It pays to stay one step ahead. We have learned this lesson over and over again from micro-organisms, and this issue contains many examples of bacteria and viruses that have subverted our cellular machinery to their own advantage.

Take, for example, the Kaposi's sarcoma virus, human herpesvirus 8, which has borrowed a cyclin and turned it against us. A Highlight on page 88 describes two of this cyclin's dastardly deeds. You might think that stimulating division of its host cells, thereby providing more host to infect, was cunning enough, but it has another trick up its sleeve: once it's done replicating, it uses the same cyclin to promote apoptosis of the host and aid its dissemination.

Viruses have also learned a thing or two about shutting off regulated intracellular proteolysis by the ubiquitin–proteasome system. The importance of this pathway in cellular regulation, discussed in a Timeline by R. John Mayer on page 145, was marked in September by the presentation of the Albert Lasker award for basic medical research to three scientists whose work crystallized its significance — Avram Hersko, Aaron Ciechanover and Alexander Varshavsky. However, the viruses got there first. By turning off proteasomal antigen processing in antigen-presenting cells, the likes of Epstein–Barr virus and cytomegalovirus can lie low in their host cells for years.

But the subverter par excellence has to be the intracellular bacterium Listeria monocytogenes, whose actin 'comet tails' are the subject of a review by Julie Theriot and colleagues on page 110, and the inspiration for this issue's cover. Listeria's habits have taught us an enormous amount about how our cells use the actin cytoskeleton to move — an unusual case of symbiosis.