ARS | Publication request: HSP70 induction during baculovirus infection

Submitted to: Society for Invertebrate Pathology Meeting
Publication Type: Abstract Only
Publication Acceptance Date: May 29, 2012
Publication Date: August 9, 2012
Citation: Breitenbach, J.E., Popham, H.J. 2012. HSP70 induction during baculovirus infection [abstract]. Society for Invertebrate Pathology Meeting. p. 127.

Technical Abstract: Baculoviruses are arthropod-specific double-stranded DNA viruses that have been employed as bio-insecticides against crop pests and to produce heterologous proteins in baculovirus expression systems. Although a consensus has emerged on the dominant molecular events driving baculovirus replication in vitro, little is known regarding the host-virus interplay in the infected insect. In our previous work, RNA-seq and 2d gel analysis revealed that the inducible 70kDa heat shock protein (hsp70) was among those cellular proteins most up-regulated following productive baculovirus infection. Transcription of hsp70 is triggered during cellular stress in an hsf-1-dependent fashion, a stress-related transcription factor we have also detected as induced following baculovirus infection. Due to its role in promoting protein sorting and proper folding, we hypothesized that baculoviruses may benefit from the presence of hsp70 during late times of infection, owing to overwhelming translation of viral proteins and their subsequent trafficking through the endoplasmic reticulum. In the present study, insects that were either permissive or non-permissive for infection revealed that induction of hsp70 was dependent on viral replication. In vivo experiments analyzing virus infection demonstrated a progressive induction of hsp70 over time, culminating in the greatest expression in the fat body prior to the death of the host, a somewhat surprising finding given that the midgut is source of primary infection. These studies add to a growing body of evidence suggesting a method by which baculoviruses may have evolved to subvert host cellular processes to promote efficient viral propagation.