Prostaglandins of the A series were found to strongly suppress the replication of vesicular stomatitis virus (VSV) in mouse L fibroblasts. The highest non-toxic dose of PGA, 4 µg/ml, decreased VSV production by 93.6%. At this dose, PGA did not alter DNA, RNA or protein synthesis in uninfected L cells for periods up to 24 h, whereas it further suppressed protein synthesis and slightly increased RNA synthesis in VSV-infected cells. The presence of PGA during virus adsorption, with no treatment after infection, reduced VSV yields by 63.6%. However, the presence of PGA during an early step of VSV replication was not essential for the antiviral action to occur (PGA treatment could be started 1 to 2 h post-infection). Apart from a slight overall inhibition of virus protein synthesis, PGA strongly suppressed the synthesis of the VSV glycoprotein G; moreover, it produced an alteration in the mobility of this protein in SDS-polyacrylamide gels. We propose that this slight decrease in molecular weight (about 4000) of the G protein in the presence of PGA could be due to an alteration in the glycosylation process.

Keyword(s): G protein , PGA1 and VSV

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