Interferon induces the production of membrane protein-deficient and infectivity-defective vesicular stomatitis virions through interference in the virion assembly process.
The reduced rate of synthesis, maturation and degradation as well as the level of accumulation of the intracellular virus proteins in VSV-infected cells may account for the overall reduction (less than 10-fold) of progeny virion yield due to interferon (IFN); however, the deficiency of the virions proteins, G and M, which apparently caused a drastic loss of infectivity of these progeny virions (about 1000-fold) cannot be easily explained, because the concentrations of G and M proteins relative to other virus proteins were not reduced in the cell. In fact, intracellular M protein was significantly increased. Moreover, the virus proteins in IFN-treated and control cells were synthesized and accumulated in large excess of the amount incorporated into the released virions. The reduction in the intracellular activity of GlcNac-P-P-Dol transferase did not appear to play a direct role in the antiviral mechanism in this system. Our results, however, do suggest that the deficiency of G and M proteins in the virion is related to specific inhibition of the incorporation of either or both of these proteins in the virus assembly process.
D007372:Interferons / Q000494:pharmacology*; D008562:Membrane Glycoproteins; D014721:Vesicular stomatitis Indiana virus / Q000187:drug effects*; D014759:Viral Envelope Proteins; D014763:Viral Matrix Proteins; D014764:Viral Proteins / Q000037:antagonists & inhibitors*; D014779:Virus Replication / Q000187:drug effects
C028391:G protein, vesicular stomatitis virus; D008562:Membrane Glycoproteins; D014759:Viral Envelope Proteins; D014763:Viral Matrix Proteins; D014764:Viral Proteins; D007372:Interferons