Vaccinia virus infection results in large rearrangements of the host actin cytoskeleton including the formation of actin tails that are strikingly similar to those seen in Listeria, Shigella and Rickettsia infections. Using actin polymerization as the driving force the intracellular enveloped form of the vaccinia virus (IEV) is propelled on the tip of actin tails at a speed of 2.8 microns/min, both intra- and intercellularly. The similarities between the actin-based motility of the vaccinia virus, Listeria, Shigella and Rickettsia suggest that intracellular pathogens have developed a common strategy to exploit the actin cytoskeleton of the host to facilitate their intercellular spread. This review focuses on our current understanding of the interactions between the vaccinia virus and the actin cytoskeleton.