefusion conformation RSV fusion glycoprotein (F), was designed by introducing the stabilized prefusion F (preF) mutations from DS-Cav1 into the encoding gene of wild-type RSV (wtRSV) F protein. The recombinant adenovirus encoding mDS-Cav1, rChAd63-mDS-Cav1, was constructed based on serotype 63 chimpanzee adenovirus vector and characterized in vitro. After immunizing mice via intranasal route, the rChAd63-mDS-Cav1 induced enhanced neutralizing antibody and F-specific CD8+ T cell responses as well as good immune protection against RSV challenge with the absence of enhanced RSV disease (ERD) in BALB/c mice. The results indicate that rChAd63-mDS-Cav1 is a promising mucosal vaccine candidate against RSV infection and warrants further development.

Detection of Notch signaling molecules in cemento-ossifying fibroma of the jaws.

BACKGROUND: The aim of this study was to evaluate the roles of Notch signaling in the oncogenesis and cytodifferentiation of cemento-ossifying fibroma, the expressions of Notch receptors and ligands were detected in COF and normal jaw bones. MATERIALS AND METHODS: The expressions of Notch1, Notch3, Jagged1, and Jagged2 were detected by reverse transcriptase polymerase chain reaction and immunohistochemistry respectively in 16 cases of normal bone tissues and 12 cases of COF of the jaws. RESULTS: The mRNAs expressions of Notch1, Notch3, Jagged1, and Jagged2 were detected in all specimens. The expression levels of mRNAs in COF were higher than those in normal bones. In COF, Notch proteins staining were showed extensively distribution in fibroblasts and osteoblasts. In normal bone tissue, Notch proteins were expressed in osteoblasts, whereas proteins staining were weaker than those in COF, but no detection in fibroblast-like bone marrow stroma cells. The expressions of Notch receptors and ligands were not detected in cementum-like products or bone matrices. CONCLUSION: Our data suggest that Notch signaling may participate in controlling cell differentiation and proliferation in normal bone and COF of the jaws. Notch signaling disorder may be a molecular incident in COF occurrence and development.