During virus entry, induces fusion of viral and cellular mbranes leading to delivery of the nucleocapsid into the cytoplasm. The fusogenic activity is inactive untill entry into host cell endosome, where a furin-like protease cleaves off a small peptide between F1 and F2. Interacts directly with heparan sulfate and may participates in virus attachment. Furthermore, the F2 subunit was identifed as the major determinant of RSV host cell specificity. Later in infection, proteins F expressed at the plasma mbrane of infected cells can mediate fusion with adjacent cells to form syncytia, a cytopathic effect that could lead to tissue necrosis. The fusion protein is also able to trigger p53-dependent apoptosis.
Respiratory syncytial virus (RSV)SH and G proteins are not essential for viral replication in vitro clinical evaluation and molecular characterization of a cold-passaged, attenuated RSV subgroup B mutant.Karron R.A., Buonagurio D.A., Georgiu A.F., Whitehead S.S., Adamus J.E., Clements-Mann M.L., Harris D.O., Randolph V.B., Udem S.A., Murphy B.R., Sidhu M.S.Proc. Natl. Acad. Sci. U.S.A. 94:13961-13966(1997)
Research Topic:Others
