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Prostaglandin A inhibits replication of human immunodeficiency virus during acute infection

Helmut Ankel

Institute of Virology, University ‘La Sapienza’, Viale di Porta Tiburtina 28, 00185 Rome, Italy

An antiviral effect of prostaglandins (PGs) of the A series on the replication of human immunodeficiency virus (HIV) has been determined. In the T cell line C8166 under single growth cycle conditions, PGA₁ reduced the number of infectious progeny 1000-fold in the absence of cytotoxicity. Thus, inhibition of HIV replication by PGA₁ represents a true antiviral phenomenon. The number and size of virus-induced syncytia, and the amount of viral antigen were also drastically reduced. The effect was specific for PGAs because PGA₂ was also inhibitory, whereas PGB₁, PGE₁ and PGE₂ were inactive. Virus adsorption and penetration do not appear to be targets of antiviral action because PGA₁ substantially reduced virus replication, even when added 5 h post-infection. PGA₁ did not inhibit viral reverse transcriptase, as determined by in vitro assays, suggesting that its antiviral action is not the consequence of a direct inhibitory effect on this enzyme. PGA₁ also inhibited the replication of HIV-1 in CEM x 174 cells, but with less potency. Previously, intravenous infusion of PGA₁ into human volunteers has shown no significant deleterious side-effects and thus these observations suggest that PGAs might have potential as antiviral agents in humans.

Present address: Department of Biochemistry, Medical College of Wisconsin, Milwaukee, Wisconsin 53226, U.S.A.

Received 12 April 1991; accepted 15 July 1991.