Treatment of virally infected cells in culture with prostaglandins of the A-series (PGA) prevents replication of RNA and DNA viruses. The antiviral effect is independent of host cell transcription and unrelated to antiviral effects that are caused by interferons. It is the aim of this research to understand antiviral action of PGAs at the molecular level. Specifically the following questions are raised and will be answered: At what level of virus assembly do PGAs act? What are the active species, the PGAs themselves or their metabolites? The RNA viruses Encephalomyocarditis and Vesicular stomatistis will be investigated, since both are highly sensitive to antiviral action of PGAs. Both virions have been studied intensely in the past and much is known about their morphogenesis from early to late events. Both, on the other hand, are fundamentally different in the individual steps that are involved in the formation of infectious progeny. Thus results pertaining to the mechanism of inhibition of both will complement each other and allow conclusions in favor of a common mechanism of inhibition, or separate ones, each specific for each virus. Suitable antiviral drugs are rare. Since a desirable drug should have the ability to block viral replication after infection has occurred, it is important to understand the mechanism of action of a drug that acts like PGA. This knowledge should suggest new chemical approaches to synthesize PGA analogs that have retained antiviral properties, yet lack those side effects that make PGA unsuited for general clinical use.
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| Ankel, H; Capobianchi, M R; Castilletti, C et al. (1994) Interferon induction by HIV glycoprotein 120: role of the V3 loop. Virology 205:34-43 |
| Parker, J; Ankel, H (1992) Formation of a prostaglandin A2-glutathione conjugate in L1210 mouse leukemia cells. Biochem Pharmacol 43:1053-60 |
| Bader, T; Ankel, H (1990) Inhibition of primary transcription of vesicular stomatitis virus by prostaglandin A1. J Gen Virol 71 ( Pt 12):2823-32 |
