Incubation of HeLa cells with Encephalomyocarditis virus (EMC) induces permeability of the cell membrane to protein toxins, such as alpha sarcin. To induce permeability to this toxin only 5 min incubation of cells with virus is needed. On the other hand, less than 1 min exposure of the susceptible cells to alpha sarcin produces maximal inhibition of protein synthesis. EMC virus treated with UV-light, although unable to replicate, can still induce the entrance of alpha sarcin into HeLa cells, but the virion loses this capacity after heating at 60 degrees C for 10 min. These findings suggest that an integral viral genome is not necessary to make the cells permeable to alpha sarcin, and that a virion protein might be involved in this phenomenon. Although human interferon prevents productive EMC infection, it does not affect the virus-induced entrance of alpha sarcin into the cells. The plasma membrane of cells that have been treated with virion particles can recover its initial lack of permeability to alpha sarcin after 2 h at 37 degrees C. Poliovirus modifies membrane permeability in human HeLa cells, but it has no effect on mouse L cells. This fact suggests that viral attachment to specific cell surface receptors is necessary to induce permeability, since receptors to poliovirus are only present in primate cells.