Alternate pathway of entry of budded Autographa californica nuclear polyhedrosis virus: fusion at the plasma membrane.

Recently we reported that the budded phenotype of Autographa californica nuclear polyhedrosis virus (AeNPV BV) functionally entered IPLB-SF-21 cells by adsorptive endocytosis and that neutralizing monoclonal antibody AcV1 acted by preventing AcNPV BV from using this entry pathway (L. E. Volkman and P. A. Goldsmith (1985), Virology 143, 185-195). Not all infectivity could be neutralized by AcV1, however, and in the study reported herein we investigated the nature of the particles responsible for this residual infectivity, and obtained evidence for an alternate entry pathway for both AcNPV BV and AcV1 treated BV. Residual infectivity was shown to be due to AcV1 linked AcNPV BV and not aberrant particles lacking the AcV1-reactive BV epitope. We obtained evidence that entry by fusion at the plasma membrane, but not phagocytosis, appeared to be an additional, functionally less efficient entry pathway. Fusion was indicated by the detection of viral envelope antigen in the host cell plasma membrane by immunoelectron microscopy. Fusion occurred even at 4 degrees , which was unexpected and highly unusual. Treatment of cells with cytochalasin B inhibited phagocytosis but did not reduce BV infectivity.