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.