Pathogens and parasites are fascinating creatures that can have very complicated and subtle relationships with their hosts. These relationships can also be life and death simple—think about an individual fly’s struggle to encapsulate and kill the parasitoid wasp larva living inside it. The important thing to remember is that there is an ongoing struggle between the host and its pathogens. These struggles, however, are not purely host vs. disease. There is a subtle play for dominance that creates strange bedfellows—interactions that are every bit as complicated as any political climate you might imagine. For example, consider the many mosquito specific viruses that cause disease in mosquitoes. This would seem to be a pretty clear-cut situation of disease equals good, at least from a human perspective. What complicates this story is the fact that many mosquito specific viruses inhibit the replications of arboviruses (viruses that infect people but are carried by mosquitoes) like West Nile or Chikungunya. This has led to lines of investigation considering using viruses for controlling the movement of vector borne diseases through the vector population. See? It’s a complicated world inside an insect.

I am a graduate student in the Entomology department, and I am interested in the ecology and evolution of insect disease. How do pathogens move through the populations they exist within? How does the insect immune system influence the evolution of pathogens and how do those same pathogens influence the evolution of the immune system? What can an insect’s immune response to a pathogen tell us about how the insect immune system works? The other main question I have is: How do pathogens evolve toward higher or lower virulence depending on the conditions they exist in?

I cut my teeth in the field. I worked on evolution of guppies in Trinidad, examined endosymbiont ecology in Colorado, looked at how spiders walk, and  studied population biology of grizzly bears in Montana while living in a tent for six months. I cannot think of a greater privilege than to get paid to learn something outside in the natural world. That said, I have also done a fair bit of laboratory bench research from studying the population dynamics of yeast evolution to drug discovery in Human African Trypanosomiasis.

I am interested in harnessing molecular biology tools to answer questions about how pathogens shape the evolution of their host’s immune system in the field. I am also interested in how those same insect immune systems shape the evolution of pathogens. In short, I try to combine laboratory techniques with field ecology questions.

To that end, my project involves looking at a behavior putatively induced by a virus. Geocoris pallens, a beneficial insect in cotton and alfalfa, are eating their own eggs at prodigious rates. We have a fair bit of evidence that suggests that this increase in egg cannibalism (they always eat some of their eggs) is the result of a viral infection. Basically, the virus turns the poor Geocoris into zombies. To discover what this virus is and whether it actually is causing the ‘zombie’ phenotype I am using a variety of techniques from RT-qPCR to RNAseq to look at all of the viruses inside my bugs, the viriome,  to see whether we can suss out if there is an association between one or more of these viruses and the cannibalism we have been observing over the last couple of years.

I welcome questions and collaborations. If you are interested in either shoot me a note. My email is:


Jensen, BC. Booster, NA. Vidadala, RSR. Maly, DJ. Parsons, M. A novel protein kinase is essential in bloodstream Trypanosoma brucei. 2016. International Journal of Parasitology.

Booster, NA. Su, FM. Adolph, SA. Ahn, AN. Effect of temperature on leg kinematics in sprinting tarantulas (Aphonopelma hentzi): high speed may limit hydraulic joint actuation. 2015. Journal of Experimental Biology