Ultraviolet-irradiated vesicular stomatitis virus and defective-interfering particles are similar non-specific inhibitors of virus infection.
The way in which ultraviolet-irradiated vesicular stomatitis virus (VSV) inhibits the early events in VSV infection has been further characterized. Comparison of several different u.v.-irradiated thermolabile, temperature-sensitive mutants before and after heat inactivation established a requirement for inhibitory activity of functional G, N and L proteins, but not M protein. Defective-interfering (DI) particles, whether irradiated or not, inhibited VSV primary transcription as efficiently as UV-VSV, suggesting that virus proteins rather than transcription products are responsible for inhibition. Addition of inhibitory UV-VSV at different times after infection established that inhibition results from an action at an intracellular site, rather than at the cell surface or in the process of internalization. A similar inhibition by UV-VSV of infection by Sendai virus, Semliki Forest virus, Sindbis virus and influenza virus suggests that UV-VSV is acting by inducing a general change in the intracellular environment.
D000818:Animals; D002213:Capsid / Q000502:physiology; D002460:Cell Line; D006224:Cricetinae; D003673:Defective Viruses / Q000502:physiology*; D014158:Transcription, Genetic; D014466:Ultraviolet Rays; D014721:Vesicular stomatitis Indiana virus / Q000502:physiology* / Q000528:radiation effects; D014762:Viral Interference; D014764:Viral Proteins / Q000502:physiology*
D014764:Viral Proteins