The virus is nature's squatter — it breaks into a cell, and then makes itself at home. Different viruses use various means of entering cells, and a report by Ari Helenius and colleagues in Science now uncovers how the simian virus 40 (SV40) gets in.

SV40 is endocytosed through caveolae — indentations in the plasma membrane — that are pinched off as vesicles that contain caveolin-1 and a single virus particle. But can SV40 actively induce its own endocytosis? As a first step in studying this, the authors tried to block the process, and found that latrunculin A (which sequesters actin monomers), and general- and tyrosine-kinase inhibitors, prevented virus uptake and infection.

Helenius and co-workers next found that, after virus entry, the number of actin stress fibres was reduced. Instead, small actin patches and tails appeared. The site for actin-tail formation corresponded to the sites of caveolin-1 expression. Moreover, dynamin II — which is involved in internalization — was also recruited to the virus-containing caveolae.

These results indicate that the virus uses actin polymerization to enhance its own internalization, and the authors showed that SV40-induced tyrosine phosphorylation in the caveolae leads to the observed transient changes. The next step, then, will be to identify the kinase(s) that are responsible.