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Virology. 1967 Aug;32(4):678-86.

The disaggregation of host polyribosomes in productive and abortive infection with herpes simplex virus.

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1
Department of Microbiology, University of Chicago, Chicago, Illinois 60637, USA.

Abstract

Herpes simplex virus strain MPdk- causes disaggregation of host polyribosomes in both permissive (HEp-2) and nonpermissive (DK) cells during the first 3 hours after infection. The following findings are discussed in this paper: (1) UV light-irradiated virus does not cause disaggregation of host polyribosome. (2) To obtain equivalent disaggregation of host polyribosomes, 1 hour after infection the nonpermissive DK cells must be infected with MPdk- virus at a multiplicity twenty- to thirty-fold higher than the permissive HEp-2 cells. (3) Actinomycin D (0-20 microg/ml of medium), 6-azauridine (0-10(-4) M), or p-fluorophenylalanine (0-10(-3) M) do not prevent the disaggregation of host polyribosomes in HEp-2 cells infected with 60 plaque-forming units (PFU)/cell of MPdk- virus. However, the drugs do prevent the disaggregation of host polyribosomes in DK cells infected with 1000 PFU/cell of MPdk- virus. (4) The differences between HEp-2 and DK cells with respect to multiplicity requirements to induce disaggregation and the ability of the drugs to prevent it are due to some property of the product specified by MPdk- in these cells. This conclusion is based on the finding that in DK cells productively infected with MPdk+sp, a multistep mutant of MPdk- virus, equivalent disaggregation of host polyribosomes is achieved with 40 PFU/cell and cannot be prevented by actinomycin D. The interpretation of these findings is based on data reported previously that the products specified by MPdk- virus in nonpermissive DK cells malfunction. We conclude that (1) in permissive cells the disaggregation of host polyribosomes is catalyzed by a highly efficient protein synthesized after infection; (2) in nonpermissive cells the protein malfunctions; to obtain comparable reduction in host functions the concentration of this protein must be higher in nonpermissive cells. This condition is satisfied by infecting nonpermissive cells at high multiplicity. (3) The reduction in synthesis or in function of this protein by the various drugs is sufficient to prevent the breakdown of host polyribosomes in nonpermissive cells but not in permissive cells.

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