POSSIBLE MECHANISM OF ROTAVIRUS PERSISTENCE

Abstract

Infection of BSC-1 cells with bovine rotaviruses usually results in a cytolytic infection. This communication describes virus:cell interactions in cells persistently infected with a bovine rotavirus. Viral persistence does not adversely affect these cells (RP-BSC-1 cells) which grow at a rate comparable to that of uninfected cells. In addition, RP-BSC-1 cells continuously produce Rotavirus and are immune to super-infection with related viruses. To further characterize virus:cell interactions during persistent infections, viral expression was examined in synchronized RP-BSC-1 cells. Viral expression was limited to mid and late G1 when 80% of cells exhibited viral antigens detectable by immunofluorescence and PAGE. Entry into S-phase caused a degradation of viral proteins and a sharp decline in viral expression. Degradation was probably brought about by factors synthesized in S-phase as exponentially growing BSC-1 cells yielded predominantly incomplete virus particles. The results suggest that some strains of rotavirus are unable to shut-down host macromolecular synthesis and therefore can only replicate in certain permissive phases of the cell cycle. As the infected cell traverses from ‘G1’ into the ‘S’ phase of the cell cycle, viral replication and viral gene expression ceases, only to resume when the cells re-enter a permissive phase.