RESPONSES OF INSECT CELLS TO BACULOVIRUS INFECTION - PROTEIN-SYNTHESIS SHUTDOWN AND APOPTOSIS

Protein synthesis is globally shut down at late times postinfection in the baculovirus Autographa californica M nuclear polyhedrosis virus ( AcMNPV)-infected gypsy moth cell line Ld652Y. A single gene, hrf-1, fr om another baculovirus, Lymantria dispar M nucleopolyhedrovirus, is ab le to preclude protein synthesis shutdown and ensure production of AcM NPV-progeny in Ld652Y cells (S, JI. Thiem, S, Du, hi, E, Quentin, and M. RI, Berner. J. Virol. 70:2211-2329, 1996; S, Du and S, M. Thiem, Vi rology 227:420-430), 1997), AcMNPV contains a potent antiapoptotic pen s, p35, and protein synthesis arrest,vas reported in apoptotic insect cells induced by infection with AcMNPV lacking p35, In exploring the f unction of host range factor, 1 (HRF-1) and the possible connection be tween protein synthesis shutdown and apoptosis, a series of recombinan t AcMNPVs with different complements of p35 and hrf-1 were employed in apoptosis and protein synthesis assays, We found that the apoptotic s uppressor AcMNPV P35 was translated prior to protein synthesis shutdow n and functioned to prevent apoptosis, HRF-1 presented protein synthes is shutdown even when the cells were undergoing appptosis, but HRF-1 c ould not functionally substitute for P35. The DNA synthesis inhibitor aphidicolin could block both apoptosis and protein synthesis shutdown in Ld652Y cells infected with p35 mutant AcMNPVs but not the protein s ynthesis shutdown in wild type AcMNPV-infected Ld652Y cells, These dat a suggest that protein synthesis shutdown and apoptosis are separate r esponses of Ld652Y cells to AcMNPV infection and that P35 is involved in inducing a protein synthesis shutdown response in the absence of la te viral gene expression in Ld652Y cells, A model was developed for th ese responses of Ld652Y cells to AcMNPV infection.