Treatment of radioactively labelled host cells with T1 or T2 bacteriophages induces a leakage of cellular P and S into the medium. Evidence is presented showing that this increased cell permeability is not the result of complete lysis of a small fraction of the cells, but rather is made up of contributions from all or most of the infected population. This leakage of cellular constituents exhibits the following characteristics: (a) Infection of a cell with a single virus suffices to evoke the reaction; (b) Increasing the multiplicity up to 7 to 8 virus particles per cell does not affect the extent of leakage produced; (c) Some leakage does occur at 0 degrees C., but much less than at 37 degrees C.; (d) Infection by T1 virus results in a smaller amount of leakage than in the case of T2, but the pattern of response to varying virus multiplicity is the same; (e) The P resulting from such leakage contains no DNA and chemically resembles that which elutes in smaller amounts from uninfected cells; (f) At 37 degrees C. the virus-induced leakage reaction appears within a matter of seconds, and usually decreases after 2 to 3 minutes; (g) The reaction is inhibited by 0.025 M Mg(++). Theoretical considerations are presented suggesting the place of this reaction in the sequence of events constituting the virus penetration reaction; its relationship to the phenomenon of lysis-from-without; and its resemblance to the leakage reaction produced by electrostatic binding of ionized compounds to cell surfaces. The existence of similar effects in avian-mammalian virus systems is noted.

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cellular p and s cellular constituents binding virus cell virusinduced leakage

T T, PUCK H H, LEE,.Mechanism of cell wall penetration by viruses. I. An increase in host cell permeability induced by bacteriophage infection.. 99 (5),481-94.

T T, PUCK H H, LEE,"Mechanism of cell wall penetration by viruses. I. An increase in host cell permeability induced by bacteriophage infection." 99

T T, PUCK H H, LEE,"Mechanism of cell wall penetration by viruses. I. An increase in host cell permeability induced by bacteriophage infection."