The incorporation of [32P]Pi and [3H]
inositol into the
inositol lipids of baby-hamster kidney cells was studied in herpes-simplex-virus-type-1(HSV-1)-infected and mock-infected cells. The
infection was conducted during incorporation of, as well as after prelabelling with, the precursors. These methods were used in order to study both synthesis de novo of, and steady-state changes in, the
phosphoinositides. Both with
infection during labelling, and after prelabelling, we found increased [32P]- and [3H]-
phosphatidylinositol 4,5-bisphosphate (PIP2) and decreased [32P]- and [3H]-
phosphatidylinositol 4-monophosphate in infected as compared with mock-infected cells, whereas no effect was observed on
phosphatidylinositol. This altered
inositol-lipid metabolism was (at least in the case of PIP2) not present until 3-6 h after
infection and remained stable, or increased slightly, throughout the
infection period.
Polyphosphoinositide metabolism constitutes an important step in signal processing in many forms of cellular stimulation, and the results obtained suggest that HSV-1
infection may induce such events in our cell system.