Modification of membrane permeability in vaccinia virus-infected cells

Abstract

Infection of mouse L cells with vaccinia virus leads to a modification in the permeability of the cell membrane. This modification permits the entry of the translation inhibitor hygromycin B (MW 550). On the basis that some inhibition of protein synthesis is also observed in the presence of the protein toxin α-sarcin (MW 16,800), it seems likely that macromolecules can also cross the membrane in vaccinia virus-infected cells. The modification of the cell membrane is observed very early during infection, in the first hour of viral adsorption. After this time the cell membrane gradually reseals, restoring its normal permeability characteristics. The multiplicities of infection needed to observe these modifications in permeability are rather low; the presence of 3 PFU/cell (150 physical particles/cell) are enough to promote the entry of the inhibitor hygromycin B. Ultraviolet (uv)-inactivated vaccinia virus (17,280 ergs/mm 2 promotes the increase in membrane permeability. Moreover, the presence of actinomycin D (25 μg/ml) and cordycepin (100 μg/ml) did not inhibit the passage of hygromycin B suggesting that a virion component is responsible for this phenomenon. That an intact virion is required to permeabilize L cells, is supported by the findings that neither purified core particles, nor virion surface proteins can induce the inhibition of translation by hygromycin B. Since interferon treatment appears to induce chemical, physical, morphological, and immunological alterations in the cell surface, the effect of interferon on changes in membrane permeability following vaccinia virus infection was investigated. We find that the permeability of the cell membrane is enhanced in interferon-treated, vaccinia virus-infected cells when compared to untreated, infected cells.