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1 Center of Virology, CNR, OO.RR., Via Circonvallazione Gianicolense 85, Rome, Italy
2* Department of Surgery
and3 Department of Biochemistry, S.U.N.Y. Downstate Medical Center, 450 Clarkson Avenue, Brooklyn, New York 11203, U.S.A.
and4 Institute of Microbiology, School of Medicine, University of Rome, Rome, Italy
Prostaglandins of the A series potently inhibited the production of vaccinia virus in mouse L fibroblasts. With the highest non-toxic dose of PGA1, 4 µg/ml, the replication of the virus was inhibited by 95.3%. The antiviral activity was dose-dependent and specific for the A series. At the dose used, PGA1 was not toxic to uninfected cells and did not alter cell metabolism as measured by DNA, RNA and protein synthesis. PGA1 did not influence the adsorption of the virus by the host cells and the antiviral activity was not dependent on the presence of PGA1 during the early stages of infection. PGA treatment delayed and partially inhibited virus DNA synthesis and, while it did not produce any change in the pattern of protein synthesis in uninfected cells, it altered both the rate and the pattern of virus protein synthesis. We conclude that PGA1 selectively inhibits one or more steps involved in the replication of vaccinia virus in mouse L fibroblasts.
Keywords: prostaglandin, vaccinia virus, virus replication, virus proteins
Received 22 February 1982;
accepted 30 June 1982.
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