Significant progress has been made in elucidating the mechanisms of vi
ral membrane fusion proteins; both those that function at low, as well
as those that function at neutral, pH. For many viral fusion proteins
evidence now suggests that a triggered conformational change that exp
oses a previously cryptic fusion peptide, along with a rearrangement o
f the fusion protein oligomer, allows the fusion peptide to gain acces
s to the target bilayer and thus initiate the fusion reaction. Althoug
h the topologically equivalent process of cell-cell fusion is less wel
l understood, several cell surface proteins, including members of the
newly described ADAM gene family, have emerged as candidate adhesion/f
usion proteins.