Membrane Fusion by Influenza Hemagglutinin
- J.J. Skehel1,
- T. Bizebard2,
- P.A. Bullough3,
- F.M. Hughson3,
- M. Knossow2,
- D.A. Steinhauer1,
- S.A. Warton1, and
- D.C. Wiley3
- 1National Institute for Medical Research, Mill Hill, London NW7 1AA, United Kingdom; 2Laboratoire de Biologie Structurale, UMR 9920, CNRS-Université Paris-Sud, 91198 Gif-sur-Yvette Cedex, France; 3Department of Biochemistry and Molecular Biology and Howard Hughes Medical Institute, Harvard University, Cambridge, Massachusetts 02138
This extract was created in the absence of an abstract.
Excerpt
Enveloped viruses infect cells by binding to cell-surface receptors and then fusing their membranes with cellular membranes to deliver their genetic material into the cell. Fusion can occur at the cell surface as is the case, for example, for paramyxoviruses (see, e.g., Kohn 1965), but in many infections it involves interactions between virus membranes and the membranes of endosomes into which the receptor-bound viruses are transferred (see, e.g., Helenius et al. 1980). This is the case for influenza viruses for which the fusion potential of the receptor-binding membrane-fusion glycoprotein, the hemagglutinin (HA), is activated at endosomal pH (Maeda and Ohnishi 1980; Huang et al. 1981; White et al. 1981) in a process that involves extensive structural changes in the molecule. We present here observations on the nature of these changes that contribute to an understanding of their requirement for fusion activity and to considerations of the mechanisms of protein-mediated membrane...
