Ebola virus (EBOV), a negative sense single stranded RNA virus of the Filoviridae family, is the pathogen behind episodic outbreaks of hemorrhagic fever. With mortality rates for infections often exceeding 50% and an outbreak currently underway in the DRC (As of June 2018), solidifying our understanding of Ebola virus pathogenesis is an urgent need. It is widely agreed that macrophages and dendritic cells, major players in the innate immune system, are the earliest cell types to sustain significant and persistent Ebola virus replication. Previous research in our lab has explored the impacts of macrophage polarization on infectability, but there is a dearth of research in the field with regard to dendritic cell infection. Multiple viruses, including SARS-CoV, measles, and Toscana virus, preferentially infect dendritic cells, harnessing their migratory capabilities to disseminate viral progeny throughout host tissue and lymphatics. The systemic nature of Ebola hemorrhagic fever suggests that EBOV may too employ this mechanism. My project seeks to address the underlying questions of this model, namely which DC populations are readily and productively infected and which receptor is used to initiate EBOV entry in these cell types.
Rogers KJ, Shtanko O, Stunz L Bohan D, et. al. CD40 signaling restricts RNA virus replication in macrophages, leading to rapid innate immune control of acute virus infection. Journal of Leukocyte Biology. In press, 2020. Selected as Leading Edge Research. Rogers KJ, Brunton B, Mallinger LL, Bohan D, et al. IL-4/IL-13 polarization of macrophages enhances Ebola virus glycoprotein-dependent infection. PLoS Negl Trop Dis. 2019;13(12):e0007819. Published 2019 Dec 11. doi:10.1371/journal.pntd.0007819
Honors and Awards
- Young Investigator Award, Autumn Immunology Conference (November 2018)
- Virology T32 Training Grant (June 2018 - June 2019)