Inhibition of Bombyx mori nuclear polyhedrosis virus (NPV) replication by the putative DNA helicase gene of Autographa californica NPV.

Abstract

Coinfection of Bombyx mori nuclear polyhedrosis virus (BmNPV) with Autographa californica NPV (AcNPV) in the BmNPV-permissive BmN cell line resulted in the complete inhibition of BmNPV replication. Coinfected BmN cells exhibited an atypical cytopathic effect (CPE) and synthesis of viral and host proteins was dramatically attenuated by 5 h postinfection (p.i.) and nearly completely blocked by 24 h p.i. Viral transcription, however, appeared to occur normally during both early (5-h-p.i.) and late (24-h-p.i.) stages of infection. Superinfection of BmN cells with AcNPV at 5 and 12 h post-BmNPV infection resulted in limited inhibition of BmNPV replication. BmN cells singly infected with AcNPV also showed similar CPE, premature inhibition of viral and host protein synthesis, and apparently normal viral transcription. BmNPV replication occurred normally following coinfection of BmNPV and eh2-AcNPV, an AcNPV mutant identical to AcNPV except for a 572-bp region in its putative DNA helicase gene originating from BmNPV (S. Maeda, S. G. Kamita, and A. Kondo, J. Virol. 67:6234-6238, 1993). Furthermore, atypical CPE and premature attenuation of host and viral protein synthesis were not observed. These results indicated that the inhibition of BmNPV replication was caused either directly or indirectly at the translational level by the putative AcNPV DNA helicase gene.