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.
ORIGINAL RESEARCH PAPER
Pelkmans, K., Püntener, D. & Helenius, A. Local actin polymerization and dynamin recruitment in SV40-induced internatlization of caveolae. Science 296, 535–539 (2002)
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Mitchell, A. A transient tail. Nat Rev Mol Cell Biol 3, 311 (2002). https://doi.org/10.1038/nrm815
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DOI: https://doi.org/10.1038/nrm815