Abstract
Entry is the first step in the infectious life cycle of a virus. In the case of rhabdoviruses, entry is facilitated exclusively by the envelope glycoprotein G and its interactions with the host cell. For vesicular stomatitis virus (VSV), attachment to the cell surface was thought to be facilitated by interactions with the lipid phosphatidylserine, however recent work suggests that it is in fact initiated by recognition of proteinaeous receptors. Clathrin-mediated endocytosis delivers the virions into endosomes where they have been proposed to traffic to multi-vesicular bodies. There, the viral envelope fuses with internal vesicles in a process mediated by glycoprotein G in a pH- and phosphatidylserine-dependent manner. A clear mechanistic understanding of glycoprotein G mediated fusion has yet to be obtained, however current data suggests that it is likely facilitated by events distinct from Class I or Class II fusion proteins of other viruses. Rhabdoviruses are also notable in that their fusion protein exists in a reversible pH-dependent equilibrium, which prevents irreversible preactivation during assembly, and may prove to be relevant in the mediation of cell-to-cell fusion - an alternate form of viral spread.