There are several distinct types of viral fusion proteins, including the class I, primarily alpha helical proteins (such as HIV TM and influenza HA), the class II, primarily beta sheet proteins (such as the flavivirus E and alphavirus E1), and mixed helix/sheet proteins (including herpes virus gB and rhabdovirus G) [3, 4] . To date, most progress with viral fusion protein inhibitors has focused on class I alpha helical proteins. The HIV TM protein provides an excellent example of targeting distinct, interacting surfaces for inhibition. The HIV TM functions as a homotrimer with each monomer contributing two alpha helical regions that interact to form a post-fusion six-helix bundle. Inhibition of the formation of this six-helix bundle can be accomplished by exogenous peptides mimicking either of the two reciprocally interacting helices [5] [6] [7] .