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Binding of virus particles to the host cell surface initiates a cascade of events that culminates with the introduction of the viral genetic material into the host cell. For enveloped viruses, this cascade begins with the envelope proteins on the virus binding to specific cellular receptors and is completed following viral glycoprotein–mediated fusion of the viral and target membranes. Presently, the best model for viral envelope–mediated membrane fusion is that of influenza hemaglutinnin (HA). HA mediates membrane fusion by first binding to its cognate receptor on the host membrane. After endocytosis, pH-induced conformational changes lead to insertion of a hydrophobic stretch of residues (the so-called fusion peptide) of HA into the host membrane. Subsequent to fusion peptide insertion, additional conformational changes are thought to take place in HA that eventually lead to membrane fusion (reviewed byCarr and Kim 1994).
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Paul Bates (1996) studied this question.
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