Prostaglandin J (PGJ) was found to suppress dramatically Sendai virus replication in African green monkey kidney cells in culture. PGJ was not toxic at the active dose to uninfected cells and did not significantly inhibit macromolecular synthesis, but it specifically stimulated the synthesis of a polypeptide of 74000 mol. wt. In Sendai virus-infected cells, PGJ partially inhibited virus protein synthesis and caused an alteration in the mobility of the virus glycoprotein HN in SDS-PAGE, corresponding to a decrease of about 4000 in its mol. wt. We propose that the PGJ-induced alteration in the molecular structure of the HN protein prevents the insertion of this protein into the cell membrane thereby blocking virus maturation. The α,β-unsaturated carbonyl group in the cyclopentane ring of the PGJ molecule may be necessary for antiviral activity.


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