Location: Biological Control of Insects ResearchTitle: Baculovirus replication induces the expression of heat shock proteins in vivo and in vitro) Author
Submitted to: Archives of Virology
Publication Type: Peer reviewed journal
Publication Acceptance Date: 1/10/2013
Publication Date: 6/29/2013
Citation: Breitenbach, J.E., Popham, H.J. 2013. Baculovirus replication induces the expression of heat shock proteins in vivo and in vitro. Archives of Virology. 158:1517-1522. Interpretive Summary: Understanding how an insect responds to stressors, such as microbial infection, is a fundamental step to developing novel means of controlling pest insects. Studying corn earworm larvae, we found the level of a messenger RNA that produces a specific heat shock protein increased in response to a fatal baculovirus infection in several different tissues of the caterpillar. A related but different heat shock gene did not respond to infection except in one tissue, very late during infection. No change in these genes was seen in larvae infected with a different baculovirus that did not cause a fatal infection. We also found these same gene responses in insect cells established from corn earworms. We have demonstrated that heat shock genes can have a different response to a virus in insects and cells based on how infective the virus is. These findings allow us to understand how different species of insects respond to baculovirus infection and can be expanded to enable the virus to control a wider range of pest insects. This work will impact scientists working on mechanisms by which an insect resists infection by a virus.
Technical Abstract: A recent handful of studies have linked baculovirus infection with the induction of heat shock proteins, a highly conserved family of cytoprotective proteins. Here, we demonstrate baculovirus-stimulated upregulation of hsp70 transcription in the natural host, Helicoverpa zea. Larvae lethally infected with the Helicoverpa zea single nucleopolyhedrovirus (HzSNPV) accumulated hsp70 transcripts throughout the 72 hour course of infection in the midgut, hemocytes, and fat body. While a maximal 20-fold induction of hsp70 was noted in the midgut and hemocytes, by 72 hours post infection, hsp70 transcription in the fat body of infected larvae was greater than two orders of magnitude over that of mock-infected larvae. These results were largely mirrored in cultures of infected cells, and a potentiation effect was observed in cells that were both heat shocked and infected. In contrast, neither Spodoptera frugiperda multiple NPV nor ultra-violet inactivated HzSNPV were able to stimulate hsp70 transcription in these experimentally non-permissive larvae and cell culture, respectively. Taken together, this report documents baculovirus-mediated upregulation of hsp70 in the natural host, and demonstrates the requirement for productive infection for hsp70 induction in vitro and in vivo.