Prostaglandin A inhibits the replication of vesicular stomatitis virus: effect on virus glycoprotein.
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 PGA1, 4 micrograms/ml, decreased VSV production by 93.6%. At this dose, PGA1 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 PGA1 during virus adsorption, with no treatment after infection, reduced VSV yields by 63.6%. However, the presence of PGA1 during an early step of VSV replication was not essential for the antiviral action to occur (PGA1 treatment could be started 1 to 2 h post-infection). Apart from a slight overall inhibition of virus protein synthesis, PGA1 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 PGA1 could be due to an alteration in the glycosylation process.
D000818:Animals; D004247:DNA / Q000096:biosynthesis; D004305:Dose-Response Relationship, Drug; D007739:L Cells; D008562:Membrane Glycoproteins; D051379:Mice; D008970:Molecular Weight; D011454:Prostaglandins A / Q000494:pharmacology*; D014176:Protein Biosynthesis; D012313:RNA / Q000096:biosynthesis; D014721:Vesicular stomatitis Indiana virus / Q000187:drug effects* / Q000502:physiology; D014759:Viral Envelope Proteins; D014764:Viral Proteins / Q000096:biosynthesis*; D014779:Virus Replication / Q000187:drug effects
C028391:G protein, vesicular stomatitis virus; D008562:Membrane Glycoproteins; D011454:Prostaglandins A; D014759:Viral Envelope Proteins; D014764:Viral Proteins; D012313:RNA; D004247:DNA; C100573:prostaglandin A1