Many pathogens actively exploit the actin cytoskeleton during infection. Th
is exploitation may take place during entry into mammalian cells after enga
gement of a receptor and/or as series of signaling events culminating in th
e engulfment of the microorganism. Although actin rearrangements are a comm
on feature of most internalization events (e.g. entry of Listeria, Salmonel
la, Shigella, Yersinia, Neisseria, and Bartonella), bacterial and other cel
lular factors involved in entry are specific to each bacterium. Another ste
p during which pathogens harness the actin cytoskeleton takes place in the
cytosol, within which some bacteria (Listeria, Shigella, Rickettsia) or vir
uses (vaccinia virus) are able to move. Movement is coupled to a polarized
actin polymerization process, with the formation of characteristic actin ta
ils. Increasing attention has focused on this phenomenon due to its strikin
g similarity to cellular events occurring at the leading edge of locomoting
cells. Thus pathogens are convenient systems in which to study actin cytos
keleton rearrangements in response to stimuli at the plasma membrane or ins
ide cells.