Prostaglandins (Pgs) have been shown to inhibit the replication of several DNA and RNA viruses. Here we report the effect of prostaglandin (PgA1) on the multiplication of a positive strand RNA virus, Classical Swine Fever Virus (CSFV) in PK15 cells. PgA1 was found to inhibit the multiplication of CSFV. At a concentration of 5 µg/ml, which was nontoxic to the cells, PgA1 inhibitis virus production in 99%. In PgA1 treated cells the size and number of characteristic Classical Swine Fever focus decreased in amount.

Prostaglandin A1 (PGA1) inibe a replicação do vírus Mayaro em células de Aedes albopictus em doses não tóxicas para células não infectadas. A presença de PGA1 durante o período de adsorção, reduz a produção do vírus em 41%. A atividade antiviral é observada mesmo quando o tratamento é iniciado com 1 ou 2 horas após a infecção. Entretanto, em células pré-tratadas com PGA1 durante 24 h a replicação viral é inalterada. A análise das proteínas marcadas com 35S-metionina, por eletroforese em gel de poliacrilamida, mostra que a PGA1 inibe a síntese de proteínas virais e induz a síntese de polipeptídeos com peso molecular de 70 Kda, 57 Kda e 23 Kda. Em células pré-tratadas com actinomicina D observa-se um bloqueio da atividade antiviral, indicando que as proteínas de estresse induzidas pela PGA1 estão envolvidas neste mecanismo.

Prostaglandin A1 (PGA1) inhibits Mayaro virus replication in Aedes albopictus cells at nontoxic doses to uninfected cells. At 10 µg/ml, PGA1 decreases virus production by 90%. The presence of PGA1 during virus adsorption, with no treatment after infection, reduces virus yield by 41%. Antiviral activity is observed even when treatment starts at one or two hours post-infection. However, in cells pre-treated with PGA1 during 24 hours, virus replication is not impaired. Thus, events ocurring during initial stages of infection and after virus adsorption and penetration must be the target of PGA1 action. SDS-PAGE analysis of 35S-methionine labelled proteins shows that PGA1 inhibits the synthesis of viral proteins and induces the synthesis of polypeptides with molecular weight of 70 kDa, 57 kDa and 23 kDa. In cells pre-treated with actinomycin D the induction of those proteins is suppressed. In addition, actinomycin D treatment prevents PGA1antiviral activity, indicating that PGA1-induced stress proteins are probably involved in this mechanism.