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The mechanism of N-methyl-izat in-thiocarbazone (methisazone, Mel ВТ) antiviral activity has been studied on Ad 1-infected HEp2 and HeLa cells. Mel ВТ did not induce interferon and did not directly inhibit viral and cell translation. The adenoviral infection was not affected by recombinant human interferon a2 (rIFN). Mel ВТ showed antiviral effect in AdI-infected HEp2 or HeLa cells when rIFN had added to HeLa cells or in the period of interferon induction during virus infection (in HEp2 cells). In the presence of this compound, the El A transcription was unchanged in infected cells as compared to untreated control, while early transcription was decreased, the beginning of viral replication being retarded. Futhermore, the VAI RNA synthesis was also greatly suppressed. These effects were independent on interferon treatment and disappeared when MeIВТ had been added during the late phase of virus growth cycle. Actually, MeIВТ can induce the delay of VAI RNA transcription promoting interferon antiviral effect

biopolymers and cell

Aromatic thiosemicarbazones, their antiviral action and interferon. 1. The decreasing of adenovirus type 1 resistance against interferon by methisazone in vitro