Mutations within the Autographa californica Nucleopolyhedrovirus FP25K Gene Decrease the Accumulation of ODV-E66 and Alter Its Intranuclear Transport

• DOI: 10.1128/jvi.73.10.8559-8570.1999
• Publication Date: 2019-12-31T18:20:13Z
• Authors: Sharon C. Braunagel; Jared K. Burks; German Rosas-Acosta; Robert L. Harrison; H. Ma; M. D. Summers
• Keywords: Autographa californica

ABSTRACT Previous reports indicate that mutations within the Autographa californica nucleopolyhedrosis virus FP25K gene (open reading frame 61) significantly reduce incorporation of enveloped nucleocapsids into viral occlusions. We report is a nucleocapsid protein both budded (BV) and occluded (ODV), we describe effects two (480-1 [N-terminal truncation] FP-βgal [C-terminal fusion]) on expression cellular localization ODV-E66 ODV-E25. Significantly decreased amounts are detected in cells infected with 480-1 or mutants, even though during infection, steady-state levels transcripts remain unchanged. While normally intranuclear microvesicles ODV envelopes by 24 h postinfection (p.i.), remains cytosolic throughout infection (up to 96 p.i.), its not until p.i. mutant virus. The nuclear ODV-E25 affected mutant; however, trafficking delayed mutant. Temporal Western blot analyses cell lysates show infections result altered accumulation patterns several structural proteins, including gp67, BV/ODV-E26, major capsid p39. In addition gp67 may interact FP25K, p39 also be components complex containing FP25K. Together, these data suggest associated complex(es) play an important role targeting intracellular transport proteins infection.