Inhibition of host protein synthesis in vaccinia virus-infected cells in the presence of cordycepin (3'-deoxyadenosine)

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Abstract
Cordycepin efficiently inhibited viral mRNA and poly(A) acid syntheses in vaccinia virus-infected [mouse Ehrlich ascites tumor] cells, but allowed the shutoff of host protein synthesis to occur. Therefore, cordycepin was used to study this shutoff in the absence of gene expression. Ribosome transit time was increased in infected cells, revealing an inhibition at the level of elongation and/or release of polypeptide chains. The disappearance of heavy polysomes in vaccinia virus-infected cells showed that the inhibition of host protein synthesis resulted predominantly from a block at the stage of initiation. This conclusion was confirmed by the recovery of heavy polyribosomes when low levels of cycloheximide were added to slow down ribosome release from the mRNA. Similar amounts of cellular mRNA (present in the polyribosomes) were found in vaccinia virus-infected cells and in mock-infected cells (exposed to cordycepin), showing that the cellular mRNA was not inactivated in these conditions. A component of the vaccinia virion apparently inhibits, in the absence of viral RNA and poly(A) syntheses, host protein synthesis at the level of initiation and, to a lesser extent, at the level of elongation (and/or release) of polypeptide chains.