Tokarz, R., Firth C., Street, C., Cox-Foster, D. L., & Kipkin, W. I. (2011). Lack of Evidence for an association between Iridovirus and Colony Collapse Disorder. PLos One, 6(6), e21844.
Hunter, W., Ellis, J., Vanengelsdorp, D., Hayes, J., Westervelt, D., Glick, E., Williams, M., Sela, I., Maori, E., Pettis, J., Cox-Foster, D., & Paldi, N. (2010). Large-scale field application of RNAi technology reductin Israeli acute paralysis virus disease in honey bees (Apis mellifera, Hymenoptera: Apidae). PLos Pathogens, 6(12), e1001160.
Singh, R., Levitt, A. L., Rajotte, E. G., Holmes, E. C., Ostiguy, N., Vanengelsdorp, D., Lipkin, W. I., Depamphilis, C. W., Toth, A. L., & Cox-Foster, D. L. (2010). RNA viruses in hymenopteran pollinators: evidence of inter-Taxa virus transmission via pollen and potential impact on non-Apis hymenopteran species. PLoS One, 5(12), e14357.
McNeil, J., Cox-Foster, D., Slavicek, J., & Hoover, K. (2010). Contributions of immune responses to developmental resistance in Lymantria dispar challenged with baculovirus. Journal of Insect Physiology, 56(9), 1167-1177.
McNeil, J., Cox-Foster, D., Gardner, M., Slavicek, J., Thiems, S., & Hoover, K. (2010). Pathogenesis of Lymantria dispar multiple nucleopolyhedrovirus in L. dispar and mechanisms of developmental resistance. Journal of General Virology, 91, 1590-1600.
Willis, J. H., & Cox-Foster D. L. (2010). Insect metamorphosis via hybridogenesis: An evidentiary rebuttal. Journal of Insect Physiology, 56(4), 333-335.
Cox-Foster, D., & vanEngelsdorp, D. (2009). Saving the Honeybee. Scientific American, 300(4), 40-47.
Department Focus Areas:
- Disease Ecology and Biology
- Chemical Ecology
Research Interests :
Insect biochemistry and physiology; evolutionary development; molecular biology; host/pathogen interactions
Insect Structure and Function
Molecular Methods in Biology
Research Activities & Interests:
I am interested in the coevolution of insects with their pathogens and parasites and the role the insect immune system plays in this interaction. We have found that insect blood cells produce reactive oxygen species when they recognize and encapsulate a metazoan invader in a cellular immune defense. We have made unique contributions by demonstrating ROS can be actively generated in vitro following a specific challenge with immunoelicitors or pathogens. We have found that a unique GMC oxidoreductase enzyme, FAD-glucose dehydrogenase (GLD), has multiple roles in insects; this enzyme is essential for both molting and cellular immune responses in Drosophila. GLD is conserved across insects as demonstrated by gene homology, enzyme activity, and immunohistochemical reactions. My working hypothesis is that the molting and immune functions share common biochemical mechanisms and use different developmental regulatory mechanisms. Our current research is (1) characterizing the enzyme interactions using assays for electron transfer and subsequent free-radical formation; (2) investigating the regulation of gene expression in epidermis and immune system; (3) characterizing the receptor/ligand reactions involved in pathogen recognition; and (4) examining the cell-cell interactions and signaling pathways underlying this activation.
We are investigating the interactions of entomopathogenic nematodes and their insect hosts. We have evidence to suggest a coevolutionary battle between the insect immune system and the nematodes. We find that the degree of cellular recognition of the nematodes during the insect's cellular immune response correlates with the insect's susceptibility/resistance to the nematodes. We have also discovered that the nematodes produce anti-oxidative factors to counteract the ROS being produced by the insect blood cells and suggest that this may allow the nematode survival. Anti-oxidant factors have been reported in some parasitic nematodes that infect mammals, but this is a unique discovery for entomopathogenic nematodes. In collaboration with Rangy Gaugler, Elizabeth Cowles, Richard Cowles, and Christopher Brey, we are isolating surface coat proteins and their genes from Steinernema glaseri that knocks out the immune system of Japanese beetle grubs in a species-specific manner. We plan to transform this gene into Heterorhabditis bacteriophora, an entomopathogenic nematode that can be easily mass-reared, in order to create a more effective biological control agent for control of Japanese beetle larvae. We are also investigating the mechanism underlying suppression of the beetle immune system and determining the host-specificity of this action. Similar interactions between the insect and nematodes may underlie vector specificity for microfilaria.
In honeybees, we are investigating the interactions of a parasitic mite, RNA-viruses (picorna and discistronidae viruses), and other microbes. We have evidence that the parasitic mites are immunosuppressing the bees and causing activation of the viruses. Both cellular immune responses and NF-kappaB mediated antimicrobial peptide synthesis is impaired. Infection or presence of other pathogens may also stimulate the progression of the viral diseases. We are beginning to investigate the role of the mites and the viruses in collapse of honeybee colonies in collaboration with Liwang Cui and Nancy Ostiguy. Our research has also revealed new information on the transmission routes of the picorna-like viruses in bees, the persistence of these viruses in the bees, and the immune system of the honeybee. We are beginning to determine what proteins are present in the mite saliva, in order to determine how the mites are suppressing the immune reactions. In collaboration with Doug Cavener and Kaori Iida, we have isolated the genes for several genes involved in honeybee immunity.
Not all invaders are met with a well-defined immune response, as during disease transmission by insect vectors. Understanding the mechanisms that underlie co-evolution between the vector and disease organism is critical to understanding how the disease transmission cycle might be disrupted. Through interdisciplinary collaboration with Drs. F. Gildow (PSU) and S. Gray (Cornell), we are examining the mechanisms underlying virus/vector specificity in aphids at the accessory salivary gland, the primary site determining transmission of different species of luteoviruses. In my lab, we have identified several proteins that bind to luteovirus in a vector-specific manner and that are also recognized by antibodies that mimic the virus. We are isolating the genes encoding these proteins for studies of the evolution of these virus/vector interactions, among different aphid and viral species. This research may further understanding of mechanisms underlying the vector-specificity of mosquitoes for transmission of alphaviruses.