Coxsackie B1 virus infection enhances the susceptibility of cultured HEp-2 cells to Shigella flexneri invasiveness. This can be reproduced partially with UV-inactivated virus, particularly the effect observed shortly after viral inoculation. The following phases of viral multiplication were correlated with the enhancing effect: uncoating of viral particles, synthesis of viral RNA and proteins, and assembly of newly produced virus particles. Uncoating of virus particles was completed within 60 min. This process was not correlated with the development of the early effect on invasiveness. Intact virus capsids seem to be necessary to enhance bacterial invasiveness in the early phase of virus infection. Separated capsid proteins had no effect either when applied to the cell surface or when microinjected into the cells. Virus protein synthesis was not required for the virus effect on bacterial invasiveness in the early infection phase, but it seems to be necessary in the late phase.
|Number of pages||8|
|Journal||APMIS. Journal of pathology, microbiology and immunology|
|Publication status||Published - Jan 1992|
- Coxsackie B1 virus
- Shigella flexneri
- viral replication